August Digest
This Month in Ovarian Cancer Research
August 2026
August was a heavy month for ovarian cancer research, and its center of gravity sat with the treatments already in wide use rather than with anything brand new. The final quality-of-life analysis from a major PARP inhibitor trial reported that maintenance treatment itself did not make people feel worse than placebo, while the cancer returning did, and that decline never fully reversed. A large European safety study put real-world numbers on the risk of second blood cancers after niraparib and located every one of them in people treated for recurrent rather than newly diagnosed disease. Antibody-drug conjugates continued their run as the most active area in recurrent disease, with real-world results for one of them and a survey of how often the three markers these drugs target actually appear together. Elsewhere, a blood test built on platelet RNA outperformed CA-125 for detection while still missing early-stage cancers, a methylation classifier separated mucinous ovarian cancer from cancer that had spread to the ovary from somewhere else, and a large surgical registry reported how much longer people lived after a second operation for recurrence. Two studies looked squarely at who is being left out: one at the near absence of Black participants from the trials that established PARP inhibitors, another at a global burden that is rising fastest where care is hardest to get.
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.
Living on a PARP inhibitor: what it costs, and what it does not.
PARP inhibitors block an enzyme that cancer cells use to repair their own DNA, and taking one as maintenance treatment after chemotherapy is now standard for many people with advanced ovarian cancer. This month’s research asked less about whether these drugs work and more about what living on them actually involves.
• Niraparib maintenance did not worsen overall quality of life compared with placebo, but the cancer coming back did, and that decline never reversed. This is the final patient-reported analysis from the PRIMA trial, in which people with newly diagnosed advanced ovarian cancer were randomly assigned two-to-one to niraparib or placebo and filled in quality-of-life questionnaires throughout. Completion stayed above 89% through cycle 24, roughly two years, and fell to 80% at the end of treatment. Early differences in digestive symptoms between the two groups resolved over time, and overall quality of life ended up no different between them. What did make a difference was progression: when the cancer grew, overall quality of life, symptom scores and general health ratings all dropped sharply in both groups and never returned to pre-progression levels, with fatigue, breathlessness, pain and appetite loss all worsening and staying worse. The pattern held regardless of whether the tumor had trouble repairing its own DNA. Two things to keep separate here: the niraparib-versus-placebo comparison was a prespecified part of a randomized trial, while the before-and-after look at progression was added afterwards and is suggestive rather than proof. Its practical message is still that delaying progression is itself a quality-of-life intervention. (Read the full paper)
• Second blood cancers after niraparib were uncommon in ordinary practice, and every case occurred in people treated for recurrent rather than newly diagnosed disease. This was a post-approval safety study run by the manufacturer and registered with the European ENCePP network, following 745 people with high-grade epithelial ovarian cancer (almost all high-grade serous) on niraparib maintenance across Germany, Italy, the Netherlands and Spain, median age 65. Nine people developed myelodysplastic syndrome or acute myeloid leukemia. All nine were among the 564 treated after recurrence, which is 1.6% of that group and a rate of 0.62 per 100 patient-years; none of the 181 people on first-line maintenance did. Six people (0.8% of the whole cohort) developed a different second cancer. Two limits matter for reading those figures. People were on niraparib a median of about 11 months and fewer than two-thirds of the recurrent group completed two years of follow-up, while the median time from starting the drug to a blood cancer appearing was 32.7 months, so longer follow-up may find more cases. And the authors are explicit that real-world and clinical trial rates cannot be directly compared, though they judged what they saw consistent with the drug’s label. Because everyone in this study took niraparib, it describes how often these events happen rather than how much of that is caused by the drug. (Read the full paper)
• A different way of reading a tumor’s DNA classified who has faulty DNA repair without relying on the standard test, which matters where that test is not available. Current tests look for the genomic “scars” left by faulty DNA repair. This phase 2 trial instead built a marker from whole-exome sequencing using tumor BRCA mutation status plus how closely the tumor’s pattern of mutations matched a known DNA-repair signature, with a lower signature threshold accepted only in tumors that do not carry extra copies of CCNE1. Of 170 people with stage IIIC or IV disease, 169 could be assessed (99.5%) and 123 (72.4%) were classified as having faulty DNA repair. Among the 45 who responded to platinum chemotherapy, had not received bevacizumab and went on to olaparib, median time without progression was 22.3 months. That is well past the 9-month benchmark the trial was designed against, though that benchmark was an assumption borrowed from older trials, and the trial’s own small placebo group of 11 people reached 16.7 months. In a 16-patient subset the new marker agreed with the commercial test 81% of the time. Because only marker-positive people were enrolled, this shows the marker can be built and applied, not that it separates those who benefit from olaparib from those who do not. (Read the full paper)
• If you carry an inherited BRCA mutation, chemotherapy may lower your white cell count more than it does for others, though this month’s direct evidence rests on very few carriers. In a retrospective single-center review, 8 BRCA carriers were compared with 33 confirmed non-carriers out of 54 people treated for stage III or IV disease. Carriers tended toward lower neutrophil counts during platinum and taxane chemotherapy, but with only 8 carriers the study had almost no power to detect a difference, and none of the comparisons reached significance. Pooling those results with previously published studies, all of them retrospective, told a clearer story: carriers had significantly higher odds of neutropenia (odds ratio 1.68) and of needing growth-factor support (odds ratio 3.09), with no significant differences in anemia, low platelets, dose delays or dose reductions. Tumors with faulty DNA repair showed no clearly increased toxicity once multiple comparisons were accounted for, though their hemoglobin ran lower throughout, starting from a meaningfully lower baseline before chemotherapy began (11.1 against 12.7 g/dL). Dose delays and reductions were no more common in carriers, but eight carriers cannot rule out an effect, and the study did not look at hospitalization or quality of life. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Whether a tumor can repair its own DNA decides who gets a PARP inhibitor, and the test is not available everywhere.
Homologous recombination deficiency, usually shortened to HRD, means a tumor has lost the ability to fix certain kinds of DNA damage, which is what makes PARP inhibitors work. Testing for it is now a gatekeeper to treatment.
• Where full HRD testing is not available, a marker that some gene panels already report may serve as a rough stand-in. Researchers looked at an Alberta, Canada cohort of 96 people with high-grade serous cancer who had HRD testing between 2023 and 2025, with confirmation in separate cohorts from other centers. Tumors with faulty DNA repair were about three and a half times more likely to be given niraparib, and among those given it, more of the HRD group were still on treatment at the time of analysis (40% against 23%). Among tumors without a BRCA mutation, extra copies of the MYC gene (five or more) were far more common in HRD tumors than in repair-proficient ones, both in the main group (43% against 3%) and in the validation groups (55% against 11%). Having MYC amplification carried an 85% probability of being HRD, against a background rate of 33%. This is an observational association rather than a validated test, but it points at something clinically usable from data many labs already generate. (Read the full paper)
• Where a national testing workflow exists, most patients get through its first step, but people who never have surgery are being missed, and that has consequences for their relatives too. The Netherlands routes ovarian cancer patients through a “Tumor-First” process, testing tumor DNA to decide who needs inherited-gene testing and who might benefit from a PARP inhibitor. In this retrospective study of the national cancer registry, 79% of the 2,221 patients diagnosed in 2023 or 2024 whose diagnosis was confirmed on tissue had tumor DNA testing, and 94% of those tests succeeded. That 79% is the tumor DNA testing rate, which is the gateway to inherited-gene testing rather than the same thing as it, and the study could not measure how many patients went on to actual germline testing. Around a hundred further patients were diagnosed clinically with no tissue sample at all and so could not be tested, and they sit outside that figure entirely. Testing was much less likely for those whose main treatment was chemotherapy rather than surgery, or who received no treatment at all, for those who died within 100 days of diagnosis, and above all for those diagnosed on a biopsy or cytology sample with no subsequent operation, where the rate fell to 58% against 87 to 95% elsewhere. If you or a relative were diagnosed without surgery, this is a reasonable thing to ask about. (Read the full paper)
• A gene-expression signature is the first serious candidate for identifying who benefits from bevacizumab, a drug given widely with no test to guide it. Bevacizumab blocks the blood-vessel growth that tumors depend on, and it is used as maintenance treatment without any way of predicting who it will help. In a retrospective analysis of stored tumor samples, researchers sequenced 244 tumors from 212 women, though only 181 patients had the clinical information needed for the survival analysis, 67 of whom had received bevacizumab and 114 of whom had not. One signature stood out: among the 99 patients whose tumors over-expressed it, adding bevacizumab to chemotherapy went with significantly longer survival (hazard ratio 0.41), and a similar pattern appeared in a previously published cohort of 377. The researchers separately confirmed that the gene pattern itself exists in a public dataset of 426 tumors from women who had not received bevacizumab. The important caveat is that the statistical test of whether the signature actually predicts who benefits reached significance only in the older published cohort and not in the researchers’ own new one, so this is a candidate marker awaiting a proper test rather than a finding ready to guide treatment. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Antibody-drug conjugates are the most active area in recurrent disease, and the question has shifted to who they suit.
These drugs work by attaching chemotherapy to an antibody that seeks out a marker on the cancer cell surface, delivering the payload where it is needed and sparing more healthy tissue.
• Folate receptor alpha is the commonest of the three markers these drugs target, and carrying all three is rare, which matters for choosing between them. In a retrospective review of tumor samples from 193 people with primary high-grade serous cancer, researchers measured folate receptor alpha, TROP2 and HER2. Folate receptor alpha was highly expressed in 51.8% and TROP2 in 24.9%, while a quarter showed only ultra-low HER2, a low-expression category rather than a positive drug target. All three together appeared in just 7.8% of tumors. High TROP2 went with more advanced stage at diagnosis, and HER2 was more common in BRCA-mutated tumors. After accounting for DNA-repair status, prior PARP inhibitor use and anti-angiogenic treatment, faulty DNA repair predicted longer time before progression and high TROP2 predicted shorter; overall survival was not shown to differ. Folate receptor alpha and HER2 did not independently predict progression but remain the targets of approved and investigational drugs. (Read the full paper)
• Trastuzumab deruxtecan worked in everyday practice at roughly the rates the trials reported, and tumor shrinkage was commonest where HER2 was strongest. This retrospective single-center review covered 40 people treated between 2022 and 2026, half with ovarian and half with endometrial cancer. Among the 20 with ovarian cancer, median time without progression was 5.8 months and 9 of 19 assessable patients (47%) responded; across both cancers the response rate was 17 of 37 assessable patients (45.9%). Responses were commonest at the highest HER2 level (6 of 7 patients, against 9 of 23 in the middle and 1 of 6 at the lowest), but time without progression was about six months at every HER2 level, so more HER2 bought more shrinkage rather than measurably longer control. Prior PARP inhibitor treatment went with possibly shorter time without progression, in only 8 patients and on a hazard ratio whose range starts at 1.0, which the authors call strictly hypothesis-generating. Four people (10%) developed lung inflammation, one of them severe. Three received the drug in combination rather than alone. The authors also found HER2 scoring disagreed 87% of the time between samples, which is a caution about the whole HER2 picture here. (Read the full paper)
• For platinum-resistant disease with high folate receptor alpha, mirvetuximab soravtansine is an approved option rather than an experimental one, at least where it is licensed. This review sets out the case: the drug pairs an antibody against folate receptor alpha with a cell-killing payload, and it appears to affect neighboring tumor cells as well as the ones it binds. The single-arm SORAYA trial showed a 32.4% response rate in 106 patients, and the randomized phase 3 MIRASOL trial then showed longer time without progression (5.6 against 4.0 months) and longer overall survival (16.5 against 12.8 months) than chemotherapy in people whose tumors express the receptor highly. The drug is approved in the United States and Europe, with approval anticipated in Japan, where these authors work. Current research is testing it in combinations, at earlier points in treatment, and as maintenance. The authors are direct about what is unresolved: resistance develops, the way the biomarker is measured still needs standardizing, and cost is a real barrier. The side effects worth knowing about are eye problems, which affect roughly half of patients and are usually mild and reversible but require eye monitoring, and rare but serious lung inflammation. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Surgery is still the backbone of treatment, and the questions this month were how much, how soon, and whether to operate again.
Removing all visible cancer gives the best outcomes, but more extensive surgery carries more risk, and balancing the two is one of the harder conversations in ovarian cancer care.
• How extensive your surgery is goes together with your risk of a serious complication, and there is now a score that begins to put numbers on that trade-off. In an observational study using two Swedish databases covering 399 women with stage III or IV disease operated on between 2009 and 2023, researchers tested a scoring system that rates how much surgery was done. A quarter of all patients had a major complication. The rate climbed steeply with surgical extent: 15% in the intermediate group, which was the least extensive category studied, 33% in the high group, and 52% in the very high group. After adjustment, the very high group had about six times the odds of a major complication compared with the intermediate group, though the range consistent with the data is wide, from twice to eighteen times, and an absolute increase of about 34 percentage points, with a range from 11 to 57. Since the same score has previously been linked to survival, it offers a way to discuss benefit and risk in the same units rather than in impressions. One thing it cannot show, being observational, is that the extra surgery itself causes the complications, since how much surgery a person needs is driven by how much disease they have. (Read the full paper)
• Operating again when ovarian cancer returns went with living substantially longer, but almost all of that advantage depended on removing every visible trace. This is an exploratory analysis of prospective registries from five specialist centers in Europe and the United States, covering 3,109 people whose cancer returned more than six months after first-line chemotherapy. About 39% had a second operation, and in 84% of those all visible disease was removed. Median survival after recurrence was 81 months when nothing visible remained, against 39 months when disease was left behind, and 34 months for those treated with chemotherapy alone. Among those who had surgery, a single site of relapse, a gap of more than 16 months since chemotherapy, age under 75, CA-125 below 105 U/mL and fully unrestricted activity were each associated with longer survival. Two findings complicate the picture: BRCA mutation carriers went longer before the cancer grew again (27.4 against 21.3 months) but did not live longer overall, and even that difference disappeared once all visible disease had been removed; and people who had previously had maintenance treatment, particularly a PARP inhibitor, had shorter survival after surgery. Because this is exploratory registry analysis from high-volume centers rather than a randomized trial, who was selected for surgery shapes the result, and the many prognostic findings were not planned in advance. (Read the full paper)
• Starting chemotherapy more than eight weeks after surgery was linked to the cancer returning sooner. Among 145 people with advanced disease who had maximal-effort cytoreductive surgery at a single specialist center between 2016 and 2021, five in six of them after chemotherapy had already started, a delay beyond eight weeks independently predicted shorter time without progression (hazard ratio 1.65), though it was not associated with overall survival. Removing all visible disease at surgery remained the strongest independent predictor of both outcomes, which is the authors’ own finding rather than an inference, and a starting CA-125 above 1,000 U/mL predicted earlier progression. Whether the operation came before or after chemotherapy made no independent difference once other factors were accounted for. This is a retrospective single-center study and cannot show that the delay itself caused earlier recurrence, since unmeasured factors such as frailty and nutrition may explain part of it, although surgical complications were notably not what drove the delays in this cohort. The authors argue for removing avoidable waits from postoperative pathways. (Read the full paper)
• A simpler laparoscopic score reliably identified who could have all their cancer removed but was much less reliable at picking out who could not. Before committing to major surgery, surgeons sometimes perform a keyhole look inside to judge whether complete removal is achievable. In a retrospective single-center study of 45 patients, a low Fagotti Score identified people who could be fully resected with a negative predictive value of 88.9%. In the other direction it was weaker: of the patients it flagged as not fully resectable, only about two-thirds actually were not (positive predictive value 66.7%, specificity 64%), so a discouraging score is not by itself a reason to abandon surgery. On overall discrimination the Fagotti Score scored higher than the laparoscopic Peritoneal Cancer Index (area under the curve 0.801 against 0.705), but with 45 patients the two ranges overlap heavily, the study did not formally test whether that difference is real, and the authors describe both tools as good, saying only that the simpler one seems to perform better. Neither score predicted survival. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Ovarian cancer is still usually found late, and the search for a better blood test continues.
CA-125, the marker in routine use, misses too much early disease to work as a screening test in the general population.
• A blood test combining platelet RNA with an ordinary blood count outperformed CA-125, and the gap was widest in pre-menopausal women, where CA-125 is least reliable. Researchers enrolled 460 people across six South Korean sites: 67 with ovarian cancer, 15 with borderline tumors, 197 with benign gynecological conditions and 181 without symptoms. They trained a machine-learning classifier on platelet RNA markers and routine blood-count values and locked the threshold before testing. In the independent test set, which contained 24 cancers, it reached an area under the curve of 0.923 with 89% specificity. Its sensitivity was 87.5% overall, but that figure splits sharply by stage: 100% for stage II to IV disease and only 57% for stage I, where all three of the missed cancers sat. The negative predictive value was 97.7%, though 43% of its positive results were false alarms even in this group, where one person in seven had cancer, and the authors expect that to be worse in a screening population. In the 100 participants who had both tests done it beat CA-125 on every measure, with sensitivity 85% against 65%, and 25 percentage points better sensitivity in pre-menopausal participants (75% against 50%), on only 12 cancers in that subgroup. This is a well-designed early study, not a screening program: it has not been tested in a general population where cancer is far rarer, and its weakest point is exactly the stage a screening test would need to catch. (Read the full paper)
• No blood test has yet been shown to reduce ovarian cancer deaths, and knowing that is worth as much as knowing what is promising. This review of early detection markers for high-grade serous tubo-ovarian cancer is blunt about the state of play: nothing has been approved for population-wide screening, and no biomarker-based test has been shown to lower mortality in the wider population. Sensitivity and specificity remain the obstacles, along with a shortage of validation in diverse populations. The authors conclude that the evidence strongly supports liquid biopsy approaches based on DNA methylation, chemical marks on DNA that change early in cancer development and can be detected in blood. (Read the full paper)
• Two routine blood-count ratios ran higher and a third ran lower in malignant ovarian tumors, but none was accurate enough to lean on by itself. Ratios between different white blood cell types and platelets are cheap, already measured in most pre-operative bloods, and reflect the body’s inflammatory response to a tumor. In a retrospective review of records from 780 people operated on for an ovarian tumor at a single Romanian hospital between 2020 and 2025, the neutrophil-to-lymphocyte and platelet-to-lymphocyte ratios were significantly higher in malignant tumors and the lymphocyte-to-monocyte ratio significantly lower, and all three stayed significant after adjusting for age and CA-125. But their individual ability to discriminate was modest (area under the curve 0.72 at best), and the authors conclude they belong alongside existing assessment rather than in place of it. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
The subtypes grouped together as “ovarian cancer” behave differently enough that treating them alike is getting harder to defend.
Low-grade serous, mucinous and carcinosarcoma each follow their own course, and each got dedicated attention this month.
• In low-grade serous ovarian cancer, how long it takes to come back is an independent predictor of what happens next. This subtype grows slowly and responds poorly to chemotherapy, and the criteria used to select people for repeat surgery were developed for the more common high-grade type and fit badly. Using France’s national rare gynecological tumor database, researchers looked back at records for 211 people with recurrent low-grade serous cancer. Median time to first recurrence was 32 months. Compared with those who relapsed between 12 and 24 months, people who relapsed between 24 and 48 months had roughly half the risk of dying afterwards, and those who relapsed after 48 months about a quarter of the risk. Adding time to recurrence improved how well prognostic models performed. It did not predict whether a second operation could remove everything, but the authors still expect it to help refine who is selected for repeat surgery. This is a multicenter retrospective study, so it describes what happened to people already treated rather than testing a decision rule. (Read the full paper)
• A methylation test told mucinous ovarian cancer apart from cancer that spread to the ovary from elsewhere with about 95% accuracy, a distinction that can point to different treatment. Mucinous ovarian cancer is frequently mistaken for a deposit from a stomach, bowel or appendix cancer, because they look alike under the microscope. Researchers profiled chemical marks across the whole genome in 58 mucinous ovarian carcinomas, 38 metastases from outside the ovary and 18 borderline mucinous tumors from six institutions, then combined those with 389 previously published profiles to build a three-step classifier. It separated the two with 95.5% accuracy on 311 independent samples, holding up at 91% in a further external set of 45. The same data split borderline tumors into two groups, one resembling normal ovary and one resembling cancer, and split the cancers themselves into two subtypes with possible prognostic meaning in the study’s own cohort, not yet confirmed elsewhere. This is the kind of finding that could reach pathology practice relatively quickly. (Read the full paper)
• In ovarian carcinosarcoma, the two very different-looking halves of the tumor share most of the same mutations, and the carcinoma half carries a marker that current antibody-drug conjugates target. Carcinosarcoma contains both carcinoma and sarcoma components and carries a poor prognosis, and its rarity means very little is known about it. This retrospective series of nine cases from one Tokyo hospital analyzed the two components separately in six of them. TP53 mutations were present in all eight tumors that could be sequenced, and most other genetic changes were shared between the two halves, which supports the idea that the sarcoma component arises from the carcinoma rather than separately, though some mutations were private to one component. Trop-2, the target of one class of antibody-drug conjugate, was present in all carcinomatous components. Immune markers were low in most cases, suggesting immunotherapy alone is unlikely to help most patients, with the exception of the one case that had high microsatellite instability linked to Lynch syndrome, which is precisely the setting where checkpoint inhibitors do work. The authors note they measured only two immune markers, so the immune-cold label should be read cautiously. Nine cases is a small series, and this is a map of possible targets rather than evidence that any of them works. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Most ovarian cancer is not inherited, but for those who carry a high-risk gene change, prevention remains the most effective tool available.
This month brought findings on what risk-reducing surgery actually finds, on its effects on the ovaries, and on what carrying more than one risk gene means.
• About one in twelve women having risk-reducing surgery for a BRCA mutation turned out to already have an undetected early cancer, and one in ten had either that or a pre-invasive tubal lesion. This was a retrospective review of records from three referral centers in Apulia, Italy, covering 291 women with an inherited BRCA1 or BRCA2 mutation who had their tubes and ovaries removed preventively between 2020 and 2025. One was excluded as a metastasis; among the remaining 290, hidden invasive or microinvasive cancer was found in 24 (8.3%), and a pre-invasive lesion in the fallopian tube in a further 5 (1.7%), giving a combined 29 of 290 (10.0%, with a range of 7.1 to 14.0%). The rate was higher in BRCA1 than BRCA2 carriers (12.6% against 6.9%), though not significantly so in this cohort. This is an argument for careful pathological examination of everything removed, and a reminder that preventive surgery is sometimes also diagnostic. (Read the full paper)
• Removing the fallopian tubes during a hysterectomy done for non-cancerous reasons is a common preventive step, and this trial could not confirm that it leaves ovarian function untouched. Because high-grade serous ovarian cancer is now thought to begin in the fallopian tubes, removing them during surgery done for other reasons has become routine. This sub-study of a Swedish randomized trial measured anti-Mullerian hormone, a marker of ovarian reserve, before surgery and a year afterwards in women under 55 having a benign hysterectomy with their ovaries left in place. Of 89 women randomized, 74 were included in the main analysis, 37 per group, with statistical imputation used for missing samples. Both groups showed reduced levels at a year, and the average difference between them was very small. But the study was designed to demonstrate that the difference stayed within a pre-set margin, and the upper bound of the uncertainty range crossed that margin, so non-inferiority was not demonstrated. This is a failure to prove equivalence in a small sample rather than a demonstration of harm, though the authors note the variation between individuals was unexpectedly large and read that as suggesting a steeper drop in some women. (Read the full paper)
• A hormonal IUD appeared to be linked to lower ovarian cancer risk, but the researchers think age explains most of it. Contraception has shifted from the pill toward intrauterine devices, and while the pill’s protective effect against ovarian cancer is well established, the hormonal IUD’s effect was largely unknown. Following 788,736 people in British Columbia between 2002 and 2021, of whom 52,888 used a levonorgestrel IUD, the analysis initially found a 43% lower risk among users after adjusting for age and prior pill use, though that rests on just 17 cancers among users and a range running from 7% to 65% lower. When users were matched one-to-one to non-users of the same age, the association was similar but no longer statistically significant. And among the 211,866 people who were over 60 by the end of follow-up, there was no reduction at all: the estimate actually pointed the other way, on only 8 cancers among users, far too few to mean anything on its own. The authors are candid that the headline association appears confounded by age, since most IUD users are young, and they advise against reading it as established protection. (Read the full paper)
• Carrying two high-risk gene changes rather than one can reshape the kind of cancer that develops, not just which gene is named on the report. Using Germany’s nationwide hereditary breast and ovarian cancer registry, researchers identified 409 people carrying more than one high-risk variant among 26,983 variant carriers, about 1.5% overall, rising to nearly 3% in the subgroup tested across 13 core genes, which is more common than previously assumed. The clearest effects they report concern breast cancer type rather than ovarian. When BRCA1 was paired with another gene, the breast cancers that developed were predominantly triple-negative even when the second gene is usually associated with hormone-receptor-positive disease, with one reported exception: women carrying BRCA1 plus CHEK2 had more hormone-receptor-positive breast cancers than BRCA1 carriers alone. Separately, people carrying a variant in both BRCA1 and BRCA2 tended to present with more severe disease than matched carriers of either alone; this was not shown for other gene combinations. This was a case-control analysis within the registry, and its practical implication is for counselling: as multigene panels become routine, a second variant may need to change the advice rather than being treated as incidental. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Treatment leaves marks that outlast it.
This month’s survivorship research looked at hormone therapy after surgical menopause, at what clinicians find hard to say, and at the grief of losing fertility.
• Hormone therapy after ovarian cancer surgery in younger women was not associated with worse survival over ten years, which is reassuring for a decision many people face without much evidence. Premenopausal women whose ovaries are removed for ovarian cancer go into immediate surgical menopause, and whether hormone therapy is safe afterwards has been genuinely uncertain. This Swedish national study followed 779 women aged 18 to 50 who had surgery between 2008 and 2015, 472 of them with epithelial ovarian cancer, 68 with non-epithelial cancer and 239 with borderline tumors, linking cancer registry records to prescription data, with a median follow-up of nearly 12 years. Among the 472 with epithelial ovarian cancer, a third used hormone therapy, and ten-year survival was 52.4% for users against 51.7% for non-users, with no significant difference. The result held among the 367 who had no residual disease after surgery. This is observational rather than randomized, so the women who were prescribed hormone therapy may have differed from those who were not, and the result cannot exclude a modest effect in either direction, but it is reassuring as far as it goes. (Read the full paper)
• Gynecologists described deliberately keeping emotional distance from patients with ovarian cancer as self-protection, and described a system that limits the care they can offer. This is worth reading if you have ever felt your appointments were about numbers rather than about you. Researchers interviewed nine gynecologists recruited from four Norwegian hospitals and analyzed what they said. Three things came through: they focused on diagnostic markers and treatment choices more than on overall wellbeing; their understanding of the disease came from medical knowledge rather than from patients’ accounts of living with it; and they created emotional distance as a way of coping with how often the disease is fatal, while holding onto hope for medical progress and acknowledging feelings of helplessness. They also described their role as constrained by a rigid system. All nine who volunteered were women, most working at university hospitals, and the authors caution that the findings should be read as an in-depth look at those clinicians rather than as representing gynecologists generally. Even so, the honesty here is useful to both sides of the consultation. (Read the full paper)
• Losing fertility to cancer treatment can be a grief in its own right, and it deserves a named place in the care plan. Fourteen women aged 22 to 48 with cervical, ovarian, uterine or endometrial cancer at a Ghanaian referral hospital were interviewed in English, Twi or Ewe about reproductive loss. Three themes emerged: psychological and emotional experience, social challenges, and coping. Fertility loss was described as a threat to womanhood, motherhood and relational security, most sharply among younger, single and childless participants, and was compounded by stigma, strained relationships, treatment symptoms, financial strain and interrupted education. Women drew on treatment adherence, dietary change, prayer and family support. Those in active treatment emphasized symptom burden, while those who had finished focused on the loss of childbearing. The authors call for fertility counselling and psychosocial support to be built into care rather than left to chance. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Epidemiology, access and health disparities research.
Where you live, and who you are, still shape what happens after an ovarian cancer diagnosis.
• Ovarian cancer cases and deaths are rising worldwide, and the gap between richer and poorer countries is persistent and widening in the least-developed settings. Drawing on Global Burden of Disease estimates across 204 countries from 1990 to 2023, researchers found annual cases more than doubled, from 158,403 to 338,615, and deaths rose from 106,301 to 220,979. The age-adjusted death rate fell slightly over that period, from 6.29 to 5.95 per 100,000, so growth in the absolute numbers reflects a larger and older world population as well as anything about risk. Two findings stand out: diagnoses before age 50 rose by an average of 0.26% a year, and how likely someone is to die of their ovarian cancer relative to being diagnosed with it tracks inversely with a country’s development level. High body mass index was estimated, in the same modelling, to account for 6.37% of ovarian cancer deaths in 2023. By 2050 the projections reach roughly 403,000 cases and 259,000 deaths a year. These are modelled estimates and projections rather than counted cases, which is worth remembering when reading figures given to the nearest person. (Read the full paper)
• The trials that established PARP inhibitors were overwhelmingly White, which limits what anyone can say about how these drugs work for everybody else. This narrative review of the landmark PARP inhibitor trials across ovarian, breast, prostate and pancreatic cancer found participation was predominantly White throughout. Black participation in the breast and ovarian cancer trials was almost always under 3%. Race and ethnicity data were frequently missing altogether, reaching about 20% in two prostate cancer trials and 13.3% in one of the major ovarian trials, and Hispanic ethnicity was reported in only 5 of the roughly 13 to 14 trials tabulated. The authors attribute this to how trials are built and where they are sited rather than to individual choices, noting that research finds willingness to participate does not differ by race, and they treat it as a question about the evidence base itself: dosing, toxicities, and quality-of-life findings all rest on a narrow population. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
General and basic-science research.
This is laboratory and mechanistic work, several steps away from anyone’s treatment decisions, covering how ovarian cancer grows, spreads, evades the immune system and resists drugs. None of it changes care now, and it is where future options begin.
Check the citations section for a comprehensive list of publications associated with this topic.
What Does This Mean for Me?
My tumor tested HRD-negative, or my hospital cannot do the test. Does any of this help?
Possibly. Two findings this month speak to this. First, among tumors without a BRCA mutation, extra copies of a gene called MYC turned out to be strongly associated with faulty DNA repair, and MYC copy number is already reported on some standard gene panels, so it may offer a rough estimate where full HRD testing is unavailable. That is an association, not an approved test, but it is worth knowing the research exists. Second, if bevacizumab is part of your treatment or is being considered, a gene-expression signature was identified that separated people who appeared to benefit from it from those who did not. That is the first serious candidate for guiding a drug currently given with no test at all, though the formal statistical test of whether it predicts benefit succeeded in one cohort and not in the researchers’ own new one, so it is not ready to guide anyone’s treatment yet. A reasonable question for your care team: what testing has my tumor actually had, and is there anything further available that would change the options in front of me?
I’m on PARP inhibitor maintenance and worried about the long-term risks. What should I make of this month’s findings?
The reassuring news is specific, and so are its limits. A post-approval safety study of 745 people on niraparib in ordinary European practice found nine cases of myelodysplastic syndrome or acute myeloid leukemia, every one of them among the 564 people treated for recurrent disease, which is 1.6% of that group, and none among the 181 on first-line maintenance. The authors judged this consistent with the drug’s label, while being explicit that real-world and trial rates cannot be directly compared. The important caveat is time: people were followed for a median of about 11 months on treatment, while these blood cancers appeared a median of 32.7 months after starting the drug, so longer follow-up may find more. Separately, the final quality-of-life analysis from the PRIMA trial found that maintenance treatment did not worsen overall quality of life compared with placebo, while the cancer progressing caused a drop in quality of life that never recovered. If you carry an inherited BRCA mutation, pooled data suggest chemotherapy is somewhat more likely to lower your white cell count and to require growth-factor support, though this month’s direct comparison involved only eight carriers and did not look at hospitalization or quality of life.
My cancer has come back. Is another operation worth it?
A large registry analysis this month gives a conditional answer. Across 3,109 people whose cancer returned more than six months after first-line treatment, those who had a second operation that removed every visible trace lived a median of 81 months afterwards, against 39 months when some disease was left behind and 34 months with chemotherapy alone. The whole advantage sits in achieving complete removal, which is why the assessment beforehand matters so much. On that assessment, a related study found that a low score on a simple laparoscopic assessment reliably identified people whose disease could be fully removed, while a high score was right only about two-thirds of the time, so a discouraging score is a reason for a careful second look rather than a closed door. Two caveats deserve weight: this was exploratory analysis of registry data from high-volume specialist centers rather than a randomized trial, so who was chosen for surgery affects the numbers, and people who had previously received maintenance treatment had shorter survival afterwards. The useful question is not “should I have surgery” but “in my case, how likely is it that all visible disease could be removed, and what does your center’s experience look like?”
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 targeted searches across the ovarian, fallopian tube, and peritoneal cancer landscape (PARP inhibitors, immunotherapy and antibody-drug conjugates, BRCA/HRD and hereditary risk, surgery, platinum resistance, early detection, subtypes, survivorship, disparities) plus a dedicated qualitative search. 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.
Living on a PARP inhibitor: what it costs, and what it does not.
Directly referenced:
1. Shahin MS et al.. “Updated patient-reported outcomes and the effect of disease progression on health-related quality of life in the PRIMA/ENGOT-OV26/GOG-3012 trial of niraparib first-line maintenance therapy in patients with newly diagnosed advanced ovarian cancer.” Gynecol Oncol. August 2026. PMID 42385609. https://doi.org/10.1016/j.ygyno.2026.06.010
2. van der Vorst MJDL et al.. “Real-World Risk of Myelodysplastic Syndrome/Acute Myeloid Leukemia and Other Second Primary Malignancies in Patients with Epithelial Ovarian Cancer Treated with Niraparib Maintenance Therapy: Results from a Postauthorization Safety Study.” Adv Ther. August 2026. PMID 42159951. https://doi.org/10.1007/s12325-026-03600-9
3. Oda K et al.. “Mutational Signature-Based Biomarker for Phase II Trial of Olaparib Maintenance in Advanced High-Grade Ovarian Cancer.” Cancer Sci. August 2026. PMID 42178168. https://doi.org/10.1111/cas.70421
4. Yoshida K et al.. “Association of germline BRCA and homologous recombination deficiency with hematologic toxicity during platinum-taxane chemotherapy in ovarian cancer.” Int J Clin Oncol. August 2026. PMID 42204036. https://doi.org/10.1007/s10147-026-03065-4
Additional citations on related topics:
5. Trecourt A et al.. “Changes in Cyclin E1 expression and CCNE1 amplification in high-grade ovarian carcinomas post-PARP inhibitor exposure.” Br J Cancer. August 2026. PMID 42086671. https://doi.org/10.1038/s41416-026-03440-y (open access: Cyclin E1 and CCNE1 copy number in tumours sampled after PARP inhibitor exposure, relevant to WEE1/CDK2 inhibitor trials)
6. Kang MS et al.. “JPI-547, a novel dual inhibitor of PARP1/2 and tankyrase is more effective than first-generation PARP inhibitors in preclinical BRCA1/2-mutated cancer models.” Br J Cancer. August 2026. PMID 42092176. https://doi.org/10.1038/s41416-026-03411-3 (open access: preclinical dual PARP1/2 and tankyrase inhibitor active in olaparib-resistant BRCA-mutant models)
7. Wang H et al.. “Arginine restriction exploits DNMT3B-ASS1-driven arginine auxotrophy and mTORC1-suppressed autophagy to overcome niraparib resistance in ovarian cancer.” Cancer Lett. August 2026. PMID 42176791. https://doi.org/10.1016/j.canlet.2026.218582 (open access: preclinical work on arginine restriction to overcome acquired niraparib resistance)
8. Suriya S et al.. “PARP inhibition induces a redox-dependent dormant reservoir vulnerable to disulfiram in high-grade serous ovarian cancer.” Biomed Pharmacother. August 5, 2026. PMID 42546410. https://doi.org/10.1016/j.biopha.2026.119821 (open access: preclinical study of dormant drug-tolerant cells surviving PARP inhibition and their vulnerability to disulfiram)
9. Zheng W et al.. “MicroRNA320e Augments the Synthetic Lethality of Olaparib by Regulating the PI3K-AKT-mTOR Pathway.” Oncol Res. August 13, 2026. PMID 42630730. https://doi.org/10.32604/or.2026.081656 (open access: laboratory study of a microRNA that augments olaparib activity)
10. Uccello M et al.. “First-Line Maintenance Therapy Patterns in BRCA Wild-Type, HRD-Negative or Biomarker-Unknown Advanced Epithelial Ovarian Cancer: A Five-Country European Real-World Study by APLUSA.” Cancers (Basel). August 19, 2026. PMID 42649993. https://doi.org/10.3390/cancers18162682 (open access: real-world first-line maintenance patterns across five European countries in patients without a BRCA mutation or HRD-positive result)
11. Namozova F et al.. “Olaparib maintenance versus placebo or standard of care in ovarian cancer: a biomarker-driven systematic review and meta-analysis of randomized trials.” Int J Clin Oncol. August 4, 2026. PMID 42550402. https://doi.org/10.1007/s10147-026-03144-6 (subscription access)
12. Haggstrom L et al.. “Long-Term Outcomes in Patients With Recurrent Ovarian Cancer and Exceptional Response to PARP Inhibitors.” JAMA Oncol. August 1, 2026. PMID 42348196. https://doi.org/10.1001/jamaoncol.2026.1924 (restricted license, CC BY-NC-ND 4.0)
13. Bergeron AM et al.. “Could chemotherapy response score act as a surrogate marker of response to PARP inhibitor maintenance treatment in patients with advanced ovarian cancer?.” Gynecol Oncol. August 2026. PMID 42296694. https://doi.org/10.1016/j.ygyno.2026.06.006 (restricted license, CC BY-NC-ND 4.0)
14. Lin Z et al.. “Habitat Radiomics Based on Diffusion-weighted MRI for Predicting PARP Inhibitor Resistance in Advanced High-grade Serous Ovarian Cancer.” Acad Radiol. August 2026. PMID 42055872. https://doi.org/10.1016/j.acra.2026.04.011 (subscription access)
15. Guo X et al.. “Silencing thyroid hormone receptor interactor 13/kinetochore-associated 1 inhibits DNA damage repair and enhances Olaparib sensitivity in ovarian cancer.” J Pharmacol Exp Ther. August 2026. PMID 42456201. https://doi.org/10.1016/j.jpet.2026.104964 (subscription access)
Whether a tumor can repair its own DNA decides who gets a PARP inhibitor, and the test is not available everywhere.
Directly referenced:
16. Maradiya R et al.. “The real-world utility of homologous repair deficiency testing in BRCA1/2 wild-type high-grade serous carcinoma and the utility of MYC amplification as a potential surrogate marker.” Gynecol Oncol. August 2026. PMID 42442041. https://doi.org/10.1016/j.ygyno.2026.06.011
17. Witjes VM et al.. “Opportunities to improve detection of genetic predisposition for ovarian cancer applying the Tumor-First workflow.” Fam Cancer. August 4, 2026. PMID 42550332. https://doi.org/10.1007/s10689-026-00592-x
18. Zolotareva O et al.. “Transcriptome signatures for the identification of bevacizumab responders in ovarian cancer.” Genome Med. August 5, 2026. PMID 42576234. https://doi.org/10.1186/s13073-026-01727-6
Additional citations on related topics:
19. Kim J et al.. “Integrative Analysis of Gene and Protein Expression Data Reveals Novel Clusters for Ovarian Cancer Prognosis.” Int J Mol Sci. August 9, 2026. PMID 42653150. https://doi.org/10.3390/ijms27167144 (open access: integrative gene and protein expression clustering for prognostic stratification)
20. Romero-Lozano P et al.. “Homologous recombination deficiency testing implementation in the routine clinical setting: real-life experience and lessons learned.” ESMO Open. August 14, 2026. PMID 42600240. https://doi.org/10.1016/j.esmoop.2026.108242 (restricted license, CC BY-NC-ND 4.0)
21. Betella I et al.. “Impact of neoadjuvant chemotherapy on homologous recombination deficiency test results in patients with advanced high-grade serous ovarian cancer.” Int J Gynecol Cancer. August 2026. PMID 42418892. https://doi.org/10.1016/j.ijgc.2026.104789 (subscription access)
22. De Paolis E et al.. “Genomic profiling as an option for ovarian cancer diagnostics.” Expert Rev Mol Diagn. August 2026. PMID 42422928. https://doi.org/10.1080/14737159.2026.2700342 (license unconfirmed)
23. Nakahara H et al.. “A prioritization framework for BRCA1/2 variants of uncertain significance identified by comprehensive genomic profiling.” Eur J Hum Genet. August 2026. PMID 41765968. https://doi.org/10.1038/s41431-026-02058-1 (restricted license, CC BY-NC-ND 4.0)
24. Gordiichuk P et al.. “STUDY OF PREDICTIVE VALUE OF RAD51 EXPRESSION FOR THE EFFECTIVENESS OF PLATINUM-BASED THERAPY OF HIGH-GRADE SEROUS OVARIAN CARCINOMA.” Exp Oncol. August 21, 2026. PMID 42634844. https://doi.org/10.15407/exp-oncology.2026.02.133 (restricted license, CC BY-NC-ND 4.0)
25. Parić A et al.. “The prognostic and decision-making impact of KELIM CA-125 in patients with advanced ovarian cancer: A real-world study from Bosnia and Herzegovina.” Eur J Obstet Gynecol Reprod Biol. August 2026. PMID 42302468. https://doi.org/10.1016/j.ejogrb.2026.115245 (subscription access)
26. Roller L et al.. “Toward precision prognosis: Predicting recurrence-free survival in high-grade serous ovarian cancer patients using multi-time point clinical and computed tomography radiomics data.” Gynecol Oncol. August 2026. PMID 42391853. https://doi.org/10.1016/j.ygyno.2026.06.007 (license unconfirmed)
27. Jeong J et al.. “Molecular Response Assessment From Circulating Tumor DNA in Patients With Ovarian Cancer Treated With the WEE1 Inhibitor Azenosertib.” JCO Precis Oncol. August 26, 2026. PMID 42647763. https://doi.org/10.1200/PO-25-00844 (restricted license, CC BY-NC-ND 4.0)
Antibody-drug conjugates are the most active area in recurrent disease, and the question has shifted to who they suit.
Directly referenced:
28. Zhao CL et al.. “Folate receptor alpha, TROP2 and HER2 in high-grade serous ovarian cancer: Expression and clinicopathological correlations.” Gynecol Oncol. August 2026. PMID 42447657. https://doi.org/10.1016/j.ygyno.2026.07.004
29. Silverstein J et al.. “Real-world clinical outcomes of Trastuzumab Deruxtecan in HER2-expressing ovarian and endometrial Cancer.” Gynecol Oncol Rep. August 12, 2026. PMID 42621866. https://doi.org/10.1016/j.gore.2026.102183
30. Mabuchi S et al.. “Mirvetuximab soravtansine in platinum-resistant ovarian cancer: from biological rationale to clinical impact and future directions.” Int J Clin Oncol. August 2026. PMID 42287581. https://doi.org/10.1007/s10147-026-03090-3
Additional citations on related topics:
31. Yan F et al.. “A phase 1 study of PF-07260437, a B7-H4 × CD3 bispecific T-cell engager, in patients with advanced or metastatic breast, ovarian, and endometrial cancer.” Invest New Drugs. August 2026. PMID 42171881. https://doi.org/10.1007/s10637-026-01614-2 (open access: first-in-human dose-escalation study of a B7-H4 targeted T-cell engager enrolling ovarian cancer)
32. Alashkar Alhamwe B et al.. “Ascites reprograms innate lymphoid immune cells in ovarian cancer by promoting ILC2 enrichment and dysfunctional NK-cell states.” J Immunother Cancer. August 26, 2026. PMID 42648752. https://doi.org/10.1136/jitc-2026-015396 (open access: how malignant ascites reshapes natural killer and other innate lymphoid cells)
33. Huang M et al.. “The PVR-TIGIT/CD96/CD226 axis: a novel immune checkpoint target in ovarian cancer.” Front Immunol. August 20, 2026. PMID 42694449. https://doi.org/10.3389/fimmu.2026.1903882 (open access: review of the CD155/TIGIT immune checkpoint axis as a therapeutic target)
34. Kujawski M et al.. “T cells are critical for pre-metastatic niche formation through the STAT3/IL-17 axis.” J Immunother Cancer. August 14, 2026. PMID 42601173. https://doi.org/10.1136/jitc-2025-013183 (open access: preclinical work on T cells in pre-metastatic niche formation)
35. Hausnerova J et al.. “Prognostic Impact of PD-L1 Expression in Ovarian Cancer: Analysis of a Real-World Cohort Treated With Primary Platinum-Based Chemotherapy.” Cancer Med. August 2026. PMID 42634178. https://doi.org/10.1002/cam4.72216 (open access: PD-L1 expression and prognosis in a real-world cohort treated with primary platinum chemotherapy)
36. Tankul A et al.. “Survival Impact of Programmed Cell Death Ligand-1 Expression in Patients With Epithelial Ovarian Carcinoma.” Cancer Rep (Hoboken). August 2026. PMID 42530487. https://doi.org/10.1002/cnr2.70636 (open access: PD-L1 expression and survival in epithelial ovarian carcinoma)
37. Flint MS et al.. “Signaling Under Stress: Targeting the Glucocorticoid Receptor in Cancer.” Cancer Res. August 4, 2026. PMID 42171510. https://doi.org/10.1158/0008-5472.CAN-25-4426 (open access: review of glucocorticoid receptor signalling in cancer, including trials adding selective GR modulators to taxane in platinum-resistant disease)
38. Gudoityte G et al.. “Functional profiling of ovarian cancer models reveals Bcl-xL/NOTCH targeting to overcome resistance.” NPJ Precis Oncol. August 4, 2026. PMID 42552331. https://doi.org/10.1038/s41698-026-01628-2 (open access: functional profiling of patient-derived models pointing to Bcl-xL and NOTCH targeting in platinum resistance)
39. Hao J et al.. “PTEN deficiency confers sensitivity to ATR inhibitor-based treatment in high-grade serous ovarian cancer.” J Clin Invest. August 2026. PMID 42412555. https://doi.org/10.1172/JCI197645 (open access: PTEN deficiency as a predictive biomarker for ATR inhibitor response)
40. Pietrasik Z et al.. “Overcoming Therapy Resistance in Ovarian Cancer: From Molecular Mechanisms to Emerging Therapeutic Strategies.” Cancers (Basel). August 14, 2026. PMID 42649936. https://doi.org/10.3390/cancers18162623 (open access: review of therapy resistance mechanisms and emerging strategies in epithelial ovarian cancer)
41. Codru IR et al.. “Perioperative Care of Cancer Patients Treated with Immune Checkpoint Inhibitors: Current Evidence and Clinical Considerations-A Scoping Review.” Cancers (Basel). August 17, 2026. PMID 42649966. https://doi.org/10.3390/cancers18162654 (open access: scoping review of perioperative care for patients treated with immune checkpoint inhibitors)
42. Clark HD et al.. “First-In-Human Trial of Encapsulated Cells Constitutively Expressing Localized IL2 in Patients with High-Grade Serous Ovarian Carcinoma.” Clin Cancer Res. August 3, 2026. PMID 42113012. https://doi.org/10.1158/1078-0432.CCR-25-4142 (restricted license, CC BY-NC-ND 4.0)
43. Marchetti C et al.. “First-line immunotherapy with or without PARP inhibitors in advanced ovarian cancer: A meta-analysis including bevacizumab use, molecular status, and PD-L1 expression.” Crit Rev Oncol Hematol. August 2026. PMID 42155872. https://doi.org/10.1016/j.critrevonc.2026.105383 (restricted license, CC BY-NC-ND 4.0)
44. Zhou S et al.. “Efficacy of PARP inhibitor and immune checkpoint inhibitor combination therapy in PD-L1-negative cancers: a systematic review and meta-analysis.” Immunotherapy. August 25, 2026. PMID 42639974. https://doi.org/10.1080/1750743X.2026.2722581 (license unconfirmed)
45. 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 (restricted license, CC BY-NC-ND 4.0)
46. Haight PJ et al.. “Response to mirvetuximab soravtansine and weekly paclitaxel based on treatment sequencing in platinum-resistant ovarian cancer: Does order matter?.” Gynecol Oncol. August 2026. PMID 42431171. https://doi.org/10.1016/j.ygyno.2026.06.021 (restricted license, CC BY-NC-ND 4.0)
47. Seguin CL et al.. “Cost-effectiveness of a bevacizumab biosimilar for the treatment of recurrent, platinum-sensitive ovarian cancer in the United States.” Gynecol Oncol. August 2026. PMID 42447659. https://doi.org/10.1016/j.ygyno.2026.06.025 (restricted license, CC BY-NC-ND 4.0)
48. de Mello Graziano L et al.. “Has next-generation antibody-drug conjugate engineering finally unlocked NaPi2b in ovarian cancer?.” Int J Gynecol Cancer. August 6, 2026. PMID 42660769. https://doi.org/10.1016/j.ijgc.2026.104905 (subscription access)
49. Eyada MF et al.. “Oral cyclophosphamide combined with bevacizumab in recurrent heavily pre-treated ovarian cancer.” Int J Gynecol Cancer. August 2026. PMID 42259216. https://doi.org/10.1016/j.ijgc.2026.104761 (subscription access)
50. Lawson BC et al.. “Folate Receptor Immunohistochemical Staining Heterogeneity in Gynecologic Cancers.” Int J Gynecol Pathol. August 4, 2026. PMID 42550590. https://doi.org/10.1097/PGP.0000000000001210 (subscription access)
51. Yu YA et al.. “Olvi-Vec oncolytic immunotherapy and reversal of platinum resistance in ovarian cancer.” Gynecol Oncol Rep. August 2026. PMID 42383154. https://doi.org/10.1016/j.gore.2026.102145 (restricted license, CC BY-NC-ND 4.0)
52. Mandal G et al.. “Isotype-switched antibodies originating from tertiary lymphoid structures can antagonize ovarian cancer progression.” iScience. August 2026. PMID 42472098. https://doi.org/10.1016/j.isci.2026.116757 (restricted license, CC BY-NC-ND 4.0)
53. Bhojnagarwala PS et al.. “Efficient in vivo assembly of DNA encoded polyvalent BTEs for dual antigen targeting for broadening therapeutic impact in ovarian cancer.” Mol Ther. August 2026. PMID 42198849. https://doi.org/10.1016/j.ymthe.2026.05.019 (restricted license, CC BY-NC-ND 4.0)
54. Wang X et al.. “Combined targeting of mesothelin and tenascin-C enhances CAR-T cell function and tumor microenvironment modulation in ovarian cancer.” Mol Immunol. August 2026. PMID 42259008. https://doi.org/10.1016/j.molimm.2026.05.010 (subscription access)
55. Qiao J et al.. “CD47 monoclonal antibody enhances the inhibitory effect of anti-HER2 chimeric antigen receptor macrophages on ovarian cancer.” Oncol Lett. August 2026. PMID 42375170. https://doi.org/10.3892/ol.2026.15711 (license unconfirmed)
56. Wang Y et al.. “VEGF/VEGFR targeting-induced vascular normalization: a key strategy to reverse cold tumor phenotype and potentiate immunotherapy in gynecologic cancers.” Int Immunopharmacol. August 2026. PMID 42127491. https://doi.org/10.1016/j.intimp.2026.116821 (restricted license, CC BY-NC-ND 4.0)
57. Uttam V et al.. “Overcoming immune resistance through tumor microenvironment reprogramming: Emerging immunotherapeutic strategies and translational advances.” Biochem Pharmacol. August 6, 2026. PMID 42562333. https://doi.org/10.1016/j.bcp.2026.118331 (subscription access)
58. de Melo MAZ et al.. “American Society of Clinical Oncology annual meeting 2026: key clinical trial updates in gynecologic oncology.” Int J Gynecol Cancer. August 2026. PMID 42435735. https://doi.org/10.1016/j.ijgc.2026.104813 (subscription access)
59. Hou Y et al.. “The biphasic role of reactive oxygen species in ovarian cancer progression and therapeutics: Crosstalk among metabolism, ferroptosis, and the tumor immune microenvironment.” Crit Rev Oncol Hematol. August 14, 2026. PMID 42600958. https://doi.org/10.1016/j.critrevonc.2026.105542 (subscription access)
60. 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 (license unconfirmed)
61. Paul BM et al.. “Natural products targeting cytokine-regulated SASP inflammation networks in Ovarian cancer: Implications on immune escape and molecular resistance.” Inflammopharmacology. August 2026. PMID 42479110. https://doi.org/10.1007/s10787-026-02346-8 (subscription access)
62. Ouyang X et al.. “Nicotinamide mononucleotide potentiates the anti-tumor efficacy of CAR-NK cell therapy targeting MSLN in ovarian cancer.” Cancer Gene Ther. August 13, 2026. PMID 42595793. https://doi.org/10.1038/s41417-026-01071-2 (subscription access)
Surgery is still the backbone of treatment, and the questions this month were how much, how soon, and whether to operate again.
Directly referenced:
63. Hunde D et al.. “Surgical extent and its association with major postoperative complications in advanced ovarian cancer: initial validation of the Karolinska surgical extent and complexity score (K-SECS).” Eur J Surg Oncol. August 2026. PMID 42242068. https://doi.org/10.1016/j.ejso.2026.111918
64. du Bois A et al.. “Secondary cytoreduction for ovarian cancer relapse: results from the high surgical quality, multi-center”Surgery in Recurrent Ovarian Cancer Research Consortium (SURROC-CON)“.” Int J Gynecol Cancer. August 8, 2026. PMID 42660770. https://doi.org/10.1016/j.ijgc.2026.104956
65. Jamdade K et al.. “Time to adjuvant chemotherapy after cytoreductive surgery and survival outcomes in epithelial ovarian cancer: a retrospective cohort study.” Front Oncol. August 7, 2026. PMID 42630181. https://doi.org/10.3389/fonc.2026.1856055
66. Tsolakidis D et al.. “Fagotti Score (FS) Compared with Peritoneal Cancer Index (PCI) for Preoperative Assessment of Optimal Cytoreduction in Upfront Laparoscopy.” Curr Oncol. August 20, 2026. PMID 42645395. https://doi.org/10.3390/curroncol33080490
Additional citations on related topics:
67. Rajavuori A et al.. “Biological features associated with poor response to neoadjuvant chemotherapy in high-grade serous ovarian carcinoma.” Int J Gynecol Cancer. August 8, 2026. PMID 42680633. https://doi.org/10.1016/j.ijgc.2026.104959 (open access: biological features associated with poor response to neoadjuvant chemotherapy)
68. Bizzarri N et al.. “Incidence and impact of low-volume lymph node metastasis in apparent early-stage ovarian cancer: MICR-OVARY study.” Int J Gynecol Cancer. August 2026. PMID 41968027. https://doi.org/10.1016/j.ijgc.2026.104638 (open access: incidence and prognostic impact of low-volume lymph node metastasis found at sentinel node biopsy in apparent early-stage disease)
69. Duan X et al.. “Comparison of long-term survival between primary and interval cytoreductive surgery in advanced ovarian cancer: A ten-year real-world cohort study.” Eur J Surg Oncol. August 2026. PMID 42258952. https://doi.org/10.1016/j.ejso.2026.111926 (restricted license, CC BY-NC-ND 4.0)
70. Suleiman R et al.. “Prehabilitation during neoadjuvant chemotherapy in advanced ovarian cancer is associated with improved surgical candidacy and chemotherapy outcomes.” Gynecol Oncol. August 2026. PMID 42296695. https://doi.org/10.1016/j.ygyno.2026.06.009 (subscription access)
71. Dumont F et al.. “Immediate Second Look After Cytoreduction for Colorectal or Ovarian Carcinomatosis: An Invisible Gorilla Effect?.” Ann Surg Oncol. August 2026. PMID 41865210. https://doi.org/10.1245/s10434-026-19493-5 (subscription access)
72. Liu JH et al.. “Diagnostic accuracy of MDCT for preoperative peritoneal cancer index estimation in advanced ovarian cancer undergoing cytoreductive surgery with hyperthermic intraperitoneal chemotherapy (HIPEC): a Sugarbaker-based analysis.” Eur Radiol. August 2026. PMID 41995741. https://doi.org/10.1007/s00330-026-12529-0 (subscription access)
73. Kouri A et al.. “A second chance for the second look: Feasibility of laparoscopic HIPEC at the conclusion of upfront treatment for epithelial ovarian cancer.” Gynecol Oncol. August 2026. PMID 42364423. https://doi.org/10.1016/j.ygyno.2026.06.018 (restricted license, CC BY-NC-ND 4.0)
74. Xu Y et al.. “Toward molecular and pathology-confirmed completeness in advanced ovarian cancer cytoreduction: Intraoperative molecular imaging and integrated theranostic strategies.” Mol Aspects Med. August 2026. PMID 42364525. https://doi.org/10.1016/j.mam.2026.101489 (subscription access)
75. Erdemoglu E et al.. “Minimally Invasive Splenectomy for Recurrent Gynecologic Cancer and Long-Term Outcomes.” J Minim Invasive Gynecol. August 22, 2026. PMID 42632538. https://doi.org/10.1016/j.jmig.2026.08.018 (subscription access)
76. Tiwari N et al.. “Feasibility, Safety, Efficacy, and Surgical Utility of CO₂ Insufflation-Assisted Peritonectomy Versus Conventional Stripping in Advanced Ovarian Cancer: an Open-Label Phase II Randomized Controlled Trial.” Indian J Surg Oncol. August 2026. PMID 42661915. https://doi.org/10.1007/s13193-025-02510-6 (subscription access)
77. Arçay Öztürk A et al.. “FAP-targeted PET imaging in peritoneal carcinomatosis.” Br J Radiol. August 1, 2026. PMID 42011156. https://doi.org/10.1093/bjr/tqag087 (subscription access)
Ovarian cancer is still usually found late, and the search for a better blood test continues.
Directly referenced:
78. Ahn E et al.. “Foretell Ovary: A Blood-Based Ensemble Algorithm Integrating Tumor-Educated Platelet RNA and Routine Hematology for Non-Invasive Ovarian Cancer Screening.” Cancers (Basel). August 14, 2026. PMID 42649941. https://doi.org/10.3390/cancers18162629
79. Atiq S et al.. “Emerging biomarkers for the early detection of high-grade serous tubo-ovarian cancer.” Crit Rev Oncol Hematol. August 2026. PMID 42202925. https://doi.org/10.1016/j.critrevonc.2026.105389
80. Gruber D et al.. “Preoperative Inflammatory Markers as Predictors of Ovarian Tumor Malignancy: A Retrospective Diagnostic Study.” Medicina (Kaunas). August 21, 2026. PMID 42654510. https://doi.org/10.3390/medicina62081613
Additional citations on related topics:
81. Park JS et al.. “Differential Diagnosis of Ovarian Tumor Using FDG PET/CT, based on Convolutional Neural Networks.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663205. https://doi.org/10.31557/APJCP.2026.27.8.2847 (open access: convolutional neural networks applied to FDG PET/CT for telling benign from malignant ovarian tumours)
82. Zhao N et al.. “STL-DeepBDC: A Robust Few-Shot Learning Framework for Multiclass Ovarian Tumor Classification in Ultrasound Outperforms Conventional Transfer Learning.” Cancer Med. August 2026. PMID 42624791. https://doi.org/10.1002/cam4.72165 (open access: few-shot deep learning for multiclass ovarian tumour classification on ultrasound)
83. Rahniayu A et al.. “MCM2 and p53 Expression Correlate with the Spectrum of Mucinous Ovarian Tumor.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663211. https://doi.org/10.31557/APJCP.2026.27.8.2901 (open access: MCM2 and p53 expression across benign, borderline and malignant mucinous ovarian tumours)
84. Jabbar NK et al.. “Alterations of Inflammatory Mediators (TNF-α and HMGB1) and Circulating microRNA-22 Expression in Pre- and Post-Menopausal Women with Early-Stage Epithelial Ovarian Cancer.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663234. https://doi.org/10.31557/APJCP.2026.27.8.3115 (open access: inflammatory mediators and circulating microRNA-22 in pre- and post-menopausal women with early-stage disease)
85. Lubena L et al.. “Selenium Levels in Early and Advanced Stages of Epithelial Ovarian Cancer.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663195. https://doi.org/10.31557/APJCP.2026.27.8.2755 (open access: selenium levels in early versus advanced epithelial ovarian cancer)
86. Arabi Belaghi R et al.. “A simulation-based comparison of Boruta, LASSO, and Elastic Net for variable selection in logistic regression, with an ovarian cancer miRNA application.” BMC Med Res Methodol. August 24, 2026. PMID 42675459. https://doi.org/10.1186/s12874-026-02939-5 (open access: methodological comparison of variable-selection approaches, illustrated on an ovarian cancer microRNA dataset)
87. Cecati M et al.. “Aging and Reproductive Cancers: An Integrative View on Cell-Free DNA and Transposable Elements.” Front Biosci (Landmark Ed). August 17, 2026. PMID 42689989. https://doi.org/10.31083/FBL50970 (open access: review of how ageing shapes cell-free DNA and its use as a biomarker in reproductive cancers)
88. Shefer A et al.. “Exosome-Associated Proteins as Mediators and Biomarkers of Ovarian Cancer Dissemination.” Biomolecules. August 7, 2026. PMID 42650816. https://doi.org/10.3390/biom16081150 (open access: review of exosome-associated proteins as mediators and biomarkers of dissemination)
89. Xing M et al.. “Cross-Regulation Between DNA Methylation and Circadian Clock Reprogramming in Ovarian Cancer: Mechanistic Insights, Biomarker Potential, and Therapeutic Implications.” Int J Cancer. August 19, 2026. PMID 42619413. https://doi.org/10.1002/ijc.70704 (open access: review of DNA methylation and circadian clock reprogramming, and their biomarker potential)
90. Li Z et al.. “Development and validation of a serum peptidomic signature for early detection of asymptomatic ovarian cancer: A multi-center prospective study.” Cell Rep Med. August 28, 2026. PMID 42664958. https://doi.org/10.1016/j.xcrm.2026.103014 (restricted license, CC BY-NC-ND 4.0)
91. Alizada A et al.. “DNA methylation of ANKRD23 as a novel biomarker for early diagnosis of ovarian cancer.” Afr J Reprod Health. August 17, 2026. PMID 42605682. https://doi.org/10.29063/ajrh2026/v30i15.2 (license unconfirmed)
92. Lou X et al.. “piR-hsa-8111406 promotes proliferation and serves as a novel biomarker for early detection of ovarian cancer: a multi-center retrospective study.” Int J Gynecol Cancer. August 2026. PMID 42391800. https://doi.org/10.1016/j.ijgc.2026.104795 (subscription access)
93. Meng F et al.. “Circulating Tumor DNA in Tracking Minimal Residual Disease and Recurrence in Ovarian Cancer: A Retrospective Cohort.” Cancer Invest. August 2026. PMID 42170700. https://doi.org/10.1080/07357907.2026.2675657 (restricted license, CC BY-NC-ND 4.0)
94. Zhang J et al.. “Current Advances of Molecular Biomarkers and Liquid Biopsies Techniques in Ovarian Cancer.” Cancer Med. August 2026. PMID 42572185. https://doi.org/10.1002/cam4.72057 (restricted license, CC BY-NC-ND 4.0)
95. Yoshida A et al.. “Comparative Diagnostic Performance of IOTA Simple Rules, O-RADS US, and Subjective Assessment in Differentiating Benign from Malignant Adnexal Masses.” J Ultrasound Med. August 2026. PMID 41699884. https://doi.org/10.1002/jum.70205 (subscription access)
96. Dueholm Hjorth IM et al.. “Prospective external validation of ADNEX and RMI for estimating risk of malignancy in adnexal masses in general gynecological settings: Danish multicenter study.” Ultrasound Obstet Gynecol. August 2026. PMID 42425520. https://doi.org/10.1002/uog.70271 (restricted license, CC BY-NC-ND 4.0)
97. Vishwakarma N et al.. “Examination of influence of microfluidic flow and antibody orientation on biosensor performance: A case study with CA125 electrochemical biosensor.” Bioelectrochemistry. August 2026. PMID 41494247. https://doi.org/10.1016/j.bioelechem.2025.109213 (subscription access)
98. Moffitt SE et al.. “Polyclonal antibodies targeting defined epitopes on cancer biomarker MUC16.” Anal Bioanal Chem. August 2026. PMID 42250137. https://doi.org/10.1007/s00216-026-06583-2 (restricted license, CC BY-NC-ND 4.0)
99. Chen Y et al.. “Projection-based tokenization with Pseudo feature learning for ovarian lesion segementation in ultrasound images.” Neural Netw. August 2026. PMID 41819618. https://doi.org/10.1016/j.neunet.2026.108806 (subscription access)
100. Yadav V et al.. “Exploring Molecular Signature and Prognostic Biomarkers in Ovarian Cancer: Insights From Late-Stage, Recurrent, and Metastatic Tumors.” Biotechnol Appl Biochem. August 2026. PMID 41588777. https://doi.org/10.1002/bab.70134 (subscription access)
The subtypes grouped together as “ovarian cancer” behave differently enough that treating them alike is getting harder to defend.
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109. Mantiero M et al.. “Case Report: Personalized therapy in gynecological neuroendocrine neoplasm: a case of BRCA2-mutated ovarian neuroendocrine carcinoma treated with PARP-inhibitor.” Front Oncol. August 4, 2026. PMID 42614412. https://doi.org/10.3389/fonc.2026.1774835 (open access: case of BRCA2-mutated ovarian neuroendocrine carcinoma treated with a PARP inhibitor)
110. Sofiyanski T et al.. “A gastric metastasis from ovarian carcinoma mimicking GIST - a case report.” Folia Med (Plovdiv). August 6, 2026. PMID 42677756. https://doi.org/10.3897/folmed.68.e153213 (open access: case of gastric metastasis from ovarian carcinoma mimicking a gastrointestinal stromal tumour)
111. Baraka B et al.. “Case Report: A diagnostic dilemma: metachronous pancreatic metastasis from high-grade serous ovarian carcinoma.” Front Oncol. August 12, 2026. PMID 42656280. https://doi.org/10.3389/fonc.2026.1901559 (open access: systematic review and case of metachronous pancreatic metastasis from high-grade serous ovarian carcinoma)
112. Pishas KI et al.. “Identifying therapeutic targets in low-grade serous ovarian carcinomas with no specific molecular profile.” J Pathol. August 2026. PMID 42138099. https://doi.org/10.1002/path.70075 (subscription access)
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116. Keegan A et al.. “Fam-Trastuzumab Deruxtecan in Recurrent Low-Grade Serous Ovarian Carcinoma WithFusion and Low Human Epidermal Growth Factor Receptor 2 Expression: A Case Report.” JCO Precis Oncol. August 21, 2026. PMID 42628006. https://doi.org/10.1200/PO-26-00288 (license unconfirmed)
117. Yang X et al.. “Malignant struma ovarii: clinicopathological and molecular features in a series of nine cases.” Virchows Arch. August 2026. PMID 41087724. https://doi.org/10.1007/s00428-025-04293-1 (subscription access)
118. Shi F et al.. “Desmoplastic Small Round Cell Tumor of the Ovary: A Case Report With Atypical Morphologic Features and Literature Review.” Int J Surg Pathol. August 2026. PMID 41823035. https://doi.org/10.1177/10668969251412899 (license unconfirmed)
119. Sulaimanova A et al.. “Pituitary Metastasis as the Initial Manifestation of an Undiagnosed Adenocarcinoma of Mullerian Origin: A Case Report and Literature Review.” Int J Surg Pathol. August 2026. PMID 41869702. https://doi.org/10.1177/10668969261420430 (license unconfirmed)
120. Wu Z et al.. “Primary Ovarian Epithelioid Angiosarcoma with Extensive Lymph Node Metastases: A Case Report and Literature Review.” J Vis Exp. August 14, 2026. PMID 42611577. https://doi.org/10.3791/72232 (license unconfirmed)
121. Rich BS et al.. “Immature teratoma of the ovary in children and adolescents: A multi-institutional study of characteristics and management.” Gynecol Oncol. August 2026. PMID 42419002. https://doi.org/10.1016/j.ygyno.2026.06.020 (subscription access)
122. Rich BS et al.. “Immature teratoma of the ovary with microscopic yolk sac tumor in children and adolescents: A multi-institutional study.” Gynecol Oncol. August 2026. PMID 42419003. https://doi.org/10.1016/j.ygyno.2026.06.026 (subscription access)
123. Wei Y et al.. “Ultrasonic, Clinical, and Pathological Characteristics of Malignant Ovarian Tumors in Children.” J Ultrasound Med. August 2026. PMID 41709043. https://doi.org/10.1002/jum.70203 (subscription access)
124. Suri A et al.. “Bilateral Ovarian Mucinous Cystadenocarcinoma in an Adolescent Girl: A Case Report.” J Pediatr Adolesc Gynecol. August 2026. PMID 41765224. https://doi.org/10.1016/j.jpag.2026.02.013 (subscription access)
125. Peng Y et al.. “Malignant transformation of ovarian teratoma into primitive neuroectodermal tumor: A clinicopathological analysis of three cases and literature review.” Ann Diagn Pathol. August 2026. PMID 42033925. https://doi.org/10.1016/j.anndiagpath.2026.152647 (subscription access)
126. Keyhanian K et al.. “Coexistent Endometrial and Fallopian Tube Carcinoma: Molecular and Pathological Features for Risk Stratification.” Mod Pathol. August 2026. PMID 42320759. https://doi.org/10.1016/j.modpat.2026.101030 (subscription access)
127. Gan W et al.. “Biological consistency and molecular heterogeneity in synchronous endometrial and ovarian carcinomas: a clinicopathological study within the FIGO 2023 framework.” J Ovarian Res. August 19, 2026. PMID 42693468. https://doi.org/10.1186/s13048-026-02213-8 (restricted license, CC BY-NC-ND 4.0)
Most ovarian cancer is not inherited, but for those who carry a high-risk gene change, prevention remains the most effective tool available.
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132. Ganesan S et al.. “Risk of ovarian cancer in women with a pathogenic or likely pathogenic variant in NBN: a systematic review and meta-analysis.” Am J Obstet Gynecol. August 2026. PMID 41707894. https://doi.org/10.1016/j.ajog.2026.02.020 (open access: systematic review and meta-analysis of ovarian cancer risk in carriers of a pathogenic NBN variant)
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134. Milambo JPM et al.. “Mapping the Prevalence of BRCA1 and BRCA2 Mutations in Hereditary Breast and Ovarian Cancer Across Africa: A Systematic Review and Meta-Analysis.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663196. https://doi.org/10.31557/APJCP.2026.27.8.2761 (open access: systematic review and meta-analysis of BRCA1 and BRCA2 mutation prevalence across Africa)
135. Mah SJ et al.. “Opportunistic salpingectomy during non-gynecologic surgery: Canadian surgeons’ experience, barriers and facilitators.” Gynecol Oncol. August 2026. PMID 42287763. https://doi.org/10.1016/j.ygyno.2026.06.005 (open access: national survey of general and urologic surgeons on opportunistic salpingectomy during non-gynaecologic surgery)
136. Paksoy B et al.. “Multigene panel testing reveals the spectrum of non-BRCA germline variants in BRCA1/2-negative breast, ovarian, and prostate cancer patients from a Turkish cohort.” Clin Transl Oncol. August 2026. PMID 41697532. https://doi.org/10.1007/s12094-026-04258-z (subscription access)
137. Butkowsky C et al.. ““Where do I go from here?” Navigating a lifelong road without a map: the care experiences of hereditary cancer patients.” Eur J Hum Genet. August 2026. PMID 41776346. https://doi.org/10.1038/s41431-026-02069-y (subscription access)
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139. Chess I et al.. ““I was in the driver’s seat”: A qualitative analysis of factors promoting and delaying previvors’ oophorectomy after risk-reducing salpingectomy.” Gynecol Oncol. August 2026. PMID 42456483. https://doi.org/10.1016/j.ygyno.2026.07.009 (subscription access)
140. English S et al.. “Population Genomic Screening for Hereditary Cancer Risk: Patient Experience, Perceptions, and Downstream Clinical Outcomes.” J Genet Couns. August 2026. PMID 42619412. https://doi.org/10.1002/jgc4.70274 (subscription access)
141. Jorgensen KA et al.. “A Multilevel Intervention to Identify Individuals for Genetic Testing and Treatment: The IGNITE-TX Pilot Randomized Clinical Trial.” JAMA Netw Open. August 3, 2026. PMID 42658496. https://doi.org/10.1001/jamanetworkopen.2026.30668 (restricted license, CC BY-NC-ND 4.0)
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Treatment leaves marks that outlast it.
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147. 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)
148. Wei H et al.. “The COMPASS-CAT risk assessment model for predicting in-hospital venous thromboembolism in patients with breast, lung, colorectal, and ovarian cancer: A retrospective cohort study.” J Int Med Res. August 13, 2026. PMID 42593353. https://doi.org/10.1177/03000605261471674 (open access: comparison of the COMPASS-CAT and Khorana models for predicting in-hospital venous thromboembolism)
149. Chambers LM et al.. “PRO-PLATINUM: A randomized, double-blind, placebo controlled study to investigate the efficacy of a probiotic intervention on the gut and vaginal microbiome of ovarian cancer patients undergoing treatment with platinum chemotherapy.” Gynecol Oncol. August 2026. PMID 42364424. https://doi.org/10.1016/j.ygyno.2026.06.016 (open access: protocol for a randomised placebo-controlled trial of a probiotic during platinum chemotherapy)
150. Xie Y et al.. “Symptom burden and symptom clusters in ovarian cancer patients during first-line maintenance therapy: a cross-sectional survey.” Support Care Cancer. August 4, 2026. PMID 42547626. https://doi.org/10.1007/s00520-026-11062-6 (restricted license, CC BY-NC-ND 4.0)
151. 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)
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153. AlAshqar A et al.. “Cardiovascular outcomes in individuals with ovarian cancer: A retrospective cohort study.” Gynecol Oncol. August 2026. PMID 42287764. https://doi.org/10.1016/j.ygyno.2026.06.008 (subscription access)
154. Wu X et al.. “Effects of traditional Chinese medicine directional drug penetration therapy on gastrointestinal function, gut microbiota, and sleep quality in postoperative ovarian cancer patients: a randomized controlled trial.” Support Care Cancer. August 19, 2026. PMID 42616157. https://doi.org/10.1007/s00520-026-11096-w (subscription access)
Epidemiology, access and health disparities research.
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157. Ritonja JA et al.. “Total moderate-to-vigorous physical activity across the adult life course and the risk of invasive ovarian cancer.” Int J Epidemiol. August 18, 2026. PMID 42665563. https://doi.org/10.1093/ije/dyag160 (open access: life-course analysis of total moderate-to-vigorous physical activity and invasive ovarian cancer risk)
158. Spaur M et al.. “Exposures to Drinking Water Contaminants in Community Water Systems and Risk of Ovarian Cancer in the California Teachers Study Cohort.” Environ Health Perspect. August 2026. PMID 42564971. https://doi.org/10.1021/EHP.6c00169 (open access: regulated drinking-water contaminants in community water systems and ovarian cancer risk in the California Teachers Study)
159. 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, including ovary)
160. Sankaran H et al.. “Associations of Age With Tumor Genomic Characteristics in Relapsed/Refractory Cancers Interrogated With the NCI-MATCH Trial Targeted Gene Panel Assay.” JCO Precis Oncol. August 7, 2026. PMID 42566732. https://doi.org/10.1200/PO-25-01183 (open access: tumour genomic characteristics by age in relapsed or refractory ovarian, breast and colorectal cancers on the NCI-MATCH trial)
161. Modugno F et al.. “Residential Context and Survival Disparities in Black and White Women With Ovarian Cancer.” JAMA Netw Open. August 3, 2026. PMID 42574015. https://doi.org/10.1001/jamanetworkopen.2026.27722 (restricted license, CC BY-NC-ND 4.0)
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163. Yin X et al.. “Geographic disparities, trial characteristics, and transparency of 3720 ovarian cancer clinical trials.” J Cancer Policy. August 14, 2026. PMID 42600890. https://doi.org/10.1016/j.jcpo.2026.100792 (subscription access)
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General and basic-science research.
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166. Kuryk L et al.. “Dynamic 3D microfluidic platform for exploring combined targeted therapy, chemotherapy, and virotherapy delivery in ovarian cancer.” Drug Deliv Transl Res. August 2026. PMID 41182668. https://doi.org/10.1007/s13346-025-01997-4 (open access: microfluidic three-dimensional platform for testing combined targeted therapy, chemotherapy and virotherapy)
167. Dos Santos JRN et al.. “Coumarin-dihydropyrimidinone hybrids as promising agents against ovarian cancer: synthesis, SAR, and in silico evaluation.” Bioorg Med Chem Lett. August 2026. PMID 41921824. https://doi.org/10.1016/j.bmcl.2026.130646 (open access: synthesis and structure-activity evaluation of coumarin-dihydropyrimidinone hybrids)
168. Li Y et al.. “Disruption of the SNRPF-DDX24-E2F4 Feedback Loop Uncouples Splicing and Transcriptional Regulation to Suppress Ovarian Cancer Progression.” Adv Sci (Weinh). August 2026. PMID 42107058. https://doi.org/10.1002/advs.202523374 (open access: the SNRPF-DDX24-E2F4 loop linking RNA splicing to transcriptional control)
169. Li J et al.. “MEOX1 Coordinates Autocrine-Paracrine Programs via SPHK1/S1P to Promote Lymph Node Metastasis in Ovarian Cancer.” Adv Sci (Weinh). August 2026. PMID 42107070. https://doi.org/10.1002/advs.202523574 (open access: MEOX1 and the SPHK1/S1P axis in lymph node metastasis)
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