August Digest
This Month in Cervical Cancer Research
August 2026
August’s cervical cancer research kept returning to the same uncomfortable fact: this is a disease that vaccination and screening can largely prevent, and most of the month’s work was about why the tools we have are not reaching everyone. The strongest thread ran through screening. A network meta-analysis pulled together the trial evidence on one-dose and two-dose HPV vaccine schedules and found reduced-dose regimens retain meaningful protection against persistent infection, which matters enormously for countries that cannot afford three doses. Two studies from Finland and Mexico showed that knowing which HPV type a woman carries, rather than just that she carries one, sharpens who needs a colposcopy now and who can safely wait. A ten-paper collection tackled the question that follows from vaccination’s success: how screening itself has to change once vaccinated women reach screening age, and its answer was more practical than expected. On the treatment side, first-line immunotherapy combinations for recurrent and metastatic disease produced two sets of early results, and a French analysis began to describe which patients get lasting benefit from checkpoint inhibitors and which do not. Running underneath was a set of studies on access: cervical cancer care in sub-Saharan Africa, the overlap between HIV and late-stage diagnosis at a referral hospital in South Africa’s Eastern Cape, and a screening laboratory in Ukraine that held its diagnostic quality through four years of war.
The papers highlighted here represent a selection of those published during the month. The papers were selected and summarized by AI. Accuracy of the summaries was confirmed by a scientist. This digest incorporates only open-access research articles that are free to be read by the entire community and that are explicitly licensed to be shared and reused.
Immunotherapy combinations are now the first thing tried when cervical cancer comes back or spreads, and this month brought early results on how they perform.
Immune checkpoint inhibitors are drugs that release a brake the cancer has put on the immune system, letting immune cells attack the tumor. Combined with chemotherapy and bevacizumab, a drug that blocks the blood-vessel growth tumors depend on, they have changed what is possible in recurrent and metastatic disease.
• A newer checkpoint inhibitor added to chemotherapy and bevacizumab shrank tumors in three quarters of people receiving it as first treatment for recurrent or metastatic cervical cancer. ASTRUM-CC01 was a multicenter single-arm phase 2 trial in China enrolling 48 people who had not previously had systemic treatment for their recurrent or metastatic disease, though 37 of the 48 (77%) had received chemotherapy earlier as part of their initial treatment. They had four to six cycles of serplulimab plus a bevacizumab biosimilar with cisplatin and paclitaxel, then serplulimab and the biosimilar as maintenance. Of the 48 enrolled, 75% had their tumors shrink (95% confidence interval 60 to 86%) and 90% had disease that at least stopped growing; the missing 10% left the trial before their first scan rather than progressing, and counting only the 43 who were actually scanned the figures were 84% and 100%. Median time before progression was 21.2 months, but that estimate is immature: the range runs from 14.4 months upwards with no firm ceiling, fewer than half had progressed at the cut-off, and median follow-up was 20.1 months. Severe (grade 3 or higher) side effects occurred in 21 of the 48 (44%), including severe fistulas in 5 (10%), a known risk of anti-angiogenic drugs in this setting. This is a single-arm trial with no comparison group, so the response rate cannot be read as better than existing options; the authors present it as grounds for a phase 3 trial. (Read the full paper)
• A two-target immunotherapy drug given at a lower dose than its label produced a 55.6% response rate in a real-world series, which matters where cost decides who gets treated, but no full-dose comparison was made. Cadonilimab is a bispecific antibody blocking two immune brakes at once, PD-1 and CTLA-4, and its price limits access in low- and middle-income countries. Researchers at Sichuan Cancer Center reviewed 137 people given cadonilimab at 6 mg/kg every three weeks as first-line therapy between January 2023 and September 2025, added to platinum-based chemotherapy, with bevacizumab in 70% of them. Among the 133 evaluable for response, 55.6% had tumors shrink, including 10.5% whose disease disappeared on imaging, and 83.5% had disease that at least stopped growing. An estimated 92.1% were alive at 12 months (95% confidence interval 86.5 to 98.0%), after a median of only 11 months of follow-up. Two things need saying plainly. There was no standard-dose group, and the authors state that this precludes any direct comparison with the approved regimen; they also note their 55.6% is numerically lower than the 79.3% reported with the standard 10 mg/kg dose in earlier work. And the safety picture is not uniformly reassuring: grade 3 or higher treatment-related events affected 78.8%, mostly low blood counts and largely attributable to the chemotherapy, while immune-related myocarditis occurred in 5.1%, which the authors call higher than in the registration data, and 10.9% stopped the drug permanently because of immune side effects. This is a retrospective single-center series, not a comparison of doses. (Read the full paper)
• Roughly one in five people in this series got lasting benefit from checkpoint inhibitors, but the series is mostly a phase 1 trial population, so the figure is not a general expectation. Researchers at Gustave Roussy in France looked back at 106 people with metastatic cervical cancer treated with checkpoint inhibitors between January 2015 and September 2023, 88% of them within clinical trials and mostly phase 1 studies of experimental combinations; fewer than half (47 of 106) received a checkpoint inhibitor on its own, and 83% had already had chemotherapy for metastatic disease. Long-term response was defined as tumor shrinkage or stable disease lasting more than 12 months, and 20 people (19%) met it. Median time without progression was 3.5 months in the other 86 and had not been reached in the long-term responders after a median 42 months of follow-up; 11 of the 20 stayed in response after stopping treatment, for a median of 22 months. Three clinical features were independently associated with long-term response: disease limited to two or fewer sites, spread confined to lymph nodes, and progression outside a previously irradiated area. The estimates are directionally clear but very imprecise, with odds ratios of 8.2 and 11.4 whose ranges extend past 50. Tumor mutational burden and mismatch repair status did not distinguish the groups, and PIK3CA mutations were more common in responders while STK11 alterations were more common in the rest, all of which rests on the 43 of 106 patients who had tumor sequencing, only 10 of them responders. This is a retrospective single-center analysis pointing at the kind of patient in whom a durable response is realistic, not a selection rule. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
For cervical cancer that has grown beyond the cervix but not spread to distant organs, chemoradiation remains the treatment, and the open questions are about what to add and what it costs the body.
Locally advanced cervical cancer is treated with radiation to the pelvis plus internal radiation called brachytherapy, given alongside chemotherapy. It cures many people, and this month’s research looked at both ends of that: whether adding more chemotherapy afterwards helps, and what the radiation does to bone.
• Adding chemotherapy after chemoradiation did not significantly improve survival for stage III cervical cancer in this small study, and its prognostic findings are too thin to act on. Researchers in Guangdong, China retrospectively compared 33 people who had chemoradiation alone with 39 who also received chemotherapy afterwards, all with 2018 FIGO stage III disease treated between May 2018 and May 2024; those 72 were what remained after 150 of 222 eligible patients were excluded, which the authors say may introduce considerable selection bias. Three-year overall survival was 79.5% with the extra chemotherapy against 63.6% without, and progression-free survival 56.4% against 45.5%. Neither difference was statistically significant, and with 72 patients a real difference either way could easily have been missed; survival was numerically better with the extra chemotherapy, so this is not evidence that it does not help. Severe toxicity showed no significant difference between the groups, though grade 3 to 4 neutropenia and anaemia were numerically more common with the extra chemotherapy and the authors flag those trends. The paper’s two prognostic signals need heavy qualification. Larger positive lymph nodes (10 mm or more, among the 55 patients who had nodal disease) tracked with earlier progression, but the overall-survival estimate was so imprecise that it did not exclude no effect at all. And the squamous cell carcinoma antigen finding rests on four patients: the marker was measured only in the 60 people with squamous carcinoma, only four had a level above 1.5 ng/mL after brachytherapy, and all four happened to be in the no-adjuvant-chemotherapy group, so the marker is entangled with treatment allocation. The authors describe these findings as hypothesis-generating, and that is the right reading. (Read the full paper)
• Small pelvic fractures show up in about one in six women after definitive chemoradiation for cervical cancer, more often than most people are told. Radiation weakens bone, and the resulting insufficiency fractures can cause pain months to years after treatment. Researchers at a Rome hospital retrospectively reviewed 202 women with locally advanced disease treated with definitive chemoradiation followed by brachytherapy, contoured the pelvic bone marrow into three regions, and recorded how much of each received 10, 20, 30 and 40 Gy. Women treated with surgery and post-operative radiation were explicitly excluded, so these figures do not apply to adjuvant pelvic radiation after an operation. Thirty-six women (17.8%) developed a fracture within the treated area, and most had no symptoms from it; pain was reported in 12 of the 36. The authors say plainly that their follow-up was neither uniform nor long enough to establish a true incidence, and that published estimates range from 10% to 29%. Age was the stronger risk factor, while the volume of the lower pelvis receiving 40 Gy was borderline, and the two combined gave only modest risk discrimination. This is a retrospective single-center study, and the authors call for their proposed dose limits to be tested by building them into treatment planning. Worth knowing if you are being planned for definitive chemoradiation: it is reasonable to ask whether your center considers bone dose when designing the plan. (Read the full paper)
• New spots lighting up on a scan after chemoradiation are not always the cancer spreading, and this case is a reminder worth having before that conversation. A woman in her mid-40s with stage IIIC1 cervical squamous cell carcinoma completed external beam radiation, brachytherapy and weekly cisplatin with curative intent. A PET scan six months after treatment showed the cervical tumor responding, but also new avid lymph nodes in the abdomen, chest and around both lungs, plus uptake in multiple vertebrae and both iliac bones. Investigation was messy rather than decisive: a lymph node biopsy at the root of the lung was largely non-diagnostic but contained cells suggesting granulomatous inflammation rather than cancer, a neck node was inconclusive, and a thyroid nodule initially suspicious for malignancy turned out to be benign. Tuberculosis was ruled out by culture. The diagnosis of a cisplatin-induced sarcoidosis-like reaction was reached by combining the imaging pattern, the primary tumor’s response and those histological findings. No treatment was given, and a PET scan three months later showed the reaction had resolved completely. This is one patient, and the authors note there is no reliable data on how often this happens. Its value is the principle they draw: widespread new uptake after platinum chemotherapy warrants confirmation before it is called metastatic disease. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
HPV vaccination is the single most effective thing that can be done about cervical cancer, and the research is now about schedules, cost and reaching the girls who are missed.
Almost all cervical cancer is caused by persistent infection with high-risk types of human papillomavirus, a very common sexually transmitted virus. Vaccinating before exposure prevents the infection. The obstacles are no longer about whether the vaccine works.
• One and two dose HPV vaccine schedules retained meaningful protection against persistent infection in this pooled analysis, which is the finding that could put vaccination within reach of countries that cannot afford three doses. Researchers combined randomized trials of different HPV vaccine dose schedules using a Bayesian network meta-analysis, searching five databases up to February 2026. Twenty-four trials met their criteria, mostly in females aged 9 to 26 although some enrolled males or older women, and only seven of the 24 contributed to the comparison against six-month persistent infection. Three-dose schedules produced the highest antibody responses and ranked highest against persistent infection. Single-dose schedules retained what the authors describe as moderate efficacy, clearly below the three-dose estimates: the bivalent one-dose regimen gave an odds ratio of 0.32 against placebo, with a wide credible interval of 0.07 to 0.96 that only just excludes no effect. Single-dose schedules also ranked best for injection-site pain in the week after vaccination, which is unsurprising given fewer injections. In girls aged 9 to 14, two doses produced antibody responses similar to three, and the authors are explicit that this is a similarity of point estimates rather than a formal demonstration that two doses protect as well. Two further limits they name: the very large antibody effect estimates are inflated because almost nobody in the placebo groups seroconverted, and the single-dose evidence rests on a handful of recent trials, leaving that part of the network sparsely connected. Their conclusion is that two doses are well supported in adolescents and one dose is a viable option in resource-constrained settings, with longer-term clinical endpoint data still needed. (Read the full paper)
• Giving the nine-type HPV vaccine after surgery for moderate cervical precancer was followed by fewer recurrences, but the comparison has enough problems that it settles nothing. Women treated for cervical intraepithelial neoplasia grade 2, meaning moderately abnormal precancerous cells, remain at risk of the lesion returning because HPV infection can persist or be newly acquired. At a Bari hospital between November 2017 and November 2024, women having a large loop excision for isolated CIN2 received their first dose of the nonavalent vaccine within a month of surgery. Recurrence occurred in 3 of 148 vaccinated women (2.03%) against 6 of 105 unvaccinated (5.71%), a 64.6% relative reduction that did not reach statistical significance. Three caveats matter more than the headline. Those 148 are what remained of 211 vaccinated women after excluding everyone who still tested positive at six months, plus those vaccinated late or off schedule, and the authors state directly that this means the true post-excision recurrence rate is higher than 2.03% and that establishing it was not their aim. The two groups had very unequal follow-up, up to 8 years for the vaccinated and up to 19 for the comparison group, giving the latter far longer to accumulate recurrences; when the authors accounted for that with a survival analysis the difference was again non-significant, with confidence intervals overlapping throughout. And the comparison group is 99 women treated before the study plus 6 treated during it who declined or could not be vaccinated, not a randomized control. The authors calculate that roughly 837 women would be needed to settle the question and call their own findings hypothesis-generating. It is still a fair thing to ask about after treatment for CIN2. (Read the full paper)
• Just over half of 15 to 17 year old girls surveyed in Lesotho said they had received an HPV vaccine dose, and only three in ten had completed the schedule. Lesotho reintroduced its national HPV vaccination program in 2022, and the WHO target is for 90% of girls to be fully vaccinated by age 15. In this population-based cross-sectional survey of 699 girls aged 15 to 17, 52.15% reported having had at least one dose (95% confidence interval 48.4 to 55.8%), of whom 21.65% had had one dose only and 30.5% had completed two. Two limits shape what this can mean. The girls surveyed are mostly older than the 9 to 14 age group the program targets, so this is retrospective recall rather than a measure of current coverage, and the girls reported it themselves with vaccination cards available for fewer than half, which the authors expect to overstate uptake. Girls aged 17 were much less likely to be vaccinated and 16 year olds marginally so, which the authors read as an artefact of who was eligible when the program restarted rather than an effect of age itself. Uptake varied widely by district, from 34.8% in Maseru to 75.4% in Butha-Buthe. Having heard of cervical cancer and having heard of sexually transmitted infections were both associated with higher uptake, though the cervical cancer question was answered by only about half the sample and the sexually transmitted infection association only just reached significance. The authors argue for sexual health education covering HPV and sexually transmitted infections, targeted at the lowest-coverage districts. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Screening is where most of the month’s research landed, and the direction of travel is towards knowing more precisely who is at risk.
HPV testing has largely replaced the Pap smear as the primary screening test because it finds more precancer, but it flags many women whose infection will clear on its own. That trade-off, high sensitivity against unnecessary colposcopies, is what this month’s work is trying to resolve.
• Letting women collect their own HPV sample nearly doubled screening participation in underserved parts of Colombia, though it did not translate into good population coverage. Self-collection means taking a vaginal swab yourself rather than having a clinician take a cervical sample, and it removes several barriers at once. This community trial randomized four municipalities across two Colombian territories, not individual women, with each area starting on one collection method and crossing to the other. Eligible women were aged 30 to 50 with no screening record in the previous 30 months or unknown results from the previous 24. Participation, measured against the number of women the study expected to invite because records of who was actually invited did not exist, was 49.6% with self-collection against 25.7% with clinician collection. Across both arms, 89.6% of women who tested positive attended the triage or treatment visit, and 71% were still in follow-up at six months; compliance was 86.7% in the self-collection arm and 97.2% with clinician collection, a difference that was not statistically significant. The authors are notably honest about their own result: they expected 1,400 women and 532 attended, so higher participation within the trial did not amount to population coverage. Campaigns outperformed routine screening for both methods, though they caution that campaigns ran first and may have reached the women most inclined to be screened. The study was funded by a grant from Pfizer, which manufactures an HPV vaccine. (Read the full paper)
• Knowing which HPV type you carry changes your risk enough that two women with the same mildly abnormal smear can need quite different management. Standard HPV tests report whether any high-risk type is present; extended genotyping reports which one. Researchers followed 2,368 women who tested positive for high-risk HPV in the Tampere region of Finland between 2017 and 2019, for up to 6.5 years, and measured how many developed high-grade precancer or worse. Across 3,099 type detections in those women, HPV16 was both the commonest (14.3% of detections) and the riskiest, carrying a 35.7% risk of high-grade precancer, followed by HPV33 at 24.6% and HPV18 at 20.8%. A clear hierarchy emerged: the lowest-risk group of types, HPV59, 39, 68, 51, 56 and 66, carried a risk below 4.2%. The striking comparison is this: a woman with HPV16 and an essentially normal or borderline smear had a 23.9% risk, higher than the 21.1% risk faced by a woman with a lowest-risk type and a low-grade or worse abnormal smear. Two things to hold alongside the numbers. Because women carried an average of about 1.3 types each, these are risks attached to detecting a given type rather than to carrying it alone. And the study reports no ranges of uncertainty around any of these percentages, so the less common types rest on small numbers. The ordering is the robust part, and the authors argue it should be built into national screening algorithms. (Read the full paper)
• Testing for five HPV types rather than HPV16 alone found every case of severe precancer in this Mexican screening program, at the cost of referring more women who turned out not to have it. Researchers screened 5,856 women aged 25 to 65 in a public screening program in Mexico City between January 2017 and August 2018, referred all 691 who tested HPV-positive for colposcopy, and analyzed the 561 who completed both colposcopy and tissue confirmation. Testing for HPV16 alone found 43.0% of the CIN3 cases, the most severe grade of precancer, with 85.4% specificity. Adding HPV18, then 33, 31 and 39 in sequence raised sensitivity to 100%, but specificity fell to 54.5%. Under that five-type strategy, 47.0% of the HPV-positive women would be referred, and 5.3% of those referred actually had CIN3, which clears the international threshold of 4% that justifies a colposcopy referral. The 100% figure needs its denominator: those percentages imply roughly 14 CIN3 cases in total, so 100% means 14 of 14, and with that few events the true sensitivity could plausibly be well below 100%. Two further limits: this applies to CIN3 among the women who completed diagnostic workup in this program, not to cervical cancer, and 130 HPV-positive women did not complete that workup. (Read the full paper)
• After Portugal switched to HPV-based screening, more cervical cancers were picked up inside the organized program without more being found outside it. Researchers linked the organized screening database in Portugal’s Central Region to hospital records for 2014 to 2023, identified 654 invasive cervical cancers, and classified each as detected within the screening program or outside it, comparing periods with Poisson regression adjusted for underlying time trends. In this retrospective population-based study, the HPV-based period (2020 to 2023) had a screen-detected cancer rate about twice that of the cytology-based period (2014 to 2019), though the estimate is imprecise, with a range consistent with anything from an 11% to a 240% increase. The rate of cancer diagnosed outside the program was not significantly different, at an incidence rate ratio of 0.94, though that range is still wide enough to accommodate a modest change in either direction. Screening participation stayed broadly stable. The authors read this as detection shifting into the screening pathway rather than more cancer occurring, and they are appropriately cautious: this covers the early phase of implementation, and other factors affecting access to diagnosis during those years cannot be excluded. Worth noting what the study measured and did not: it tracked where cancers were found, not stage at diagnosis, treatment or survival. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Vaccination has worked well enough that screening now has to be redesigned around it, and a dedicated collection of papers this month took that question apart.
As the first vaccinated cohorts reach screening age, the arithmetic of screening changes: fewer of them have precancer, so a positive test means less than it used to, and the balance between finding disease and causing unnecessary procedures shifts. Nine of the ten papers in this collection sit behind a restricted license and appear below by citation only.
• Screening tests that measure changes in the cervical cells themselves, rather than just the presence of the virus, may hold up better in vaccinated women, though the evidence is thinner than the principle. This review, led by a US National Cancer Institute epidemiologist with Belgian and Slovenian co-authors, explains the logic. In vaccinated populations the mix of HPV types shifts towards less carcinogenic ones that are less likely to progress, so a positive HPV test carries lower risk than the same result in an unvaccinated woman. But vaccines do not affect infections a woman already has, so the rare vaccine-type infections that do occur in vaccinated women carry undiminished risk. In principle, then, tests linked to the cancer process in the cells, such as cytology, dual stain and host methylation, should degrade less than tests that mostly detect infection. The direct evidence is mixed: cytology’s sensitivity fell only 1 to 7% in the genotype strata used as a stand-in for vaccinated populations, but the one large study in genuinely vaccinated women found methylation markers had limited discriminative power there, which cuts against the expectation for that test. The authors conclude that combining HPV genotyping, limited or extended, with a triage biomarker can stratify risk usefully for vaccinated and unvaccinated women alike. This is a review synthesizing existing data, much of it from genotype subgroups rather than from vaccinated women directly. (Read the full paper)
• Tailoring screening to vaccination status turns out not to require looking up individual women at all, which is the practical answer to a problem most countries cannot solve. Written by two authors at the International Agency for Research on Cancer with a co-author from Karolinska Institutet, this paper examines what vaccination-informed screening actually needs. Registry linkage studies have already confirmed the vaccines work against infection, lesions and invasive cancer, and it is accepted that screening should be adjusted for vaccinated cohorts. The obstacle is individual-level data, and the authors’ examples are mostly of linkage not achieved: in Sweden the barrier is legal rather than technical, since regulations do not permit linking the vaccination registry to screening invitations, while Argentina has no linkage to vaccination data and Bangladesh has not attempted it. Their conclusion follows from that. Rather than tailoring by individual vaccination status, they report that a European working group recommends risk-based screening for whole birth cohorts once those cohorts reach at least 50% vaccination coverage. Italy has already acted on this logic, moving the age at which HPV-based screening starts from 25 to 30 for vaccinated cohorts. So if you have been vaccinated and your own screening schedule has not changed, that is by design rather than an oversight: the recommended approach adjusts the schedule for your whole birth cohort, not for you individually. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Surgery for early cervical cancer is being done less radically than a decade ago, and the research is catching up with what that means for cure rates and for fertility.
For cancer confined to the cervix, the traditional operation removes the uterus and surrounding tissue. Less extensive options can preserve the ability to carry a pregnancy, and this month brought evidence on how safe they are and how people actually weigh the choice.
• Removing just the abnormal cone of cervical tissue plus checking the lymph nodes was followed by recurrence in about one woman in twenty-five with early cervical cancer and no lymph node involvement. Conization means cutting out a cone-shaped piece of the cervix rather than removing the uterus and combining it with lymph node assessment is being explored as a way to reduce surgical harm. This systematic review and meta-analysis pooled 12 mostly small studies covering 548 women. The pooled recurrence rate was 4%, with a range of uncertainty from 2 to 7%, rising to 5% (3.5 to 7%) when studies of fewer than 30 women were excluded, and varying little between studies. Lymph node positivity pooled at 3%, but here the authors found clear evidence of publication bias favoring small studies with extreme results, and excluding those raised the estimate to 6%. That correction is worth noticing: it means the chance of finding involved lymph nodes is probably higher than the headline figure. Two limits on how far these numbers travel: the pooled analysis does not state over what period the recurrences were counted, so the 4% has no time horizon attached, and a pooled single-arm rate cannot be compared with hysterectomy. The authors conclude the approach is feasible, and the honest framing is that it looks reasonable in carefully selected women while resting on 548 patients across a dozen small studies. (Read the full paper)
• When the same trade-offs were put to patients and to their surgeons, patients weighted the chance of pregnancy more heavily and were less put off by added risk of dying from the cancer. Researchers in the Netherlands built 16 hypothetical scenarios varying four factors and asked 58 of 205 invited former patients (28.3%) aged 25 to 42 at the time of their surgery, and 33 of 55 Dutch gynecologic oncologists (60%), to rate their preference between fertility-sparing surgery and hysterectomy on a five-point scale. Patients leaned modestly towards fertility-sparing surgery at 3.48 (95% confidence interval 3.22 to 3.74); clinicians sat at 3.16 (2.95 to 3.36), an interval that includes the neutral midpoint. All four factors mattered to both groups, but the ranking differed: for patients the most influential single factor was the likelihood of achieving pregnancy, which raised their score by 1.07 points when the chance of conception was 85%, while for clinicians the most decisive factor was cancer-related death, which pushed their score 1.84 points away from fertility-sparing surgery for a 10% additional risk. This is a hypothetical scenario study rather than a record of real decisions, only 28.3% of invited patients took part, and the authors report no formal test comparing how the two groups weighted the attributes. What it suggests is a difference in how the two sides of the consultation read the same numbers, which is an argument for asking rather than assuming. (Read the full paper)
• German surgeons pulled back sharply from keyhole radical hysterectomy after a major trial questioned it, then partly returned to it. The LACC trial, published in 2018, found worse survival with minimally invasive radical hysterectomy than with open surgery for early cervical cancer and unsettled what had become standard practice. This retrospective study pooled 391 patients with early-stage disease treated at four German university hospitals between 2014 and 2024, with a median age of 44. Laparoscopic operations, radical and non-radical together, fell from 66.5% of procedures before 2019 to 50.0% afterwards, bottoming out at 30.2% in 2021 and rebounding to 60% by 2024; formal incorporation of the trial into German guidelines in 2022 produced no further significant change. Laparoscopic radical hysterectomy specifically accounted for 98 of the 391 operations. Fertility-sparing procedures held steady, conization at 11.3% and trachelectomy at 7.4%. Two headline figures need unpacking, because both are averages across very different situations. Recurrence occurred in 22 of the 391 patients, but that splits into 1 of 138 (0.7%) among those with the smallest microinvasive tumors against 21 of 253 (8.3%) at stage IB or above, and the authors warn that the cohort’s favorable overall numbers reflect how many low-risk tumors it contained. Similarly, 84.4% of patients had no recorded complications across all procedures including conizations, but the rate was 19.2% after radical hysterectomy against 11.5% after non-radical hysterectomy, and the authors add that retrospective record review probably understates complications. Median follow-up was 46.6 months overall and only 28.6 months for those treated from 2019 onwards, so the recurrence figures will rise. The authors do not claim the trial caused the change and observe that no single operative standard has emerged. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Most cervical precancer never becomes cancer, and the research question has shifted from how to remove it to whether it always needs removing.
CIN stands for cervical intraepithelial neoplasia, precancerous changes in the surface cells of the cervix, graded 1 to 3. Grade 2 sits in the middle and often regresses on its own, particularly in younger women, which is why treating every case with surgery has come under scrutiny: excision can weaken the cervix and raise the risk of preterm birth in a later pregnancy.
• Australian gynecologists interviewed about watching moderate precancer rather than cutting it out considered it safe for carefully selected lower-risk women, and were explicit about who that does not include. Active surveillance for CIN2 means repeat testing over time instead of immediate excision, accepting that many lesions regress. Researchers conducted 25 in-depth interviews with obstetrics and gynecology specialists and trainees across Australian secondary and tertiary settings and analyzed them thematically. Participants viewed active surveillance positively for patients they assessed as at lower risk of progression, typically younger women without HPV 16 or 18 who could reliably attend follow-up and were comfortable recommending either surveillance or immediate excision depending on the balance of risk factors. The authors add a caution the interviews themselves do not carry: the supporting evidence comes largely from women under 30, in whom regression rates are relatively high, and above 30 the 20-year risk of invasive cancer is higher with surveillance than with immediate treatment. What participants consistently agreed on was resourcing, describing active surveillance as an added burden on a public system already facing long colposcopy waits, and calling for more clinics, equipment and staff; several also suggested phone, email or text reminders to reduce loss to follow-up. Two limits on reading this as Australian practice: the 25 participants volunteered and the authors say they generally held positive views, most working in urban or suburban settings, and they reported that many of their colleagues still prefer immediate treatment. (Read the full paper)
• A light-activated treatment may be able to clear the milder grade of high-grade cervical precancer without cutting the cervix, which would matter most for younger women who still want to have children. Photodynamic therapy works less directly than its name suggests. The drug given, 5-aminolevulinic acid, is not itself the active agent: cells convert it into protoporphyrin IX, and abnormal cells accumulate more of it because the enzyme that would clear it works less well in them. Light of a specific wavelength then drives a reaction with oxygen inside those cells, damaging them while leaving the structure of the cervix intact. This review sets out that biology and summarizes clinical reports of 84.5 to 90.9% complete remission and 64.4 to 92.5% HPV clearance at six to twelve months, though those figures pool CIN1, CIN2 and CIN3 together, 7 to 25% of lesions persisted, and the authors say randomized trials with longer follow-up are needed to establish whether the treatment is oncologically equivalent to excision. The proposed mechanism involving autophagy, a cellular recycling process HPV suppresses, is not settled either: the authors note the effect is context-dependent, and that blocking autophagy with chloroquine also makes the treatment work better. They flag that candidate markers for predicting who will not respond, including PAX1 methylation and iron-transport proteins, are proposed but not yet validated. Their positioning is specific: an alternative worth developing for younger women with CIN2, with excision still preferred for CIN3. (Read the full paper)
• A two-part immunotherapy aimed at clearing HPV16 infection itself was followed by the virus becoming undetectable in five of eleven women, which is several times the rate expected without treatment, though nothing measured predicted who cleared it. PVX2 combines a DNA vaccine targeting the HPV16 E7 protein, given at weeks 0 and 4, with a fusion protein vaccine at week 8. This paper is not the trial report but a correlative analysis: researchers went back to blood samples from the twelve women in the safety run-in group of an earlier single-arm trial, all with HPV16 infection and CIN grade 1 or less, and looked for immune signatures tracking with viral clearance. HPV16 was undetectable in 5 of 11 evaluable participants at six months. For context the authors supply themselves, in a comparable natural-history cohort of similar age with low-grade cytology, only about 9% of HPV16 infections cleared spontaneously by six months, against 45% here, and HPV16 is the most persistent of the high-risk types. The search for a correlate largely failed. Clonal T-cell expansion occurred in all participants, though the authors caution much of it may be non-specific bystander activation rather than HPV-directed, and antibody rises across the group were weak. Neither T-cell receptor diversity, clonal expansion nor shared clonotypes was associated with clearance, although overall repertoire composition did differ between those who cleared and those who did not. One finding did reach statistical significance: baseline MCP-1, an inflammatory marker, was higher in those who did not clear. A second, a higher proportion of vaccine-antigen-specific T-cell reads in those who cleared, pointed the same way without reaching significance. With 12 participants and no control group this cannot show the immunotherapy caused the clearances, which is why the authors treat it as a signal worth testing in a randomized trial. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Cervical cancer is not one disease, and August brought work on the subtypes that behave differently and on the markers that might track disease without another biopsy.
Most cervical cancers are squamous cell carcinomas caused by HPV, but a minority are adenocarcinomas, and a smaller minority of those arise without HPV involvement at all. Those HPV-independent cancers respond poorly to standard treatment, and finding something to target in them is an active problem.
• An HPV-independent cervical adenocarcinoma that resists standard treatment responded in the laboratory to a drug that is already approved for another cancer. Gastric-type endocervical adenocarcinoma is not caused by HPV and behaves aggressively. Researchers in Japan profiled gene expression across gastric-type tumors, the more common usual-type endocervical adenocarcinoma, and a lesion called lobular endocervical glandular hyperplasia suspected of being its precursor. Gastric-type tumors had a transcriptional profile distinct from usual-type, supporting their status as a separate subtype, while the suspected precursor clustered closely with them, supporting a shared lineage. One protein, PGC, rose stepwise from precursor to cancer and was confirmed by tissue staining, making it a candidate diagnostic marker. Pathway analysis flagged several activated growth pathways, and upstream regulator analysis predicted that a receptor called RET was driving the tumors; treating them with vandetanib markedly suppressed growth in cells and in mice. Two things to keep straight. RET activation was predicted computationally rather than demonstrated directly, and vandetanib blocks several growth receptors besides RET, so its effect does not by itself prove the tumors depend on RET. And this is laboratory and animal work, identifying a target and a candidate drug rather than showing benefit in patients. The reason it is worth watching is that vandetanib is already approved for medullary thyroid cancer, which shortens the route from a finding like this to a trial. (Read the full paper)
• A gene linked to poor outcomes in cervical cancer also, in a computer simulation, looked capable of binding an existing chemotherapy drug. Researchers in Taiwan mined public datasets, including single-cell sequencing and spatial transcriptomics, for the role of UBE2C, an enzyme that regulates the exit from cell division. Higher UBE2C was consistently found in tumors compared with normal tissue and tracked with advanced stage, metastasis and shorter disease-free survival. Dependency screens indicated the gene matters for cell viability and DNA replication, and the team backed the computational work with laboratory experiments: silencing UBE2C in cervical cancer cell lines slowed growth and reduced mitotic regulators, and they stained human tumor tissue to confirm the protein-level picture. The spatial data placed high UBE2C expression alongside macrophage signals in tumor regions, though the authors are careful that co-location does not establish cause, that they used no animal models, and that their own single-cell data awkwardly put the highest UBE2C signal in the macrophages rather than the tumor cells. The drug finding is the weakest part and should be read as such: a docking simulation predicted that topotecan, a chemotherapy already used in cervical cancer, could fit a pocket on UBE2C. No experiment tested whether it actually binds, and topotecan’s established mechanism is inhibiting topoisomerase I, not UBE2C, so this is a new and untested hypothesis rather than an explanation of why the drug already works. (Read the full paper)
• Looking in blood for HPV DNA shed by the tumor is the most developed of these tests in cervical cancer, and a negative result is still not reliable enough to safely reduce treatment on. Liquid biopsy means detecting fragments of tumor-derived DNA circulating in blood or other fluids, and minimal residual disease means cancer left behind that scans cannot see. In cervical cancer the target is viral rather than the patient’s own mutated DNA, which makes it biologically specific. This narrative review assesses the evidence across endometrial and cervical cancer and is unusually clear about where the line sits. Post-treatment HPV circulating tumor DNA has the strongest disease-specific prospective evidence: when it stays detectable, recurrence is strongly more likely. But the sensitivity figures are sobering. In the largest longitudinal cohort a single post-treatment test caught only 45% of recurrences, rising to 61% if any positive test over follow-up counts, and 9 of 23 patients who relapsed never tested positive at all. That is precisely why the authors say a negative result does not justify reducing treatment on its own. Methylation testing of cervicovaginal or urine samples shows preliminary promise for detecting recurrence that has already established itself, particularly local recurrence, but has not been shown to give advance warning. Circulating tumor cells, extracellular vesicles, microRNAs and platelet-based tests remain exploratory. Their verdict is that liquid biopsy should stay an investigational add-on until prospective, disease-specific trials with predefined margins show that acting on the result improves outcomes. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Where a woman lives and what else is happening in her life still shape whether her cervical cancer is caught early, and this is the part of the field where the gap between what is possible and what happens is widest.
Around 90% of cervical cancer deaths occur in low- and middle-income countries. The research below is about the specific mechanisms of that gap rather than the fact of it.
• Barriers to cervical cancer care in sub-Saharan Africa run right along the care pathway rather than sitting at screening alone, and the review that says so also catalogues what is being tried. Researchers searched six databases with a systematic, PRISMA-reported search strategy, then synthesized 38 studies thematically rather than pooling them, interpreting the findings through five dimensions of healthcare access alongside a social determinants framework. Barriers fell into three interacting groups: individual, including knowledge, income and beliefs; community, including cultural acceptance, social norms and support networks; and health system, including resource limits, service quality and weak policy implementation. On the other side they catalogue opportunities, split between approaches such as community-driven health education, culturally informed care and multi-stakeholder engagement, and technologies such as mobile health platforms, telehealth, electronic records, digital patient navigation and reminder systems. Two things about the evidence base matter for how far this travels. Almost all the included studies covered a single stage of care, 11 on screening and 14 on diagnosis and treatment against only three on follow-up and three on palliative care, so it is the review that spans the continuum rather than the studies; the authors name primary prevention, follow-up and palliative care as persistent research gaps. And the studies were English-language only and geographically skewed, with 20 of the 32 single-country studies from Eastern Africa and several of the highest-burden countries barely represented. (Read the full paper)
• Six in ten women in a cervical cancer registry at a South African referral hospital were living with HIV, and roughly seven in ten arrived with stage III disease despite near-universal antiretroviral coverage. Women living with HIV are more likely to have HPV infections that persist and progress. Researchers analyzed records for 606 women diagnosed with cervical cancer in a hospital-based registry at Nelson Mandela Academic Hospital in Mthatha, Eastern Cape, so these are one referral hospital’s figures rather than a provincial estimate. HIV prevalence in this group was 60.23%, with status unrecorded for about one woman in ten, so the true share is likely higher. Of the 606, 369 were on antiretroviral therapy, which is almost exactly the number who were HIV-positive, meaning coverage among HIV-positive women was close to complete; the two figures overlap oddly enough that the paper’s own numbers do not fully reconcile. And 68.48% presented with stage III cancer. HIV-positive women were on average 9.2 years older than HIV-negative women in this cohort, and older age was associated with later stage at presentation. The combination is what carries the message: HIV treatment coverage was essentially complete and women were still arriving with advanced cancer, which points at the seam between the two services rather than at either alone. This is a retrospective cross-sectional analysis of secondary data, a snapshot the authors note cannot establish cause, with no data on antiretroviral adherence and no HPV vaccination status recorded. (Read the full paper)
• A Ukrainian screening laboratory held its diagnostic quality through four years of war, and testing volumes ended up higher than before the invasion. Ukraine launched its national cervical cancer screening program in 2025, during active armed conflict. Researchers analyzed 946,451 Pap smears and 114,974 HPV tests from one laboratory’s database covering 2021 to 2025 and compared the results against Bethesda System and College of American Pathologists benchmarks. Pap test volume fell 21.5% in 2022, recovered in 2023, and by 2025 was 85.3% above the pre-war 2021 baseline. The Bethesda category proportions stayed inside international benchmark ranges throughout, with one exception the authors flag: the rate of unusable samples drifted upward across the period and slightly exceeded the international threshold in 2024, at 1.03% against a limit of 1.0%. High-grade lesion detection also fell significantly over the period, from 0.62% to 0.31%, ending barely above the recommended floor. HPV testing grew far faster than cytology, from 1,452 tests in 2021 to 40,363 in 2025, and HPV positivity fell from 21.07% to 17.16%. The authors attribute that fall to dilution, testing reaching a broader and lower-risk previously unscreened population, with the actual decline concentrated in women aged 30 to 65 while under-25s stayed at 30 to 35% positive. HPV18’s share among positive results nearly doubled, from 5.6% to 10.4%, which they say must be read as a shift in relative genotype distribution among people tested rather than a real change in community transmission. This is one large private urban laboratory, with specimens from occupied and frontline regions absent from the database, so it shows that quality can be held rather than that it was held nationally. As a demonstration of what a health system can hold onto under extreme pressure, it is still remarkable. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
General and basic-science cervical cancer research.
This is laboratory and computational work on how cervical cancer starts, grows, evades the immune system and resists treatment, including a growing body of work on the vaginal microbiome. None of it changes anyone’s care now, and it is where future treatments come from.
Check the citations section for a comprehensive list of publications associated with this topic.
What Does This Mean for Me?
My HPV test came back positive. How worried should I be?
Less worried than the word “positive” suggests, and this month’s research is part of why. Most high-risk HPV infections clear on their own without ever causing precancer. What August added is that not all high-risk types carry the same risk. In the Finnish study, detecting HPV16 carried roughly a one in three chance of high-grade precancer over six and a half years, while the lowest-risk types, HPV59, 39, 68, 51, 56 and 66, carried less than one in twenty-five. That difference is large enough that it is worth asking your clinician whether your test reported which type you have, and if it did, whether that changes the plan. Not every laboratory does extended genotyping, and not every country’s guidelines use it yet, so the answer may be no. If you have been told you have HPV16 or HPV18, take the follow-up appointment seriously even if your smear was normal or borderline, because that is the combination the Finnish data flags as carrying more risk than a worse smear with a lower-risk type. One caveat on those percentages: they come from one Finnish region, are reported without ranges of uncertainty, and are risks attached to detecting a type rather than to carrying it as your only infection.
I have been told I have CIN2. Do I have to have it treated?
Possibly not, but the answer depends a good deal on your age and your other risk factors, which is different from saying watchful waiting is generally safe. CIN2 sits between mild and severe precancer and often regresses on its own. The Australian gynecologists interviewed this month were comfortable offering active surveillance to women they judged lower risk, and reliable follow-up was the condition they kept returning to. But the authors of that study add an important qualification: the evidence supporting surveillance comes largely from women under 30, and above 30 the 20-year risk of invasive cancer is higher with surveillance than with immediate treatment. So, the useful conversation is not “is watching safe” but “am I in the group for whom it is”. If you do choose surveillance, ask specifically how you will be tracked, who will contact you, and what happens if you move or change clinics, because the safety of this option rests entirely on the follow-up happening. If you have excision instead, one further finding is worth raising: in the Italian study, women given the nine-type HPV vaccine after excision for CIN2 had fewer recurrences than an unvaccinated comparison group, though the difference was not statistically significant, the comparison group had been followed far longer, and the authors call their own result hypothesis-generating. It is still reasonable to ask whether vaccination after treatment is offered where you are.
I want to have children, and I have been diagnosed with early cervical cancer.
There are real options, and this month’s research is directly about how to weigh them. Fertility-sparing approaches range from removing a cone of cervical tissue to removing the cervix while keeping the uterus, and the meta-analysis published this month found recurrence in about 4 to 5% of women after conization with lymph node assessment, in early disease without lymph node involvement. Two honest details in that paper: the authors found publication bias in the lymph node data, and correcting for it raised the estimated chance of involved nodes from 3% to 6%; and the pooled analysis does not say over what period recurrences were counted. The other study worth knowing about asked patients and surgeons to weigh identical hypothetical scenarios and found they weighed them differently, with patients placing more weight on the chance of pregnancy and being less deterred by added mortality risk than their clinicians were. Neither answer is wrong, but the difference is a good reason to say out loud what matters most to you rather than waiting to be asked. Useful questions: what is my individual recurrence risk with each option, what is my realistic chance of carrying a pregnancy afterwards, and how many of these operations does this center do a year?
I have had the HPV vaccine. Do I still need screening?
Yes, and the ten-paper collection published this month is about how that answer will change over the next decade. Vaccination substantially reduces but does not eliminate cervical cancer risk: it does not clear infections you already had, and no current vaccine covers every high-risk type. What is changing is the arithmetic of screening for vaccinated women, because when precancer becomes rarer a positive test means less than it used to and unnecessary procedures become a larger share of screening’s harms. The practical answer the IARC authors reach is worth knowing, because it is not the one most people would guess: rather than looking up whether you individually were vaccinated, which is legally or technically impossible in many countries, the recommended approach adjusts screening for whole birth cohorts once their vaccination coverage is high enough. Italy has already moved the starting age from 25 to 30 for vaccinated cohorts. So, if your own schedule has not changed, that is by design rather than an oversight. Until your cohort’s schedule changes, follow your national screening program as it stands.
This digest is prepared by OCRA (Ovarian Cancer Research Alliance) for patients, caregivers, and advocates. It is intended to inform, not to guide individual treatment decisions. Please speak with your care team about what research findings may mean for your specific situation.
A note on how this digest was made: This edition was built by searching PubMed for papers published in August 2026, using a two-tier strategy: targeted thematic searches across the cervical cancer landscape (treatment, immunotherapy, ADCs, HPV vaccination, screening, disparities, surgery, molecular subtypes, precancer, survivorship, rare subtypes) plus a dedicated qualitative search and a broad MeSH sweep. Papers summarized in full are open-access under a permitted license (CC0, CC BY, CC BY-SA, CC BY-ND, or CC BY-NC); on-topic papers under other licenses are listed by citation only. A companion methodology report, available separately, documents the full search-and-screening process and every paper reviewed.
Sources
Citations are grouped by the topic sections above. Within each section, the papers directly referenced in the digest are listed first, followed by additional on-topic papers published this month that are either not discussed above or are behind access restrictions.
Immunotherapy combinations are now the first thing tried when cervical cancer comes back or spreads, and this month brought early results on how they perform.
Directly referenced:
1. Liu H et al.. “Serplulimab combined with bevacizumab and chemotherapy as first-line treatment for recurrent or metastatic cervical cancer (ASTRUM-CC01): a phase II trial.” Front Immunol. August 18, 2026. PMID 42682706. https://doi.org/10.3389/fimmu.2026.1923961
2. Liu X et al.. “Real-world efficacy and safety profile of low-dose cadonilimab in recurrent or metastatic cervical cancer as first-line therapy.” Front Immunol. August 18, 2026. PMID 42682635. https://doi.org/10.3389/fimmu.2026.1871890
3. Barraud S et al.. “Clinico-molecular predictors of durable response to immune checkpoint inhibitors (ICI) in metastatic cervical cancer (mCC).” Br J Cancer. August 2026. PMID 42151561. https://doi.org/10.1038/s41416-026-03438-6
Additional citations on related topics:
4. Zhao D et al.. “Cellular Immunotherapy for Cervical Cancer: Next Therapeutics Frontiers.” Oncol Res. August 13, 2026. PMID 42630674. https://doi.org/10.32604/or.2026.084736 (open access: review of cellular immunotherapy platforms for cervical cancer: tumour-infiltrating lymphocytes, TCR-engineered T cells, CAR-T and CAR-NK cells)
5. Deng Q et al.. “HDAC2 restrains IGF2BP1-associated m6A dysregulation in cervical cancer immunotherapy resistance.” PLoS One. August 27, 2026. PMID 42658872. https://doi.org/10.1371/journal.pone.0355606 (open access: laboratory work on an epigenetic mechanism of acquired resistance to immunotherapy)
6. Lou H et al.. “Iparomlimab and tuvonralimab in previously treated patients with cervical cancer.” Cell Rep Med. August 4, 2026. PMID 42551432. https://doi.org/10.1016/j.xcrm.2026.102944 (subscription access)
7. Liu F et al.. “Adverse events associated with immune checkpoint inhibitors in cervical cancer: A systematic review and meta-analysis of randomized controlled trials.” Eur J Obstet Gynecol Reprod Biol. August 2026. PMID 42320227. https://doi.org/10.1016/j.ejogrb.2026.115263 (subscription access)
8. Ikeda S et al.. “Salvage tacrolimus therapy for steroid-refractory immune-related adverse event-associated sclerosing cholangitis.” Clin J Gastroenterol. August 2026. PMID 42283999. https://doi.org/10.1007/s12328-026-02375-4 (subscription access)
9. Fukunaga C et al.. “Right Ventricular Metastasis From Cervical Cancer Treated With Pembrolizumab-Containing Chemotherapy: A Case Report and Literature Review.” Am J Case Rep. August 4, 2026. PMID 42550800. https://doi.org/10.12659/AJCR.952931 (subscription access)
10. Schröder C et al.. “Tumoral PD-L1 Expression as a Prognostic Marker in Invasive Cervical Cancer.” Anticancer Res. August ??, 2026. PMID 42527062. https://doi.org/10.21873/anticanres.18294 (subscription access)
11. Ricardo M et al.. “PD-L1 expression in cervical cancer tissue is strongly associated with the expression of CD73/TGF-β1, the percentage of CD8+/PD-1+ T cells and disease progression.” Immunol Lett. August 2026. PMID 41707877. https://doi.org/10.1016/j.imlet.2026.107150 (subscription access)
12. Sinha R et al.. “Impact of Interruptions in Chemotherapy on Survival for Patients With Metastatic or Recurrent Cervical Cancer.” Am J Clin Oncol. August 2026. PMID 41355394. https://doi.org/10.1097/COC.0000000000001279 (subscription access)
13. Kataria B et al.. “Consensus statements from the first Gynecologic Cancer InterGroup Cervical Cancer Consensus Conference in Clinical Research.” Lancet Oncol. August ??, 2026. PMID 42508438. https://doi.org/10.1016/S1470-2045(26)00215-9 (subscription access)
14. Peters S et al.. “Antibody-drug conjugates in selected solid tumours: a position statement update based on findings from the third workshop held by the ETOP IBCSG Partners Foundation.” ESMO Open. August 2026. PMID 42431135. https://doi.org/10.1016/j.esmoop.2026.108316 (subscription access)
For cervical cancer that has grown beyond the cervix but not spread to distant organs, chemoradiation remains the treatment, and the open questions are about what to add and what it costs the body.
Directly referenced:
15. Yang H et al.. “Efficacy comparison of concurrent chemoradiotherapy alone versus concurrent chemoradiotherapy plus adjuvant chemotherapy in stage III Locally Advanced Cervical Cancer: A single-center, retrospective observational cohort study.” PLoS One. August 10, 2026. PMID 42574435. https://doi.org/10.1371/journal.pone.0354207
16. Autorino R et al.. “Pelvic insufficiency fractures in cervical cancer patients treated with definitive chemoradiation: impact of dosimetric and clinical factors.” Strahlenther Onkol. August 2026. PMID 42168624. https://doi.org/10.1007/s00066-026-02518-z
17. Healsmith S et al.. “Cisplatin-induced sarcoidosis-like reaction after primary chemoradiotherapy for locally advanced cervical cancer.” BMJ Case Rep. August 28, 2026. PMID 42665296. https://doi.org/10.1136/bcr-2025-271654
Additional citations on related topics:
18. Girbovan AH et al.. “Molecular Biomarkers of Radiosensitivity and Radioresistance in Cervical Cancer: A Systematic Review.” Int J Mol Sci. August 5, 2026. PMID 42589685. https://doi.org/10.3390/ijms27157033 (open access: systematic review of molecular markers of radiation sensitivity and resistance)
19. Prapan A et al.. “Dihydroquinine Enhances Radiosensitivity in Cervical Cancer Cells Accompanied by Radiation-Induced Cellular Responses.” Cells. August 18, 2026. PMID 42645212. https://doi.org/10.3390/cells15161484 (open access: laboratory study of dihydroquinine as a radiosensitiser in cervical cancer cells)
20. Ronsini C et al.. “Exploratory Analysis of Systemic Inflammatory Indices Across Locoregional Tumor Progression Parameters in Cervical Cancer: The CERTIFIKO Prospective Study.” Medicina (Kaunas). August 17, 2026. PMID 42654467. https://doi.org/10.3390/medicina62081570 (open access: prospective study relating routine blood inflammatory ratios to locoregional tumour extent)
21. Qu A et al.. “Nimotuzumab Plus Image-Guided Radiation Therapy for Elderly Patients with Locally Advanced Cervical Squamous Cell Carcinoma: Interim Analysis of a Prospective Multicenter Phase II Trial.” Int J Radiat Oncol Biol Phys. August 2026. PMID 41197740. https://doi.org/10.1016/j.ijrobp.2025.10.029 (subscription access)
22. Mayadev JS et al.. “ARTIA-Cervix: a prospective trial of adaptive radiation therapy for cervical cancer.” Int J Gynecol Cancer. August 2026. PMID 41407635. https://doi.org/10.1016/j.ijgc.2025.102823 (subscription access)
23. Shinde P et al.. “Spatially fractionated radiotherapy using straight and bending virtual rods as an alternative for cervical cancer brachytherapy-results from preclinical in-silico dose comparison and quality assurance.” Br J Radiol. August 1, 2026. PMID 42179164. https://doi.org/10.1093/bjr/tqag075 (subscription access)
24. Cilla S et al.. “Unsupervised clustering analysis unravels the role of systemic inflammatory indices in the prognosis of patients with locally advanced cervical cancer treated with chemoradiation.” Strahlenther Onkol. August 2026. PMID 41843108. https://doi.org/10.1007/s00066-026-02513-4 (subscription access)
25. de Melo Neto AB et al.. “ATF4, ZIK1, and PNMA3 Transcriptomic Signatures Predict Chemoradiotherapy Response in Cervical Cancer.” Cancer Med. August ??, 2026. PMID 42509645. https://doi.org/10.1002/cam4.72053 (subscription access)
26. Ramalho NM et al.. “Effect of topical vaginal estrogen after radiotherapy for cervical cancer: a randomized, double-blind pilot trial.” Int J Gynecol Cancer. August 2026. PMID 42468465. https://doi.org/10.1016/j.ijgc.2026.104831 (subscription access)
HPV vaccination is the single most effective thing that can be done about cervical cancer, and the research is now about schedules, cost and reaching the girls who are missed.
Directly referenced:
27. Ye J et al.. “Immunogenicity, efficacy, and safety of different dose schedules of human papillomavirus vaccines: a Bayesian network meta-analysis of randomized controlled trials.” Front Immunol. August 6, 2026. PMID 42625665. https://doi.org/10.3389/fimmu.2026.1883217
28. Pinto V et al.. “The Role of Adjuvant Nonavalent HPV Vaccination After LLETZ in Patients with Isolated CIN2: A Controlled Cohort Study.” Pathogens. August 1, 2026. PMID 42654751. https://doi.org/10.3390/pathogens15080814
29. Tebeje TM et al.. “Magnitude of human papillomavirus vaccination uptake and its determinants among adolescent girls in Lesotho: a cross-sectional study.” BMJ Open. August 3, 2026. PMID 42547243. https://doi.org/10.1136/bmjopen-2025-110615
Additional citations on related topics:
30. Thompson JH et al.. “Co-creating HPV Vaccination Messages for Rural Washington: Application of a Boot Camp Translation Approach.” Health Educ Behav. August 2026. PMID 41439412. https://doi.org/10.1177/10901981251399649 (open access: community co-design of HPV vaccination messages for rural Washington State using a boot camp translation approach)
31. Yang H et al.. “Personal vs professional HPV vaccination and screening among female healthcare workers in China.” Vaccine. August 2026. PMID 42349131. https://doi.org/10.1016/j.vaccine.2026.128879 (open access: national survey of the gap between female healthcare workers’ own HPV vaccination and screening and what they recommend professionally)
32. Jindal R et al.. “Addressing HPV vaccine hesitancy and misinformation in India through public health communication strategies.” Hum Vaccin Immunother. August 3, 2026. PMID 42544634. https://doi.org/10.1080/21645515.2026.2711551 (open access: commentary on tackling HPV vaccine misinformation during India’s national rollout)
33. Lynn T et al.. “Integrated service delivery to improve adolescent health and human papillomavirus (HPV) vaccination in Lao PDR: a quasi-experimental mixed-methods study - study protocol.” BMJ Open. August 3, 2026. PMID 42547242. https://doi.org/10.1136/bmjopen-2025-098836 (open access: study protocol for an integrated adolescent health and HPV vaccination service model in Lao PDR)
34. John A et al.. “Perceptions and practices among students, parents, and teachers of the Human Papillomavirus (HPV) Vaccination: A pilot feasibility study from Rural Kerala.” PLoS One. August 10, 2026. PMID 42574468. https://doi.org/10.1371/journal.pone.0340559 (open access: pilot study of HPV vaccination knowledge and attitudes among students, parents and teachers in rural Kerala)
35. Demirdağ B et al.. “Effect of human papillomavirus education on human papillomavirus knowledge and gynecologic cancer awareness among women aged 18-49: a randomized controlled study.” Rev Assoc Med Bras (1992). August 7, 2026. PMID 42585526. https://doi.org/10.1590/1806-9282.20260313 (open access: randomised study of a structured HPV education programme for women aged 18 to 49)
36. Boudova S et al.. “Patient and Provider Knowledge and Attitudes Regarding Vaccination with the 9-Valent HPV Vaccine during Pregnancy.” Am J Perinatol. August 21, 2026. PMID 42601048. https://doi.org/10.1055/a-2936-5812 (open access: patient focus groups and a national provider survey on giving the 9-valent HPV vaccine during pregnancy)
37. Ibrahim FM et al.. “HPV prevention awareness, vaccination willingness, and vaccine-related perceptions among middle-school girls in three Arab countries: an exploratory online survey.” Front Public Health. August 3, 2026. PMID 42609547. https://doi.org/10.3389/fpubh.2026.1902409 (open access: survey of HPV awareness and vaccination willingness among middle-school girls in Egypt, Saudi Arabia and the United Arab Emirates)
38. Sahoo SS et al.. “Content Quality of YouTube Videos on Human Papillomavirus Vaccine: A Systematic Analysis.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663224. https://doi.org/10.31557/APJCP.2026.27.8.3029 (open access: systematic assessment of the quality and reliability of YouTube videos about HPV vaccination in India)
39. Pitakkarnkul S et al.. “Knowledge, Attitude, and Clinical Practice of HPV Vaccination and Cervical Cancer Screening: A National Survey of OB-GYN Practitioners in Thailand.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663232. https://doi.org/10.31557/APJCP.2026.27.8.3097 (open access: national survey of Thai obstetricians and gynaecologists on HPV vaccination and screening knowledge and practice)
40. Bennett C et al.. “What are the barriers and enablers to the uptake of the HPV vaccine in Romania, Bulgaria and Croatia? A mixed methods systematic review.” BMJ Public Health. August 25, 2026. PMID 42689009. https://doi.org/10.1136/bmjph-2025-003253 (open access: mixed-methods systematic review of barriers and enablers to HPV vaccine uptake in Romania, Bulgaria and Croatia)
41. Samuelson N et al.. “Purification of Disassembled Capsid Protein by Hydroxyapatite Chromatography Enhances Virus-Like Particle Recovery.” Biotechnol Bioeng. August 16, 2026. PMID 42604587. https://doi.org/10.1002/bit.70346 (open access: manufacturing science: a chromatography method that improves recovery of HPV virus-like particles during vaccine production)
42. Kyei GK et al.. “Expanding HPV Vaccination in the United States Through Policy Action: A Call for Legislative Support.” Policy Polit Nurs Pract. August 2026. PMID 41406054. https://doi.org/10.1177/15271544251404015 (subscription access)
43. Wakui N et al.. “HPV Education and Its Impact on Vaccination Willingness and Recommendation Intentions Among Unvaccinated Japanese University Students: A Cross-Sectional Study.” J Cancer Educ. August 2026. PMID 40968245. https://doi.org/10.1007/s13187-025-02733-9 (subscription access)
44. Rai I et al.. “Call for Increased Community Education Regarding Common HPV-Associated Cancers Within the Urban Safety-Net Hospital Population.” J Cancer Educ. August 2026. PMID 40888851. https://doi.org/10.1007/s13187-025-02722-y (subscription access)
45. Jiba DF et al.. “Human Papillomavirus Vaccine Hesitancy and Uptake Among Adolescent Girls Living with HIV in Sierra Leone: A Call for Integration of Cervical Cancer Services.” AIDS Behav. August 2026. PMID 41964808. https://doi.org/10.1007/s10461-026-05065-x (subscription access)
46. Dejene K. “Navigating stigma, faith, and fear: understanding HPV vaccine acceptance among adolescent girls in rural parts of Central Ethiopia.” Cult Health Sex. August 2026. PMID 41389081. https://doi.org/10.1080/13691058.2025.2600046 (subscription access)
47. Alamgir M et al.. “Behavioural and social drivers of HPV vaccine uptake in Tonga: a mixed-methods study using the WHO BeSD framework and Talanoa in a Pacific Island setting.” Vaccine. August 2026. PMID 42308978. https://doi.org/10.1016/j.vaccine.2026.128843 (subscription access)
48. Zundong Y et al.. “Entering into life-course immunization: Process, significance, and prospects of HPV vaccine inclusion into the national immunization program of China.” Vaccine. August 4, 2026. PMID 42551399. https://doi.org/10.1016/j.vaccine.2026.129000 (subscription access)
49. Lal A et al.. “Evaluating the Impact of an Educational Intervention on Medical Students’ Knowledge and Attitudes Toward Human Papillomavirus.” J Community Health. August 20, 2026. PMID 42622728. https://doi.org/10.1007/s10900-026-01630-6 (subscription access)
50. Gross S et al.. “Frequent detection of high-risk HPV types other than HPV 16/18 in a cohort of French women who claimed to have been vaccinated.” Arch Virol. August 28, 2026. PMID 42663706. https://doi.org/10.1007/s00705-026-06722-1 (subscription access)
51. Tague C et al.. “Human papillomavirus: Role of HPV2 and HPV9 in reducing the burden of cervical cancer in sub-Saharan Africa.” Int J Infect Dis. August 2026. PMID 42044725. https://doi.org/10.1016/j.ijid.2026.108733 (subscription access)
52. Wang L et al.. “Quantification of HPV-16 and HPV-18 neutralizing antibodies via a magnetic bead-based competitive chemiluminescence platform.” J Virol Methods. August 27, 2026. PMID 42660319. https://doi.org/10.1016/j.jviromet.2026.115452 (subscription access)
53. Gyamfi-Samakome A et al.. “Impact of health education intervention on knowledge and attitude towards HPV vaccination in Africa: A systematic review.” Vaccine. August 2026. PMID 42468223. https://doi.org/10.1016/j.vaccine.2026.128930 (subscription access)
54. Shah K et al.. “Modelling the impact of awareness campaigns on HPV transmission dynamics: a neural network-enhanced mathematical model.” Sci Rep. August 6, 2026. PMID 42557263. https://doi.org/10.1038/s41598-026-51555-2 (subscription access)
Screening is where most of the month’s research landed, and the direction of travel is towards knowing more precisely who is at risk.
Directly referenced:
55. Fernández-Deaza G et al.. “Participation and Follow-Up Compliance in Cervical Cancer Screening According to Delivery Strategy for HPV Self-Collection: A Community Trial in Underserved Colombian Areas.” Cancer Med. August ??, 2026. PMID 42603309. https://doi.org/10.1002/cam4.72171
56. Leino A et al.. “Improving cervical screening risk stratification through extended human papillomavirus genotyping and age-specific data.” Eur J Public Health. August 4, 2026. PMID 42606565. https://doi.org/10.1093/eurpub/ckag139
57. Meneses-León J et al.. “Extended HPV typing as an efficient alternative within HPV-based screening programs.” Int J Cancer. August 2026. PMID 41902757. https://doi.org/10.1002/ijc.70428
58. Sousa R et al.. “Invasive Cervical Cancer Detection After Transition to Primary Human Papillomavirus Screening: Population-Based Linkage Study in Portugal.” Acta Med Port. August 3, 2026. PMID 42556424. https://doi.org/10.20344/amp.24709
Additional citations on related topics:
59. Hulmi J et al.. “Histological outcomes and colposcopic findings in patients with persistent high-risk human papillomavirus infection without major cytological findings.” Am J Obstet Gynecol. August 2026. PMID 41895365. https://doi.org/10.1016/j.ajog.2026.03.016 (open access: colposcopy findings and histological outcomes in women with persistent high-risk HPV but no major cytological abnormality)
60. Šavrova A et al.. “Nationwide Study on the Cervical Cancer Screening Pathway in Estonia.” Int J Cancer. August 2026. PMID 41957967. https://doi.org/10.1002/ijc.70466 (open access: nationwide study of how completely women with a positive screening test are followed up in Estonia)
61. Flannelly G et al.. “The importance of quality assurance in colposcopy in the elimination of cervical cancer: A position paper by the European Federation for Colposcopy.” Eur J Obstet Gynecol Reprod Biol. August 2026. PMID 42263348. https://doi.org/10.1016/j.ejogrb.2026.115238 (open access: European Federation for Colposcopy position paper on quality assurance in colposcopy)
62. Memmel L et al.. “HPV Self-Collection Experience in US Hispanic/Latinx Women Using a Device Designed for at-Home Collection.” Hisp Health Care Int. August 13, 2026. PMID 42593217. https://doi.org/10.1177/15404153261470020 (open access: analysis of HPV self-collection experience and preferences among Hispanic and Latinx women in the United States)
63. Nogueras Gonzalez GM et al.. “Barriers to cervical cancer screening and experiences using mailed at-home HPV self-collection kits among US and foreign-born Hispanic women in a safety net health system.” Gynecol Oncol. August 2026. PMID 42468446. https://doi.org/10.1016/j.ygyno.2026.07.012 (open access: comparison of screening barriers and mailed HPV self-collection experience among foreign-born Hispanic, US-born Hispanic and US-born non-Hispanic women)
64. Zhang Q et al.. “Analysis of the clinical utility of p16/Ki-67 dual staining in screening cervical lesions among women positive for high-risk HPV.” Medicine (Baltimore). August 21, 2026. PMID 42629682. https://doi.org/10.1097/MD.0000000000050102 (open access: clinical utility of p16 and Ki-67 dual staining to triage women who test positive for high-risk HPV)
65. d’Avenia M et al.. “Relative HPV Viral Load Measured by ΔCt for Risk Stratification in Cervical Cancer Screening.” Cancers (Basel). August 10, 2026. PMID 42649882. https://doi.org/10.3390/cancers18162568 (open access: relative HPV viral load as a risk-stratification tool in screening)
66. Živadinović AR et al.. “Clinical Significance of High-Risk HPV Positivity with Negative Cytology: Can Further Evaluation Be Safely Delayed?.” Medicina (Kaunas). August 3, 2026. PMID 42654390. https://doi.org/10.3390/medicina62081493 (open access: whether further evaluation can safely be delayed in women with high-risk HPV and negative cytology)
67. Mostafa HH et al.. “Application of Cobas 6800 HPV testing and qPCR utilizing three genomically-optimized primer sets for detecting HPV DNA in the blood of HPV Positive dysplasia and cancer patients.” PLoS One. August 25, 2026. PMID 42640927. https://doi.org/10.1371/journal.pone.0354671 (open access: pilot study detecting HPV DNA in blood plasma using a commercial platform plus optimised PCR)
68. Miao S et al.. “High diagnostic concordance between vulvar and cervical samples for human papillomavirus detection: a cross-sectional study.” Microbiol Spectr. August 14, 2026. PMID 42599100. https://doi.org/10.1128/spectrum.04026-25 (open access: concordance between vulvar and cervical samples for HPV detection, as a less invasive sampling option)
69. Qin H et al.. “Improving cervical cancer screening uptake through theory-informed education: a comprehensive systematic review and meta-analysis.” Acta Oncol. August 5, 2026. PMID 42555395. https://doi.org/10.2340/1651-226X.2026.45119 (open access: systematic review and meta-analysis of theory-informed education to increase screening uptake among underserved women)
70. Kusuma F et al.. “Effectiveness of different educational interventions on knowledge, attitude and willingness to undergo cervical cancer screening in rural Indonesia: a quasi-experimental study.” BMJ Open. August 10, 2026. PMID 42575548. https://doi.org/10.1136/bmjopen-2025-103814 (open access: quasi-experimental comparison of educational approaches to increase screening willingness in rural Indonesia)
71. Deng X et al.. “Nursing intervention and follow-up compliance after abnormal cervical cancer screening.” Medicine (Baltimore). August 21, 2026. PMID 42629693. https://doi.org/10.1097/MD.0000000000049893 (open access: retrospective study of a structured nursing programme to improve follow-up after an abnormal screening result)
72. Lumia C et al.. “Economic incentives for cervical cancer screening: A qualitative study of healthcare professionals’ perspectives.” Public Health. August 2026. PMID 42302570. https://doi.org/10.1016/j.puhe.2026.106385 (open access: qualitative study of Italian health professionals’ views on paying women to attend screening)
73. Muchtariza S et al.. “Predictors of Cervical Cancer Screening Uptake Among Women of Reproductive Age in Indonesia: A Nationwide Cross-Sectional Study Based on the 2023 Indonesian Health Survey.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663222. https://doi.org/10.31557/APJCP.2026.27.8.3013 (open access: nationwide analysis of screening uptake predictors among Indonesian women of reproductive age)
74. Tibenderana JR et al.. “Cervical cancer screening predictors in Tanzania: a variance component models’ approach of national survey 2022.” Medicine (Baltimore). August 21, 2026. PMID 42629684. https://doi.org/10.1097/MD.0000000000050260 (open access: national survey analysis of cervical cancer screening predictors in Tanzania)
75. Adam J et al.. “Factors Associated With Cervical Cancer Awareness Among Women of Reproductive Age in the Democratic Republic of the Congo: Evidence From a Nationwide DHS Analysis.” Cancer Rep (Hoboken). August ??, 2026. PMID 42543153. https://doi.org/10.1002/cnr2.70633 (open access: nationwide analysis of cervical cancer awareness among women of reproductive age in the Democratic Republic of the Congo)
76. Urundai Meeran SB. “Enhanced Diagnosis of Cervical Cancer Using Archer Fish Hunting Optimizer-Optimized Xception Network with AI Interpretability via Grad-CAM.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663198. https://doi.org/10.31557/APJCP.2026.27.8.2783 (open access: deep-learning classifier for cervical cytology images with explainable-AI heat maps)
77. Sırma T et al.. “Evaluating Performance of Transvaginal Doppler Parameters in Differentiating Cervical Neoplastic Severity.” Diagnostics (Basel). August 16, 2026. PMID 42650995. https://doi.org/10.3390/diagnostics16162592 (open access: prospective study of transvaginal Doppler ultrasound parameters across the spectrum from precancer to cancer)
78. Hsiao K et al.. “Diagnostic Performance of HPV Testing Using Self-Collected Urine and Vaginal Samples for Detecting Cervical Precancer or Worse: A Meta-Analysis.” J Obstet Gynaecol Res. August ??, 2026. PMID 42547988. https://doi.org/10.1111/jog.70434 (subscription access)
79. Senian AA et al.. “Evaluation of Sample Pooling Strategies for Point-of-Care HPV DNA Testing Using the STANDARD™ M10 Platform.” J Med Virol. August ??, 2026. PMID 42572963. https://doi.org/10.1002/jmv.71101 (subscription access)
80. Zhou H et al.. “Head-to-head comparison of the MyGene human papillomavirus-sexually transmitted infection assay versus the Cobas 4800 human papillomavirus test for detecting high-grade cervical intraepithelial neoplasia.” Int J Gynaecol Obstet. August 2026. PMID 41721577. https://doi.org/10.1002/ijgo.70869 (subscription access)
81. Dhillon SK et al.. “Clinical Validation of the Sansure Human Papillomavirus DNA Diagnostic Kit for Use in Primary Cervical Cancer Screening.” J Med Virol. August ??, 2026. PMID 42605738. https://doi.org/10.1002/jmv.71106 (subscription access)
82. Yoda RA et al.. “Implementation and impact of primary HPV testing in cervical cancer screening: Historical perspectives and institutional experience at a large academic medical center.” Cancer Cytopathol. August ??, 2026. PMID 42482480. https://doi.org/10.1002/cncy.70129 (subscription access)
83. Joura E et al.. “European Society of Gynaecological Oncology/European Network of Gynaecological Advocacy Groups Position on risk-based cervical cancer screening.” Int J Gynecol Cancer. August 2026. PMID 42341405. https://doi.org/10.1016/j.ijgc.2026.104794 (subscription access)
84. Bertelsen VM et al.. “Assessing the clinical value of cervical biopsies in individuals with transformation zone type 3 at colposcopy: A cross-sectional study.” Acta Obstet Gynecol Scand. August 2026. PMID 42141730. https://doi.org/10.1111/aogs.70243 (subscription access)
85. Nieberle LS et al.. “Comparison of Ex-House and In-House Cytology for the New Cervical Cancer Screening Assessment.” Geburtshilfe Frauenheilkd. August 2026. PMID 42592404. https://doi.org/10.1055/a-2900-6511 (subscription access)
86. Zhang Y et al.. “A combined PAX1/JAM3 methylation and HPV viral load model for exploratory risk stratification of ≥CIN2 among women with positive cervical screening results.” BMC Cancer. August 27, 2026. PMID 42661176. https://doi.org/10.1186/s12885-026-16788-4 (subscription access)
87. Li N et al.. “PAX1 and ZNF582 Methylation as a Triage Strategy in Cytologic and hrHPV+ Scrapings in Both Chinese and Dutch Cohorts.” Cancer Epidemiol Biomarkers Prev. August 3, 2026. PMID 42171339. https://doi.org/10.1158/1055-9965.EPI-26-0015 (subscription access)
88. Feng P et al.. “Diagnostic value of FAM19A4/SOX1/PAX1 methylation in non-16/18 high-risk HPV cervical lesions.” Gynecol Oncol. August 2026. PMID 42335608. https://doi.org/10.1016/j.ygyno.2026.06.012 (subscription access)
89. Rao S et al.. “Integrating a”see-and-treat” approach with opportunistic human papilloma virus deoxyribonucleic acid (HPV DNA) based cervical cancer screening in India: a retrospective cross-sectional study.” AJOG Glob Rep. August 2026. PMID 42667092. https://doi.org/10.1016/j.xagr.2026.100678 (subscription access)
90. Kovacevic IN et al.. “Effect of Organized Cervical Cancer Screening Programs on Incidence and Mortality: A Systematic Review and Meta-analysis.” J Prev (2022). August 2026. PMID 41776131. https://doi.org/10.1007/s10935-026-00908-8 (subscription access)
91. Audiger C et al.. “Area-based socioeconomic inequalities in cervical cancer screening coverage in France.” J Epidemiol Popul Health. August 2026. PMID 41955933. https://doi.org/10.1016/j.jeph.2026.203350 (subscription access)
92. Dong F et al.. “[Diagnostic efficacy and teaching value of artificial intelligence-assisted diagnostic systems in cervical liquid-based cytology screening].” Zhonghua Bing Li Xue Za Zhi. August 8, 2026. PMID 42547423. https://doi.org/10.3760/cma.j.cn112151-20260119-00048 (subscription access)
93. Geetha SD. “Can large language models like ChatGPT and Gemini interpret cervical cytology accurately?.” Ann Diagn Pathol. August 2026. PMID 41931983. https://doi.org/10.1016/j.anndiagpath.2026.152641 (subscription access)
94. Lin R et al.. “Label-free cervical cancer detection in tissue samples using Raman spectroscopy combined with machine learning technology.” Anal Methods. August 6, 2026. PMID 42396761. https://doi.org/10.1039/d6ay00509h (subscription access)
95. Singh SK et al.. “Synergistic U-bent geometry and bimetallic plasmonics for ultra-sensitive fibre-optic SPR biosensing of cervical cancer.” Analyst. August 24, 2026. PMID 42473840. https://doi.org/10.1039/d6an00563b (subscription access)
96. Saini K et al.. “Emerging frontiers in cervical cancer diagnostics: Recent innovations in biosensors for HPV detection.” Talanta. August 2026. PMID 41931971. https://doi.org/10.1016/j.talanta.2026.129750 (subscription access)
97. Aleshire M et al.. “Acceptability of At-Home hrHPV Cervical Cancer Screening For Transmasculine Individuals: A Qualitative Descriptive Study.” West J Nurs Res. August 9, 2026. PMID 42571636. https://doi.org/10.1177/01939459261464522 (subscription access)
98. Frisell T et al.. “Cervical human papillomavirus status among women with chronic inflammatory rheumatic diseases: matched cohort study.” J Natl Cancer Inst. August 17, 2026. PMID 42606905. https://doi.org/10.1093/jnci/djag222 (subscription access)
99. Uner FO et al.. “Rapid Reduction in Cancer Worry Through a Mindfulness-based Coping Programme: Evidence from a Randomised Trial with Women Awaiting Biopsy Results.” Semin Oncol Nurs. August 2026. PMID 42364950. https://doi.org/10.1016/j.soncn.2026.152284 (subscription access)
Vaccination has worked well enough that screening now has to be redesigned around it, and a dedicated collection of papers this month took that question apart.
Directly referenced:
100. Wentzensen N et al.. “How to evaluate and select cervical screening and triage tests in vaccinated populations.” J Natl Cancer Inst Monogr. August 1, 2026. PMID 42670622. https://doi.org/10.1093/jncimonographs/lgag013
101. Basu P et al.. “How practically feasible is tailored screening for cervical cancer based on human papillomavirus vaccination status?: the role of data linkage and registers.” J Natl Cancer Inst Monogr. August 1, 2026. PMID 42670621. https://doi.org/10.1093/jncimonographs/lgag014
Additional citations on related topics:
102. Gray P et al.. “Evidence for type replacement as a consequence of vaccination and implications for cervical screening.” J Natl Cancer Inst Monogr. August 1, 2026. PMID 42670618. https://doi.org/10.1093/jncimonographs/lgag011 (subscription access)
103. El-Zein M et al.. “The need to change cervical cancer screening in the post-human papillomavirus vaccination era: the interplay between disease prevalence and risk, test characteristics, and efficiency of screening programs.” J Natl Cancer Inst Monogr. August 1, 2026. PMID 42670619. https://doi.org/10.1093/jncimonographs/lgag007 (subscription access)
104. Waller J et al.. “Effective communications to support risk-adapted cervical screening in human papillomavirus-vaccinated women: lessons learned and ways forward.” J Natl Cancer Inst Monogr. August 1, 2026. PMID 42670620. https://doi.org/10.1093/jncimonographs/lgag006 (subscription access)
105. Bonde J et al.. “Deintensification of cervical cancer screening in the era of high human papillomavirus-vaccination coverage.” J Natl Cancer Inst Monogr. August 1, 2026. PMID 42670623. https://doi.org/10.1093/jncimonographs/lgag010 (subscription access)
106. Almonte M et al.. “Cervical cancer screening in vaccinated populations: challenges and implications for low- and middle-income countries.” J Natl Cancer Inst Monogr. August 1, 2026. PMID 42670624. https://doi.org/10.1093/jncimonographs/lgag009 (subscription access)
107. Adsul P et al.. “From evidence to practice: leveraging implementation science for transitioning to risk-adapted cervical cancer screening.” J Natl Cancer Inst Monogr. August 1, 2026. PMID 42670625. https://doi.org/10.1093/jncimonographs/lgag012 (subscription access)
108. Simms KT et al.. “Benefits, harms, and cervical cancer elimination timing of human papillomavirus screening approaches tailored to birth cohort as a proxy for vaccination status in the United States: a comparative modeling study.” J Natl Cancer Inst Monogr. August 1, 2026. PMID 42670626. https://doi.org/10.1093/jncimonographs/lgag008 (subscription access)
109. Bruni L et al.. “Developments in human papillomavirus vaccines, schedules, and implementation strategies.” J Natl Cancer Inst Monogr. August 1, 2026. PMID 42670627. https://doi.org/10.1093/jncimonographs/lgag015 (subscription access)
110. Jiang C et al.. “Cervical cancer incidence rates by birth cohort against the backdrop of human papillomavirus vaccination in the United States.” J Natl Cancer Inst. August 1, 2026. PMID 41502005. https://doi.org/10.1093/jnci/djaf374 (subscription access)
111. Jiang C et al.. “State-level progress in reducing cervical cancer incidence among US young women between the pre- and post-human papillomavirus vaccination eras.” J Natl Cancer Inst. August 1, 2026. PMID 41730310. https://doi.org/10.1093/jnci/djag051 (subscription access)
Surgery for early cervical cancer is being done less radically than a decade ago, and the research is catching up with what that means for cure rates and for fertility.
Directly referenced:
112. Dantas NMM et al.. “Conization With Lymph Node Assessment in Early-Stage Cervical Cancer: A Systematic Review and Meta-Analysis.” J Obstet Gynaecol Res. August ??, 2026. PMID 42576341. https://doi.org/10.1111/jog.70411
113. Wolswinkel JT et al.. “Balancing fertility potential and oncologic and obstetric risks: a vignette study on decision-making in fertility-sparing surgery for early-stage cervical cancer.” Int J Gynecol Cancer. August 2026. PMID 42385629. https://doi.org/10.1016/j.ijgc.2026.104802
114. Steinkasserer L et al.. “Analysis of the temporal changes in management of early-stage cervical cancer over a 10-year period in Germany: a multicenter retrospective analysis of the JAGO/NOGGO.” Front Oncol. August 5, 2026. PMID 42620224. https://doi.org/10.3389/fonc.2026.1916573
Additional citations on related topics:
115. Jalink M et al.. “The diagnosis to surgery interval and overall survival in patients with cervical cancer.” Cancer Epidemiol. August 4, 2026. PMID 42551070. https://doi.org/10.1016/j.canep.2026.103190 (open access: population-based study of the interval from diagnosis to surgery and overall survival in Ontario)
116. Paternostro C et al.. “Incidence and Risk Factors of Postoperative Bleeding After LLETZ.” Med Sci (Basel). August 13, 2026. PMID 42646612. https://doi.org/10.3390/medsci14040478 (open access: retrospective study of the incidence and risk factors of bleeding after large loop excision of the transformation zone)
117. Andrade MB et al.. “Prevalence of Pelvic Floor Dysfunction in Women with Cervical Cancer: A Cross-Sectional Study.” Int Urogynecol J. August 2026. PMID 41874630. https://doi.org/10.1007/s00192-026-06582-y (open access: cross-sectional study of pelvic floor dysfunction in women newly diagnosed with cervical cancer, before any treatment)
118. Chen X et al.. “Predictive value of triglyceride combined with age-adjusted D-dimer in patients with early-stage cervical cancer.” J Int Med Res. August 21, 2026. PMID 42630064. https://doi.org/10.1177/03000605261476782 (open access: dual-centre study of preoperative triglyceride and age-adjusted D-dimer as prognostic markers in early-stage disease)
119. Raspagliesi F et al.. “Revisiting the Concept of Nerve-Sparing Radical Hysterectomy: A Proof-of-Concept Prospective Study From a Cervical Cancer Cohort.” Ann Surg Oncol. August 2026. PMID 42002718. https://doi.org/10.1245/s10434-026-19671-5 (subscription access)
120. Hamada K et al.. “Nationwide trends in surgery selection and minimally invasive surgery for cervical cancer with preoperative T1B1/T1B2 disease in Japan.” Int J Clin Oncol. August 2026. PMID 42286379. https://doi.org/10.1007/s10147-026-03095-y (subscription access)
121. LeJeune CL et al.. “Analysis of indocyanine green-guided sentinel lymph node mapping for cervical cancer during pregnancy.” Int J Gynecol Cancer. August 2026. PMID 42424759. https://doi.org/10.1016/j.ijgc.2026.104810 (subscription access)
122. Kang O et al.. “Neoadjuvant Paclitaxel-Carboplatin Chemotherapy Followed by Cesarean Radical Hysterectomy in Pregnant Patients With Cervical Cancer: Obstetric, Neonatal, and Surgical Outcomes.” J Obstet Gynaecol Res. August ??, 2026. PMID 42489393. https://doi.org/10.1111/jog.70403 (subscription access)
123. Zhao G et al.. “Construction and Validation of a Risk Prediction Model for Lower Limb Lymphedema After Cervical Cancer Surgery: A Prospective Cohort Study.” Cancer Med. August ??, 2026. PMID 42608880. https://doi.org/10.1002/cam4.72194 (subscription access)
124. Li B et al.. “Identification of Risk Factors and Development of a Prediction Model for Postoperative Urinary Retention Following Radical Hysterectomy for Cervical Cancer Based on Preoperative Urodynamic Profiling.” Arch Esp Urol. August ??, 2026. PMID 42684283. https://doi.org/10.56434/j.arch.esp.urol.aeu006 (subscription access)
125. Ozkaya Ucar Y et al.. “Postoperative Sexual Quality of Life and Associated Factors After Loop Electrosurgical Excision Procedure Versus Cold Knife Conization in 185 Sexually Active Women With Preinvasive Cervical Lesions.” Med Sci Monit. August 30, 2026. PMID 42668418. https://doi.org/10.12659/MSM.954246 (subscription access)
126. Hong Q et al.. “Loop electrosurgical excision procedure and perinatal outcomes post-human papillomavirus cervical screening: A longitudinal cohort study.” Int J Gynaecol Obstet. August 2026. PMID 41709079. https://doi.org/10.1002/ijgo.70872 (subscription access)
127. Takemura H et al.. “Reproductive and Perinatal Outcomes After Trachelectomy: Vaginal Microbiota and Early Preterm Birth.” J Obstet Gynaecol Res. August ??, 2026. PMID 42572375. https://doi.org/10.1111/jog.70437 (subscription access)
128. Zhang M et al.. “Epidemiology and treatment options for cervical cancer patients aged <25 Years based on SEER database and real world research.” Surg Oncol. August 2026. PMID 42308701. https://doi.org/10.1016/j.suronc.2026.102480 (subscription access)
129. Samaranayake S et al.. “Benchmarking Cervical Cancer Care Pathways-Measuring Timelines and Identifying Factors Associated With Delay for Women Undergoing Definitive Radiotherapy in New South Wales, Australia.” Aust N Z J Obstet Gynaecol. August ??, 2026. PMID 42576690. https://doi.org/10.1111/ajo.70174 (subscription access)
130. Debnath A et al.. “Time to treatment initiation delays in cervical cancer worldwide: A systematic review and meta-analysis.” Cancer Epidemiol. August 2026. PMID 42092224. https://doi.org/10.1016/j.canep.2026.103095 (subscription access)
Most cervical precancer never becomes cancer, and the research question has shifted from how to remove it to whether it always needs removing.
Directly referenced:
131. Luo D et al.. “Gynaecologists’ Views and Acceptability of Active Surveillance for Women Diagnosed With Cervical Intraepithelial Neoplasia 2: A Qualitative Study.” Aust N Z J Obstet Gynaecol. August ??, 2026. PMID 42530454. https://doi.org/10.1111/ajo.70165
132. Termini L et al.. “Photodynamic therapy: a promising alternative for high-grade squamous intraepithelial lesion treatment.” Front Oncol. August 7, 2026. PMID 42630880. https://doi.org/10.3389/fonc.2026.1899399
133. Palande V et al.. “Exploration of immune correlates of viral clearance after PVX2 immunotherapy in patients with human papillomavirus type 16 infection and cervical intraepithelial neoplasia grade ≤1.” J Virol. August 2026. PMID 42505425. https://doi.org/10.1128/jvi.00643-26
Additional citations on related topics:
134. Arnholdt M et al.. “Preclinical Characterization of Dielectric Barrier Discharge as a Complementary Plasma Technology for Low-Thermal Argon Plasma Devitalization of Cervical Intraepithelial Neoplasia.” ACS Appl Mater Interfaces. August 27, 2026. PMID 42678941. https://doi.org/10.1021/acsami.6c13697 (open access: preclinical characterisation of a new cold-plasma device for treating cervical intraepithelial neoplasia)
135. Schleicher OM et al.. “Regression of high-grade squamous intraepithelial lesions in women aged 30 years or younger: a retrospective cohort study.” J Cancer Res Clin Oncol. August 1, 2026. PMID 42542454. https://doi.org/10.1007/s00432-026-06578-7 (subscription access)
136. Ssedyabane F et al.. “Recent treatment outcomes of cervical intraepithelial neoplasia in south western Uganda: a six year retrospective study.” Gynecol Oncol Rep. August 2026. PMID 42383152. https://doi.org/10.1016/j.gore.2026.102149 (subscription access)
137. Zhao C et al.. “Cervical HSIL and Microinvasive Squamous Cell Carcinoma With Superficial Spread to Endometrium and/or Fallopian Tube Epithelium: Clinical and Pathological Findings in 2 Patients and Literature Review.” Int J Surg Pathol. August 2026. PMID 41731703. https://doi.org/10.1177/10668969251414163 (subscription access)
138. Jiang A et al.. “Malignant transformation risk and management dilemmas of atypical lobular endocervical glandular hyperplasia: A retrospective cohort study comparing Peutz-Jeghers syndrome versus sporadic cases.” Gynecol Oncol. August 2026. PMID 42349040. https://doi.org/10.1016/j.ygyno.2026.06.017 (subscription access)
139. Qi J et al.. “Human papillomavirus 42: from a low-risk genotype to a potentially oncogenic virus.” Clin Exp Dermatol. August 17, 2026. PMID 41852134. https://doi.org/10.1093/ced/llag141 (subscription access)
140. Wang Z et al.. “Vaginoscopic Resection of Cervical Botryoid Sarcoma in a Pediatric Patient.” J Pediatr Adolesc Gynecol. August ??, 2026. PMID 42498328. https://doi.org/10.1016/j.jpag.2026.01.288 (subscription access)
Cervical cancer is not one disease, and August brought work on the subtypes that behave differently and on the markers that might track disease without another biopsy.
Directly referenced:
141. Yamada H et al.. “Transcriptome profiling identifies RET activation as a therapeutic target in gastric-type endocervical adenocarcinoma.” Biomed Pharmacother. August 2026. PMID 42361625. https://doi.org/10.1016/j.biopha.2026.119696
142. Raj EN et al.. “Multi-Omics Identification of UBE2C as a Prognostic Biomarker and Therapeutic Target Linked to Topotecan Sensitivity in Cervical Cancer.” Oncol Res. August 13, 2026. PMID 42630722. https://doi.org/10.32604/or.2026.079551
143. Pepe L et al.. “Liquid Biopsy for Minimal Residual Disease Assessment in Endometrial and Cervical Cancers: Molecular Rationale, Clinical Evidence, and Translational Barriers.” Int J Mol Sci. August 10, 2026. PMID 42653160. https://doi.org/10.3390/ijms27167155
Additional citations on related topics:
144. Jia M et al.. “An interpretable Hallmark pathway activity classifier for distinguishing CIN3/HSIL from invasive cervical squamous carcinoma: Development, external validation, and feature stability assessment.” PLoS One. August 28, 2026. PMID 42664194. https://doi.org/10.1371/journal.pone.0356465 (open access: transcriptomic pathway classifier distinguishing CIN3/HSIL from invasive squamous carcinoma, with external validation)
145. Song J et al.. “Bulk and single cell RNA sequencing data reveal lactylation-related gene signatures for prognosis and immunity in cervical cancer.” Braz J Med Biol Res. August 21, 2026. PMID 42659456. https://doi.org/10.1590/1414-431X2026e15368 (open access: lactylation-related gene signatures for prognosis and immune landscape, from bulk and single-cell RNA sequencing)
146. Armerinayanti NW et al.. “MicroRNA-21 (miR-21), Mutant Tumor Protein p53, and Matrix Metalloproteinase-9 (MMP-9) as Risk Markers for High-Grade Tumor Budding (HGTB) in Cervical Carcinoma: A Case-Control Study in a Balinese Population.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663214. https://doi.org/10.31557/APJCP.2026.27.8.2931 (open access: case-control study of miR-21, mutant p53 and MMP-9 as markers of high-grade tumour budding in a Balinese population)
147. Taizhanova D et al.. “Biomarkers of Hypercoagulability and Thromboinflammation in Cervical Cancer-Associated Thrombosis: A Systematic Review with Translational Insights from Breast Cancer.” Int J Mol Sci. August 16, 2026. PMID 42653312. https://doi.org/10.3390/ijms27167302 (open access: systematic review of blood-clotting and inflammation biomarkers in cervical cancer-associated thrombosis)
148. Gao M et al.. “Human Wings Apart-Like Protein as a Serum Diagnostic Biomarker in Cervical Cancer: An Integrative Bioinformatics Analysis with Serum Validation.” J Vis Exp. August 21, 2026. PMID 42631579. https://doi.org/10.3791/72194 (subscription access)
149. Wahid A et al.. “Extracellular Vesicles as Emerging Cervical Cancer Diagnostic and Molecular Signatures of Tumor and Immune Dynamics.” ACS Biomater Sci Eng. August 10, 2026. PMID 42446503. https://doi.org/10.1021/acsbiomaterials.6c00063 (subscription access)
150. Singh P et al.. “Integrating non-coding RNA profiling with HPV genotyping for cervical cancer risk stratification and early detection.” Mol Biol Rep. August 28, 2026. PMID 42663722. https://doi.org/10.1007/s11033-026-12662-5 (subscription access)
151. Lin X et al.. “Oncogenic DNMT3B as a therapeutic target for cervical cancer.” Chin Med J (Engl). August 2026. PMID 42402721. https://doi.org/10.1097/CM9.0000000000004130 (subscription access)
152. Alredha RDA et al.. “Evaluation of serum Cytokeratin 5 and p63 as non-invasive biomarkers for the diagnosis and staging of cervical cancer: a case-control study.” Clin Transl Oncol. August 2026. PMID 41722012. https://doi.org/10.1007/s12094-026-04238-3 (subscription access)
153. Virarkar M et al.. “Quantitative imaging biomarkers as prognostic indicators in squamous cell cervical carcinoma: a retrospective cohort analysis.” Abdom Radiol (NY). August 2026. PMID 41454940. https://doi.org/10.1007/s00261-025-05351-7 (subscription access)
154. Wang B et al.. “Preoperative prediction of parametrial invasion in early-stage cervical cancer: a radiomics nomogram fusing multi-parametric MRI and clinical biomarkers.” Abdom Radiol (NY). August 2026. PMID 41697314. https://doi.org/10.1007/s00261-025-05353-5 (subscription access)
155. Juneja S et al.. “MedFusionNet: A hybrid transformer-based multimodal deep learning framework for chronic disease prediction in women’s health.” Comput Med Imaging Graph. August 2026. PMID 42424829. https://doi.org/10.1016/j.compmedimag.2026.102795 (subscription access)
156. Ogura J et al.. “HPV18-Positive Cervical Large Cell Neuroendocrine Carcinoma With Rapid Progression Despite Pembrolizumab Combined With Chemotherapy: A Case Report With Immunogenomic Insights.” J Obstet Gynaecol Res. August ??, 2026. PMID 42521492. https://doi.org/10.1111/jog.70426 (subscription access)
Where a woman lives and what else is happening in her life still shape whether her cervical cancer is caught early, and this is the part of the field where the gap between what is possible and what happens is widest.
Directly referenced:
157. Mengistie N et al.. “Access to cervical cancer care in sub-Saharan Africa: a narrative review of barriers and opportunities.” Front Public Health. August 18, 2026. PMID 42682464. https://doi.org/10.3389/fpubh.2026.1881652
158. Milambo MJP et al.. “Intersecting Burdens: HIV Prevalence and Cervical Cancer Progression Among Women in the Eastern Cape, South Africa: A Retrospective Descriptive Study.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663199. https://doi.org/10.31557/APJCP.2026.27.8.2795
159. Botsun P et al.. “Cervical screening under wartime: resilience and quality of laboratory services in Ukraine during the Russian invasion.” Front Public Health. August 11, 2026. PMID 42643660. https://doi.org/10.3389/fpubh.2026.1909774
Additional citations on related topics:
160. Chokunonga E et al.. “Trends in the incidence of cancers of the breast and female genital tract in Harare, Zimbabwe 1990-2019.” Int J Cancer. August 2026. PMID 41803021. https://doi.org/10.1002/ijc.70436 (open access: thirty-year incidence trends for five women’s cancers in Harare, Zimbabwe, with cervix the highest by far)
161. Nguyen DTN et al.. “Cervical cancer burden and elimination readiness in the US-affiliated Pacific Islands: A structured narrative review.” Cancer Epidemiol. August 2026. PMID 42372369. https://doi.org/10.1016/j.canep.2026.103144 (open access: structured narrative review of cervical cancer burden and elimination readiness across the US-affiliated Pacific Islands)
162. Ramaliba TM et al.. “Incidence patterns and temporal trends of breast, prostate, oesophageal and cervical cancer in rural Eastern Cape Province, South Africa 1998-2021.” Cancer Epidemiol. August 2026. PMID 42391785. https://doi.org/10.1016/j.canep.2026.103151 (open access: incidence patterns and trends for four cancers including cervix in rural Eastern Cape Province, South Africa, 1998 to 2021)
163. Urquhart-Ducharme R et al.. “Eliminating cervical cancer in Canada is within reach.” Can J Public Health. August 14, 2026. PMID 42601588. https://doi.org/10.17269/s41997-026-01240-8 (open access: commentary on Canada’s plan to eliminate cervical cancer by 2040, including First Nations, Inuit and Metis specific actions)
164. Andersson M et al.. “Prevalence of cervical human papillomavirus infections and cytological abnormalities in asymptomatic women living with HIV in Addis Ababa, Ethiopia.” Sci Rep. August 1, 2026. PMID 42538348. https://doi.org/10.1038/s41598-026-64488-7 (open access: prevalence of cervical HPV infection and cytological abnormalities among asymptomatic women living with HIV in Addis Ababa)
165. Renzaho AMN et al.. “Co-Designing Culturally Tailored Bowel, Cervical and Breast Cancer Screening Interventions With Migrant Communities: Towards Closing the Migration-Related Cancer-Equity Gap in New South Wales, Australia.” Health Expect. August ??, 2026. PMID 42555149. https://doi.org/10.1111/hex.70805 (open access: co-design of culturally tailored screening interventions with migrant and refugee communities in New South Wales)
166. Allicock MA et al.. “Formative Work to Guide Implementation of an Evidence-Based Breast and Cervical Cancer Prevention and Early Detection Behavioral Health Program in Clinics: Qualitative Study Guided by the Consolidated Framework for Implementation Research.” JMIR Form Res. August 13, 2026. PMID 42594355. https://doi.org/10.2196/89393 (open access: qualitative implementation study of a community health worker screening programme for medically underserved Latinas)
167. Deribe KS et al.. “Multi-level determinants of comprehensive palliative care delivery for breast and cervical cancer patients in Ethiopia: using the socio-ecological model as an analytical framework.” BMC Palliat Care. August 25, 2026. PMID 42642742. https://doi.org/10.1186/s12904-026-02300-z (open access: socio-ecological analysis of what enables and blocks comprehensive palliative care for women with breast and cervical cancer in Ethiopia)
168. Afaya A et al.. “Fertility in the Shadow of Cancer: Experiences of Reproductive Loss Among Women with Gynecological Cancers in Ghana.” PLoS One. August 14, 2026. PMID 42599904. https://doi.org/10.1371/journal.pone.0343859 (open access: interviews with fourteen women in Ghana about reproductive loss after gynaecological cancer treatment)
169. Feng X et al.. “Research trends in depression associated with gynecologic cancers from 2006 to 2025: a multidatabase bibliometric and visual analysis.” Front Oncol. August 12, 2026. PMID 42657127. https://doi.org/10.3389/fonc.2026.1910076 (open access: bibliometric analysis of research on depression in gynaecologic cancers)
170. Li X et al.. “HPV52 predominates in cervical infections and precancerous lesions in Chongqing, China: a 6-year study linking genotypes to vaginal microecology.” Front Public Health. August 14, 2026. PMID 42666361. https://doi.org/10.3389/fpubh.2026.1879232 (open access: six-year study of HPV genotype distribution and vaginal microecology in Chongqing, China, where HPV52 predominates)
171. Kwesi-Maliepaard EM et al.. “Genotype distribution of high-risk and potential high-risk HPV types among women in different screening and clinic settings in Ghana and Kenya.” PLoS One. August 28, 2026. PMID 42664253. https://doi.org/10.1371/journal.pone.0355868 (open access: HPV genotype distribution across screening and clinic settings in Ghana and Kenya)
172. Gupta RK et al.. “Human Papillomavirus (HPV) Proportion and Genotype Distribution among Reproductive age Women of a Hilly District of Nepal.” J Nepal Health Res Counc. August 3, 2026. PMID 42638245. https://doi.org/10.33314/jnhrc.v24i01.5135 (open access: high-risk HPV prevalence and genotype distribution among reproductive-age women in a hilly district of Nepal)
173. McCormick LJ et al.. “Cervical Cancer Screening Coverage Increased in Malawi, Tanzania, Zambia, and Zimbabwe: Findings From Sequential Population-Based HIV Impact Assessment Surveys 2015-2017 and 2020-2023.” J Acquir Immune Defic Syndr. August 1, 2026. PMID 41983477. https://doi.org/10.1097/QAI.0000000000003880 (subscription access)
174. Naicker N et al.. “Diagnostic accuracy of the Xpert HPV assay in women starting antiretroviral treatment in South Africa.” Int J STD AIDS. August 2026. PMID 42288973. https://doi.org/10.1177/09564624261459075 (subscription access)
175. Shastri S et al.. “Cancer Screening in India: Lessons, Limitations, and Pragmatic Solutions for the Next Decade.” JCO Glob Oncol. August 13, 2026. PMID 42594327. https://doi.org/10.1200/GO-26-00018 (subscription access)
176. Schnall R et al.. “Factors Related To Improving the Quality of Cervical Cancer Screening for Women Living with HIV in La Romana, Dominican Republic: A Qualitative Descriptive Study.” AIDS Behav. August 2026. PMID 41831114. https://doi.org/10.1007/s10461-026-05074-w (subscription access)
177. Sivakumar I et al.. “Long-term trends and post-pandemic deviations in cervical cancer burden in South India, 1990-2023: a Global Burden of Disease 2023 study.” Osong Public Health Res Perspect. August 26, 2026. PMID 42642978. https://doi.org/10.24171/j.phrp.2026.0252 (subscription access)
178. Gregory K et al.. “Aotearoa New Zealanders’ views of policies and funding for human papillomavirus vaccination and screening for cervical and lung cancers: a national survey.” N Z Med J. August 28, 2026. PMID 42659668. https://doi.org/10.26635/6965.7538 (subscription access)
179. Watson JL. “The Cancer That Could Disappear.” Clin J Oncol Nurs. August 3, 2026. PMID 42555791. https://doi.org/10.1188/26.CJON.252-253 (subscription access)
180. Derveeuw S et al.. “Navigating racialised healthcare: Intersectional experiences shaping cancer screening among Black women in Belgium.” Soc Sci Med. August 2026. PMID 42217484. https://doi.org/10.1016/j.socscimed.2026.119449 (subscription access)
181. Chepkorir J et al.. “Patient portal notifications for breast and cervical cancer screening results: Perspectives of women with limited english proficiency.” Patient Educ Couns. August 2026. PMID 42085773. https://doi.org/10.1016/j.pec.2026.109651 (subscription access)
182. Kou H et al.. “Changes in Depressive Symptoms Following Mindfulness Training in Female Patients With Abdominal or Abdominopelvic Cancer: A Preliminary Non-Randomized Controlled Study.” Psychooncology. August ??, 2026. PMID 42609116. https://doi.org/10.1002/pon.70585 (subscription access)
183. Lee A et al.. “Validity of HINT-8 in evaluating health-related quality of life among cervical cancer patients.” J Comp Eff Res. August 2026. PMID 42496163. https://doi.org/10.57264/cer-2025-0194 (subscription access)
184. Li T et al.. “[Prevalence of cervical human papillomavirus infection among women in Honghe Hani and Yi Autonomous Prefecture, Yunnan Province, China].” Zhonghua Zhong Liu Za Zhi. August 23, 2026. PMID 42595548. https://doi.org/10.3760/cma.j.cn112152-20251202-00597 (subscription access)
General and basic-science cervical cancer research.
Additional citations on related topics:
185. Li X et al.. “Spatial multi-omics guides ASCT2-targeted delivery of glycolysis inhibitor for cervical cancer suppression and chemoresistance reversal.” J Adv Res. August 2026. PMID 41253274. https://doi.org/10.1016/j.jare.2025.11.035 (open access: spatial multi-omics guiding a targeted delivery system for a glycolysis inhibitor to reverse chemoresistance)
186. Zhang C et al.. “HNRNPU K181 Lactylation Drives Cervical Cancer Growth by Upregulating PHGDH and Reprogramming Serine Metabolism.” Adv Sci (Weinh). August 2026. PMID 42201673. https://doi.org/10.1002/advs.202520222 (open access: mechanism study of HNRNPU lactylation driving growth through serine metabolism)
187. Li Z et al.. “β-Elemene Triggers Drp1-Dependent Mitochondrial Fission Through CDK1/Cyclin B1 Signaling in Cervical Cancer Cells.” J Biochem Mol Toxicol. August ??, 2026. PMID 42506883. https://doi.org/10.1002/jbt.71032 (open access: laboratory study of beta-elemene triggering mitochondrial fission in cervical cancer cells)
188. Fauzia RP et al.. “Exploring the in-vitro evaluation of folic acid-modified gadolinium nanoparticles in HEK-293, HeLa, and KB cancer cells for targeted-MR-imaging agent candidate.” Sci Rep. August 7, 2026. PMID 42567852. https://doi.org/10.1038/s41598-026-38700-7 (open access: in-vitro evaluation of folic-acid-modified gadolinium nanoparticles as a targeted MRI contrast agent)
189. Khaled RK et al.. “Folic acid-loaded amino-functionalized MCM-41 as a drug delivery system for cervical cancer modulating apoptotic and survival signals.” Sci Rep. August 13, 2026. PMID 42595795. https://doi.org/10.1038/s41598-026-65500-w (open access: folic-acid-loaded mesoporous silica as a drug delivery system, tested in cervical cancer cells)
190. He S et al.. “[Expression of Concern] MicroRNA‑145‑5p suppresses fascin to inhibit the invasion and migration of cervical carcinoma cells.” Mol Med Rep. August 14, 2026. PMID 42596825. https://doi.org/10.3892/mmr.2026.13988 (open access: Expression of Concern relating to a previously published cervical carcinoma microRNA study)
191. Spurgeon ME. “The cervicovaginal microbiome: an emerging determinant of HPV infection and disease.” J Virol. August 2026. PMID 42489460. https://doi.org/10.1128/jvi.01706-25 (open access: review of the cervicovaginal microbiome as a determinant of HPV infection and disease)
192. He Y et al.. “The microbiota-host metabolic axis in cervical cancer: from homeostatic disruption to mechanisms of therapy resistance.” Front Cell Infect Microbiol. August 5, 2026. PMID 42621466. https://doi.org/10.3389/fcimb.2026.1890330 (open access: review of the microbiota-host metabolic axis from healthy cervix to invasive cancer and therapy resistance)
193. Wang W et al.. “The implications and mechanisms of vaginal microbiota metabolites on cervical cancer progression.” Front Cell Infect Microbiol. August 14, 2026. PMID 42666586. https://doi.org/10.3389/fcimb.2026.1886165 (open access: review of how vaginal microbiota metabolites influence cervical cancer progression)
194. Wang X et al.. “Elevated neutrophil extracellular traps formation driven by the HPV-mediated CXCL8-CXCR1/2-ROS-p21 axis promotes the growth and metastasis of cervical cancer.” Front Immunol. August 20, 2026. PMID 42694332. https://doi.org/10.3389/fimmu.2026.1861481 (open access: mechanism study of neutrophil extracellular traps promoting growth and metastasis via an HPV-driven signalling axis)
195. Rahimi-Moghaddam A et al.. “Dual Inhibition of PI3K-AKT Signaling Pathway by miR-542 Overexpression in Cervical Cancer.” Biochem Genet. August 2026. PMID 41082028. https://doi.org/10.1007/s10528-025-11257-2 (subscription access)
196. Yan Y et al.. “Distinct miR319a identified frommediates cross-kingdom suppression of cervical cancer by targeting ITGA3.” Acta Biochim Biophys Sin (Shanghai). August 28, 2026. PMID 41988664. https://doi.org/10.3724/abbs.2026010 (subscription access)
197. Habiba U et al.. “Machine Learning-driven Prediction of Cervical Cancer Cell Viability After Treatment With Thymoquinone, Curcumin, and 5-Fluorouracil.” Appl Biochem Biotechnol. August 2026. PMID 42105068. https://doi.org/10.1007/s12010-026-05704-y (subscription access)
198. Weng X et al.. “Exosomes derived from M2-polarized tumor-associated macrophages contribute to immune escape in cervical cancer.” Biochem Biophys Res Commun. August 2026. PMID 42241976. https://doi.org/10.1016/j.bbrc.2026.154046 (subscription access)
199. Wu C et al.. “OGT-mediated O-GlcNAcylation of STAT1 impairs its Ser727 phosphorylation and weakens antitumor immunity of tumor-associated macrophages in cervical cancer.” Biochem Biophys Res Commun. August 2026. PMID 42269272. https://doi.org/10.1016/j.bbrc.2026.154090 (subscription access)
200. Zhang Y et al.. “Advances and prospects of MIL-based drug delivery systems in the diagnosis and treatment of cervical cancer.” Dalton Trans. August 4, 2026. PMID 42329079. https://doi.org/10.1039/d6dt00965d (subscription access)
201. Yang F et al.. “PCK2 Promotes Ribosome Biogenesis in Cervical Cancer Cells via Interaction with hnRNPK.” Reprod Sci. August 2026. PMID 42443589. https://doi.org/10.1007/s43032-026-02143-2 (subscription access)
202. Fan Y et al.. “The Expression and Clinical Value of miR-483-5p in Cervical Cancer and Its Regulation of Cervical Cancer via TIMP2.” J Obstet Gynaecol Res. August ??, 2026. PMID 42493346. https://doi.org/10.1111/jog.70396 (subscription access)
203. Yilihamu Y et al.. “Tumor microenvironment-activated HA@GOx/IR-820@MnOnanosheets for dual-modal imaging guided phototherapy of cervical cancer.” J Mater Chem B. August 12, 2026. PMID 42518188. https://doi.org/10.1039/d6tb01062h (subscription access)
204. Kul Köprülü T et al.. “Aloe vera extract disrupts mitochondrial bioenergetics and suppresses HeLa cervical cancer cell proliferation: Transcriptomic and metabolic insights into cisplatin co-treatment.” J Bioenerg Biomembr. August 6, 2026. PMID 42560575. https://doi.org/10.1007/s10863-026-10127-9 (subscription access)
205. Huang C et al.. “Recurrent PIK3CA-E545K mutation promotes cervical cancer growth and invasion via AKT/mTOR signaling.” Mol Genet Genomics. August 7, 2026. PMID 42562966. https://doi.org/10.1007/s00438-026-02495-z (subscription access)
206. Liu C et al.. “USP1 Promotes Malignant Progression of Cervical Cancer Cells by Deubiquitinating and Stabilizing ATG13 to Enhance Autophagic Activity.” J Biochem Mol Toxicol. August ??, 2026. PMID 42573051. https://doi.org/10.1002/jbt.71060 (subscription access)
207. Zhou J et al.. “GATA1 knockdown enhances CD8T cell responses and protects against immune escape in cervical squamous cell carcinoma through FGL1 downregulation.” J Mol Histol. August 13, 2026. PMID 42593543. https://doi.org/10.1007/s10735-026-10940-x (subscription access)
208. Lu M et al.. “Circ_0070190 suppresses the malignant progression of cervical cancer by sponging miR-587.” J Mol Histol. August 18, 2026. PMID 42611339. https://doi.org/10.1007/s10735-026-10934-9 (subscription access)
209. Xing T et al.. “Drug Resistance and Therapeutic Reversal Strategies in Ovarian, Cervical, and Endometrial Cancers.” J Vis Exp. August 21, 2026. PMID 42631593. https://doi.org/10.3791/71197 (subscription access)
210. Liu X et al.. “HuB/HuR inhibition decreases HPV E6 and E7 proteins, stabilizes p53, and induces integrated stress to impair cervical cancer cell growth.” Proc Natl Acad Sci U S A. August 26, 2026. PMID 42647117. https://doi.org/10.1073/pnas.2401248123 (subscription access)
211. Masood S et al.. “PARP1 genetic variants modulate gene expression and cervical cancer susceptibility in a North Indian case-control study.” Mol Biol Rep. August 27, 2026. PMID 42658306. https://doi.org/10.1007/s11033-026-12655-4 (subscription access)
212. Gholami Fashkhami M et al.. “Chrysin treatment is associated with altered microrna expression and reduced levels of HPV16 E6 protein in caski cervical cancer cells.” Med Oncol. August 29, 2026. PMID 42667494. https://doi.org/10.1007/s12032-026-03381-9 (subscription access)
213. Chen J et al.. “[Mechanism study on baicalein inhibiting cervical cancer driven by persistent HPV infection via restoring MAVS-IRF3-IFN-β mitochondrial antiviral signal].” Zhongguo Zhong Yao Za Zhi. August ??, 2026. PMID 42693064. https://doi.org/10.19540/j.cnki.cjcmm.20260330.704 (subscription access)