August Digest
This Month in Uterine Cancer Research
August 2026
August was a substantial month for uterine and endometrial cancer research, and much of it was about refining decisions rather than adding new ones. Several studies asked what molecular tumor testing has made unnecessary. One large, pooled analysis of clinical trial data concluded that tumor grade no longer needs to influence treatment planning for one whole molecular subtype. Two teams reached genuinely different conclusions about whether lymph nodes should be checked during surgery for precancer, which is a useful disagreement to watch. On the treatment side, a major randomized trial reported that adding a second drug to immunotherapy maintenance delayed progression without helping people live longer, and a nationwide real-world study found that immunotherapy performs less well outside a clinical trial than inside one. Alongside this, a smaller but welcome group of studies listened directly to patients about the information they did and didn’t receive, and about the grief of losing fertility.
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.
Molecular tumor testing is changing what doctors need to look at and what they can stop looking at.
Endometrial cancers are now sorted into four molecular groups that predict how a tumor behaves: POLE-mutated (a gene change linked to unusually good outcomes), mismatch repair deficient or MMR-d (a feature that often makes a tumor respond to immunotherapy), p53-abnormal (generally the most aggressive), and “no specific molecular profile.” A theme this month was working out which older measurements these groups replace.
• If your tumor is MMR-deficient, its grade may no longer matter for planning your treatment. Researchers pooled data from three randomized trials (PORTEC-1, -2 and -3) and five clinical cohorts, molecularly classifying 2,621 endometrial cancers, of which 730 were MMR-deficient. Over a median 7.2 years, low-grade and high-grade MMR-deficient tumors had nearly identical five-year recurrence (18.0% vs 18.8%) and cancer-specific death (12.3% vs 14.2%), and grade was not independently predictive after accounting for age, stage, histology, lymphovascular invasion and adjuvant treatment, so the authors conclude grade can be left out of risk assessment for this group. This is practice-relevant evidence drawn from trial-quality data. (Read the full paper)
• Artificial intelligence may eventually let more hospitals offer molecular classification, though not yet. Molecular typing currently needs immunohistochemistry and gene sequencing, which cost money, take time, and simply aren’t available everywhere. This pathologist-authored review examines deep learning models that try to predict molecular subtype directly from the ordinary stained tissue slide already made for every patient, and finds the idea biologically reasonable and promising, while being clear that the methods have real limitations and are not ready for clinical use. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
How your surgery is done matters less than you might fear, and what gets checked during it is still not agreed upon.
Most endometrial cancers are treated first with surgery to remove the uterus, and surgeons increasingly also check the first lymph nodes the cancer would drain to (the sentinel nodes) rather than removing many nodes. This month brought reassurance about surgical platform, and open disagreement about who needs node sampling.
• Robotic and standard laparoscopic surgery appear to give you the same cancer outcomes, so the choice can be made on practical grounds. A meta-analysis of 42 comparative studies covering 91,151 patients found no significant difference in recurrence, progression-free survival or overall survival between robotic-assisted and conventional laparoscopic hysterectomy, with similar lymph node yields. Robotic surgery involved less blood loss and fewer conversions to open surgery, while intraoperative complications were slightly more frequent; the authors suggest platform choice should follow institutional resources, surgeon expertise and your own circumstances. This is practice-ready evidence, though pooled from observational studies rather than randomized trials. (Read the full paper)
• If you are having a hysterectomy for endometrial precancer, whether to also sample lymph nodes is a real open question, and two studies this month landed on opposite sides. Both start from the same fact: atypical hyperplasia (also called endometrial intraepithelial neoplasia, or EIN) often turns out to be cancer once the uterus is examined. In a multicenter retrospective study of 411 patients, 47% had occult cancer, sentinel node spread was found in 4.7% of those, and node results changed the adjuvant treatment decision for 11 of the 22 patients who received any, which escalated chemotherapy for five patients and supported its omission for another six. A separate two-hospital study of 107 patients found cancer in 48% of those who had node dissection (versus 15% of those who had hysterectomy alone) but nodal spread in only 1 of 78 (1.2%, isolated tumor cells alone), with no resulting change in management, and argued for selective rather than routine node evaluation. Both found the procedure safe; they differ on whether it earns its place. (Read the full paper) (Read the full paper)
• Finding a few scattered tumor cells in a lymph node may not mean a worse outcome, but it currently triggers a lot more treatment. Among 1,219 women who had surgery in Stockholm-Gotland, Sweden between 2010 and 2024, those with isolated tumor cells had no clearly worse overall survival than node-negative patients (hazard ratio 1.94, but with a wide confidence interval of 0.75-5.06 that includes no difference), and among node-positive patients, survival did not differ clearly by how much tumor was in the nodes. Yet 47% of those with isolated tumor cells received adjuvant therapy compared with 11% of node-negative patients. Age over 68 and p53 mutation were what tracked with worse survival. The authors are careful that their estimates are imprecise and a modest effect cannot be ruled out. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
In advanced and recurrent disease, immunotherapy remains the centerpiece, and August was a month for honest accounting.
Immune checkpoint inhibitors such as dostarlimab and pembrolizumab release a brake on the immune system so it can attack tumor cells. They have genuinely changed outcomes in advanced endometrial cancer. Three studies this month tested the limits of that progress.
• Adding niraparib to immunotherapy maintenance delayed progression but did not help people live longer, and cost considerably more side effects. In Part 2 of the phase 3 RUBY trial, 291 people with primary advanced or recurrent endometrial cancer were randomized to dostarlimab plus chemotherapy followed by niraparib (a PARP inhibitor, which blocks a DNA-repair enzyme) plus dostarlimab maintenance, or to placebo throughout. The niraparib combination cut the risk of progression or death by 40% overall (hazard ratio 0.60) and by 37% in mismatch repair proficient tumors, but at 36.2 months there was no overall survival benefit (hazard ratio 1.2), while severe treatment-related side effects rose to 70.7% from 37.5% and treatment discontinuation to 38.7% from 11.5%. The authors state plainly that dostarlimab plus chemotherapy followed by dostarlimab alone remains the only regimen to show a significant survival benefit here. (Read the full paper)
• When immunotherapy clears the cancer completely, that remission often holds, including after treatment stops. Of 192 people treated with PD-1/PD-L1-directed immunotherapy at one institution, 57 (29.7%) had a complete response, at a median of 7.2 months; two-thirds were being treated for recurrent disease. At last follow-up 37 (64.9%) were alive and disease-free, and 86.5% of those were off treatment. Among 30 people with recurrent disease who stopped immunotherapy for reasons other than progression or death, 27 (90%) remained recurrence-free. Complete responses occurred in both MMR-deficient and MMR-proficient tumors, with a trend toward greater durability in MMR-deficient disease. This is retrospective, single-institution evidence, so it describes what happened rather than proving when it is safe to stop. (Read the full paper)
• Outside a clinical trial, immunotherapy results were more modest than the trial that led to its approval, which is worth knowing when you read trial numbers. Using France’s national health data system, researchers followed all 148 women who received dostarlimab on its own through the country’s early access program. Median age was 71, median overall survival was 17.0 months and real-world progression-free survival 9.0 months, which is less favorable than in the GARNET trial that supported approval. Severe digestive side effects affected 9.5% and anemia 8.1%. The gap most likely reflects a broader, older, unselected population rather than a different drug. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Keeping your uterus is possible for some early cancers and precancers, and molecular testing is starting to say for whom.
Fertility-sparing treatment uses hormonal therapy, sometimes with hysteroscopic removal of the tumor, instead of hysterectomy. It has usually been offered only for the earliest, lowest-grade disease. This month pushed at both edges of that boundary: which tumors, and which patients.
• A standardized fertility-sparing protocol worked for grade 2 tumors, not just grade 1, but recurrence was common. Twenty-five women (median age 34) with stage IA grade 2 endometrioid endometrial cancer without invasion into the uterine muscle were treated at one tertiary center with hysteroscopic resection followed by both oral megestrol acetate and a levonorgestrel intrauterine device. All 25 achieved a complete response, 84% within six months. Fifteen tried to conceive and eight (53.3%) became pregnant, with three term deliveries, three ongoing pregnancies and two miscarriages. Recurrence occurred in 56% at a median of 16.6 months; six went on to definitive surgery and eight were successfully re-treated conservatively, leaving 96% with no evidence of disease at last follow-up. This is a small, single-center series in carefully selected patients, which is encouraging, but a larger study with longer follow-up is needed. (Read the full paper)
• Your tumor’s molecular and hormone-receptor profile may predict whether hormonal treatment will work. A meta-analysis of 18 retrospective studies covering 965 reproductive-aged women with atypical hyperplasia or endometrial cancer found that tumors with no specific molecular profile had higher odds of complete remission, while p53-abnormal and MMR-deficient tumors were significantly less likely to achieve it; POLE-mutated tumors did about as well as no-specific-profile tumors. Progesterone receptor positivity was also strongly associated with complete remission (odds ratio 7.73). Because the underlying studies are retrospective, this is best read as a framework for selecting patients rather than a rule. (Read the full paper)
• A tissue stain called PTEN could help avoid some hysterectomies done for a precancer diagnosis that was wrong, but it cannot be used alone. Distinguishing atypical hyperplasia from hyperplasia without atypia decides whether you need surgery or can be managed with hormones, and it is genuinely difficult under the microscope. Across 27 studies and 2,274 women, PTEN immunohistochemistry had 84.7% specificity but only 58.0% sensitivity, meaning it is reasonably good at confirming atypia and poor at ruling it out. The authors position it as a complementary test that could reduce over-diagnosis of atypia, and call for standardized staining and multi-marker approaches. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
The tests used to find, stage and follow endometrial cancer got a careful look, including the ultrasound cutoff used on thousands of women a year.
Endometrial cancer is usually investigated after abnormal bleeding, starting with a transvaginal ultrasound measurement of the endometrial lining. Where that threshold sits determines who gets a biopsy.
• A 4 mm endometrial thickness cutoff looks like the better balance between missing cancer and causing unnecessary biopsies. In a prospective study of 1,170 women aged 50 and over referred for endometrial evaluation at an ethnically diverse academic medical center, 82 (7.0%) had endometrial cancer and 42 (3.6%) had hyperplasia. Among the 975 with a clearly visualized endometrial stripe, sensitivity for detecting neoplasia was 100% at 3 mm, 97.8% at 4 mm and 90.2% at 5 mm, while specificity ran the other way (9.5%, 16.1% and 24.4%). The 3 mm and 4 mm thresholds were both significantly more sensitive than 5 mm, and 4 mm was significantly more specific than 3 mm, meaning that 4 mm caught nearly everything while sparing more women an invasive procedure. (Read the full paper)
• Blood tests that look for tumor DNA are promising for tracking endometrial cancer, but two reviews agree they are not ready to change your care. A systematic scoping review of 93 records found that circulating tumor DNA (fragments of tumor DNA shed into the blood) showed more potential than general cell-free DNA for prognosis, molecular profiling and monitoring, while noting that study designs and reporting were too heterogeneous to support any specific clinical use. A narrative review focused on minimal residual disease reached the same conclusion from the other direction: ctDNA measured around the time of surgery has prognostic support from an 11-study, 1,298-patient meta-analysis, with post-operative detection more informative than pre-operative, but assay differences and thin independent replication mean liquid biopsy should stay an investigational add-on until trials show that acting on the result improves outcomes. (Read the full paper) (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Weight and metabolic health are part of endometrial cancer care, not a side issue.
Obesity is the strongest modifiable risk factor for endometrial cancer, and for many people with early-stage disease the long-term health threat is not the cancer.
• For women with early-stage endometrial cancer and severe obesity, treating the obesity may matter as much as treating the cancer, though it hasn’t yet been shown to extend survival. This review synthesizes the evidence that women with early-stage disease face a greater risk of dying from obesity-related conditions than from cancer recurrence, and that weight reduction improves quality of life and long-term health burden. It finds that minimally invasive metabolic and bariatric surgery combined with hysterectomy appears feasible in selected patients with severe obesity and endometrial hyperplasia or carcinoma, and that GLP-1 receptor agonists (the weight-loss and diabetes drug class) may act on both body-wide metabolic conditions and some tumor pathways. The authors are explicit that a direct antitumor effect and a cancer-specific survival benefit have not been established, and that prospective studies are needed before this enters formal guidelines. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Some of the month’s most useful findings came from asking people with endometrial cancer about their own experience.
Qualitative research, such as interviews and thematic analysis, is the primary evidence for what care feels like from the inside, and three studies this month addressed information, fertility loss, and surgery in later life.
• Most women reported being left without the information they needed, and the worst gap was before diagnosis. Among 82 women identified through the Queensland Cancer Register and diagnosed within the previous 13 months, moderate-to-high unmet information needs were reported by 58% before diagnosis, 71% at diagnosis and 57% during treatment, with satisfaction lowest before diagnosis and improving later. Interviews with 24 of them found that what people needed varied a great deal and shifted with their emotional and cognitive capacity at the time; what they valued was clear, compassionate information delivered progressively rather than all at once. Many described delayed and inconsistent communication about their own diagnosis. (Read the full paper)
• Losing fertility to gynecological cancer treatment can be a grief in its own right, and it deserves named support in the care plan. Fourteen women aged 22 to 48 with cervical, ovarian, uterine, or endometrial cancer at a Ghanaian tertiary referral hospital were interviewed in English, Twi, or Ewe about reproductive loss. Three themes emerged: psychological and emotional experience, social challenges, and coping and resilience. 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 intimate relationships, treatment symptoms, financial strain and interrupted education. Women drew on treatment adherence, dietary change, prayer and family support. The authors call for fertility counseling, psychosocial support and guidance on other routes to family, such as adoption, to be built into care. (Read the full paper)
• For women over 65 facing endometrial cancer surgery, frailty and nutrition help predict how recovery will go. In a retrospective cohort of women aged 65 and older who had primary endometrial cancer surgery between 2016 and 2024, severe complications occurred in 7.1% and unplanned readmission within 90 days in 8.1%. A five-item frailty index and a composite of routine inflammation and nutrition blood tests each predicted both outcomes, and adding them to a standard clinical model improved its ability to discriminate risk (area under the curve rising from 0.69 to 0.77 for severe complications). The authors describe the gains as modest and requiring external validation before being used to guide decisions. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Rarer uterine cancers behave differently and telling them apart is the first step to treating them right.
Uterine sarcomas and unusual carcinoma types make up a small share of uterine cancers but account for a disproportionate share of poor outcomes.
• A rare uterine cancer type called mesonephric-like adenocarcinoma behaves much more aggressively than the common endometrial cancer it can resemble. Across 83 cases collected from institutions across Japan, 78 were confirmed as mesonephric-like adenocarcinoma (47 in the uterus, 31 in the ovary). Uterine cases had significantly shorter progression-free and overall survival than endometrial endometrioid carcinomas, closer to that of copy-number-high tumors, and lymphovascular space invasion independently predicted progression. The study also found a possible origin: adenomyosis (endometrial tissue growing within the uterine muscle) was far more common alongside uterine cases than alongside endometrioid cancers (62% vs 28%), and among the 36 uterine cases carrying a KRAS hotspot mutation, the same mutation was found in the adjacent adenomyosis in 12 (two-thirds of the adenomyosis actually examined) suggesting these tumors may arise from displaced endometrial tissue. (Read the full paper)
Check the citations section for a comprehensive list of publications associated with this topic.
Epidemiology, access and health disparities research.
Black women have roughly twice the endometrial cancer mortality of White women, and three studies this month examined where that gap comes from. All three are behind access restrictions, so they are listed here by citation only.
Check the citations section for a comprehensive list of publications associated with this topic.
General and basic-science uterine cancer research.
These laboratory and mechanistic studies are early-stage work on how endometrial cancer grows, evades the immune system and resists treatment. None of them changes care now, but they are where future treatments start.
Check the citations section for a comprehensive list of publications associated with this topic.
What Does This Mean for Me?
If I’ve had molecular testing, what should I be asking about it?
Molecular classification is no longer just a prognosis label; it increasingly determines what treatment you are offered and what you can safely skip. This month’s pooled trial analysis suggests that for MMR-deficient tumors, grade should not be driving adjuvant treatment decisions, and the fertility-sparing meta-analysis found that molecular subtype and progesterone receptor status predict whether hormonal treatment is likely to work. A reasonable question for your care team: “Which molecular group is my tumor in, and what specifically does that change about the treatment you’re recommending?” If molecular testing hasn’t been done, it’s worth asking whether it is available to you and whether it would alter the plan.
My doctor is recommending sentinel lymph node sampling for a precancer diagnosis. Is that right?
This is genuinely unsettled, and the two studies published this month reached opposite conclusions from similar starting points. One found node results changed adjuvant treatment for half the patients who needed any, the other found almost no nodal spread and no change in management. What both agree on is that a diagnosis of atypical hyperplasia or EIN frequently turns out to be cancer on final pathology (around 40 to 50% of patients in these two cohorts) and that the procedure itself is safe. So the useful conversation is not “yes or no” but “in my case, what would a positive or negative node result actually change?” If the answer is nothing, that’s an argument for skipping it.
Should I want the newest drug combination?
Not automatically. The RUBY Part 2 results are a clear example of why: adding niraparib to immunotherapy maintenance meaningfully delayed cancer progression, yet after three years it had not helped anyone live longer, while severe side effects nearly doubled and more than a third of people stopped treatment because of them. Delayed progression and longer life are not the same outcome, and it is fair to ask which one a proposed treatment has actually been shown to improve. The French real-world study is a second useful caution: results in ordinary practice, in older and less selected patients, were more modest than in the trial that led to approval.
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 uterine and endometrial cancer landscape (molecular classification, immunotherapy and targeted therapy, surgery and staging, uterine sarcoma, fertility preservation, 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.
Molecular tumor testing is changing what doctors need to look at and what they can stop looking at.
Directly referenced:
1. Wakkerman FC, et al. “No prognostic role for FIGO grading in mismatch repair deficient endometrial carcinoma.” Eur J Cancer. August 2026. PMID 42320406. https://doi.org/10.1016/j.ejca.2026.116885
2. Jeong Y, et al. “Artificial Intelligence and Digital Pathology for Molecular Classification of Endometrial Cancer.” Int J Mol Sci. August 17, 2026. PMID 42653345. https://doi.org/10.3390/ijms27167341
Additional citations on related topics:
3. Maloberti T, et al. “Molecular Characterization of Endometrial Cancer Using a Laboratory-Developed Multi-Gene NGS Panel.” Int J Mol Sci. August 18, 2026. PMID 42653388. https://doi.org/10.3390/ijms27167384 (open access — expanded gene-panel profiling of 70 endometrial tumors)
4. Hachisuga K, et al. “Clinicopathological Differences in HER2 Immunohistochemical Expression Between Low-Grade Endometrial Cancer with p53-Abnormal Expression and High-Grade Endometrial Cancer.” Cancers (Basel). August 15, 2026. PMID 42649950. https://doi.org/10.3390/cancers18162638 (open access — HER2 expression across molecular and grade groups)
5. Bakshi N, et al. “Molecular classification-driven stage migration and prognostic risk stratification in endometrial cancers: FIGO 2023 vs FIGO 2009.” Virchows Arch. August 2026. PMID 41345523. https://doi.org/10.1007/s00428-025-04366-1 (subscription access)
6. Roy A, et al. “FIGO 2023 staging may result in overtreatment of early-stage endometrial cancer.” Gynecol Oncol. August 2026. PMID 42349039. https://doi.org/10.1016/j.ygyno.2026.06.014 (subscription access)
7. Jeong S, et al. “Validation of the 2025 ESGO/ESTRO/ESP postoperative risk stratification system in endometrial cancer: A same-cohort comparison with the 2020 molecular classification.” Gynecol Oncol. August 2026. PMID 42447656. https://doi.org/10.1016/j.ygyno.2026.07.003 (subscription access)
8. Kuriakose S, et al. “Molecular subtypes and survival patterns of endometrial cancer in a South Indian cohort.” Int J Gynaecol Obstet. August 2026. PMID 41773470. https://doi.org/10.1002/ijgo.70837 (subscription access)
9. Pinninti R, et al. “Impact of Molecular Classification on Multidisciplinary Treatment Decision Making in Early-Stage Endometrial Cancer: A Prospective Real-World Study From India.” JCO Glob Oncol. August 7, 2026. PMID 42566739. https://doi.org/10.1200/GO-26-00172 (license unconfirmed)
10. Walia S, et al. “Utilization of Key Morphologic and Molecular Prognostic and Predictive Parameters in Endometrial Malignancies: A Survey of Gynecologic Pathologists.” Int J Surg Pathol. August 2026. PMID 41755714. https://doi.org/10.1177/10668969261417319 (subscription access)
11. Pereira RA, et al. “Molecular subtypes and lymph-node metastasis in endometrial cancer: An updated systematic review and meta-analysis.” Surg Oncol. August 2026. PMID 42242033. https://doi.org/10.1016/j.suronc.2026.102463 (subscription access)
12. Zhou Q, et al. “Current Treatment Options Guided by Molecular Classification in Endometrial Cancer.” Curr Treat Options Oncol. August 27, 2026. PMID 42658373. https://doi.org/10.1007/s11864-026-01409-w (subscription access)
13. Wang J, et al. “Integrating laboratory tests with FIGO staging using machine learning improves long-term prognostic assessment in endometrial cancer.” Eur J Obstet Gynecol Reprod Biol. August 2026. PMID 42275941. https://doi.org/10.1016/j.ejogrb.2026.115219 (subscription access)
14. Saegusa M. “The Molecular Pathology of Morules in Endometrial Carcinoma: Biological Significance and Clinical Implications.” Pathol Int. August 2026. PMID 42659029. https://doi.org/10.1111/pin.70168 (restricted license, CC BY-NC-ND)
15. Johnson JE, et al. “Identification of Lynch syndrome among people newly diagnosed with endometrial cancer: a prospective audit.” J Med Genet. August 26, 2026. PMID 42209212. https://doi.org/10.1136/jmg-2026-111578 (subscription access)
16. Nchako CM, et al. “Role of Genetics in Gynecologic Malignancies.” Surg Clin North Am. August 2026. PMID 42419314. https://doi.org/10.1016/j.suc.2026.03.004 (subscription access)
How your surgery is done matters less than you might fear, and what gets checked during it is still not agreed upon.
Directly referenced:
17. Kalas N, et al. “Robotic-assisted surgery versus conventional laparoscopy in endometrial cancer: a systematic review and meta-analysis.” Eur J Surg Oncol. August 2026. PMID 42235434. https://doi.org/10.1016/j.ejso.2026.111861
18. Catozzo A, et al. “Clinical utility of sentinel lymph node biopsy in atypical endometrial hyperplasia: A multicenter cohort study.” Gynecol Oncol. August 2026. PMID 42462287. https://doi.org/10.1016/j.ygyno.2026.06.027
19. Dubé AJ, et al. “Clinical Significance of Sentinel Lymph Node Dissection in Preoperative Endometrial Intraepithelial Neoplasia: A Single-Institution Analysis.” J Obstet Gynaecol Can. August 2026. PMID 42242419. https://doi.org/10.1016/j.jogc.2026.103412
20. Chilianu A, et al. “Prognostic significance of isolated tumor cells and nodal tumor burden in endometrial cancer: a population-based cohort study.” Acta Oncol. August 11, 2026. PMID 42578630. https://doi.org/10.2340/1651-226X.2026.45813
Additional citations on related topics:
21. Pongsuvareeyakul T, et al. “Prognostic Value of Lymphovascular Space Invasion and Its Quantification in Endometrial Carcinoma in Northern Thailand.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663223. https://doi.org/10.31557/APJCP.2026.27.8.3021 (open access — substantial lymphovascular invasion independently predicted worse survival in 843 patients)
22. Margherita R, et al. “Sentinel lymph node biopsy in atypical endometrial hyperplasia: impact on staging and adjuvant treatment.” Eur J Obstet Gynecol Reprod Biol. August 2026. PMID 42385287. https://doi.org/10.1016/j.ejogrb.2026.115264 (subscription access)
23. Martin D, et al. “Gynecologic Pathologist Agreement on Presence and Quantification of Lymphovascular Invasion in Low-stage, Low-grade Endometrial Endometrioid Adenocarcinoma.” Am J Surg Pathol. August 2026. PMID 42109001. https://doi.org/10.1097/PAS.0000000000002563 (subscription access)
24. He Z, et al. “Reduced-port robotic surgery versus multiport robotic surgery in endometrial cancer: a systematic review and meta-analysis.” J Robot Surg. August 12, 2026. PMID 42584727. https://doi.org/10.1007/s11701-026-03795-7 (subscription access)
25. Dayan-Schwartz A, et al. “Robotic-Assisted Cytoreductive Surgery for Recurrent Endometrial Carcinoma with Iliac Vessel Involvement: A Multidisciplinary Approach.” Ann Surg Oncol. August 2026. PMID 42143650. https://doi.org/10.1245/s10434-026-19669-z (subscription access)
26. 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)
In advanced and recurrent disease, immunotherapy remains the centerpiece, and August was a month for honest accounting.
Directly referenced:
27. Powell MA, et al. “Poly(adenosine diphosphate-ribose) polymerase inhibitor maintenance therapy with niraparib in patients with primary advanced or recurrent endometrial cancer receiving dostarlimab plus chemotherapy.” Int J Gynecol Cancer. August 2026. PMID 42391799. https://doi.org/10.1016/j.ijgc.2026.104774
28. O’Connor RM, et al. “Outcomes following complete response to immune checkpoint inhibitors in endometrial cancer.” Gynecol Oncol. August 2026. PMID 42456481. https://doi.org/10.1016/j.ygyno.2026.07.006
29. Singier A, et al. “Use, survival, and adverse events of dostarlimab monotherapy in advanced or recurrent endometrial cancer: a nationwide cohort study in France.” Oncologist. August 6, 2026. PMID 42610707. https://doi.org/10.1093/oncolo/oyag316
Additional citations on related topics:
30. Kuchimanchi M, et al. “Exposure-Response Relationship of Dostarlimab in Primary Advanced/Recurrent Endometrial Cancer: Results From Interim Analysis 2 of Part 1 of the RUBY Trial.” Clin Pharmacol Drug Dev. August 2026. PMID 42555284. https://doi.org/10.1002/cpdd.70087 (open access — dostarlimab blood levels versus survival and side effects)
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 of a new immune-engaging antibody)
32. Moiola CP, et al. “A mouse PDX clinical trial reveals broad efficacy of niraparib and vc-seco-DUBA anti-HER2 ADC SYD985 in HER2/neu expressing endometrial cancer.” Biomed Pharmacother. August 4, 2026. PMID 42551191. https://doi.org/10.1016/j.biopha.2026.119830 (open access — preclinical combination testing across 15 patient-derived tumor models)
33. Ruggiero A, et al. “A Delicate Balance: Immunotherapy for Endometrial Cancer in a Patient With Multiple Sclerosis.” J Med Cases. August 2026. PMID 42490778. https://doi.org/10.14740/jmc5260 (open access — a single case of immunotherapy alongside pre-existing multiple sclerosis)
34. Poggi A, et al. “Natural killer cells at the interface of tumor immune escape and immunotherapy resistance in endometrial cancer.” Front Immunol. August 7, 2026. PMID 42630891. https://doi.org/10.3389/fimmu.2026.1784443 (open access — review of NK cells in checkpoint-resistant tumors)
35. Santin AD, et al. “A Phase II Evaluation of the Efficacy and Safety of Sacituzumab Govitecan in Patients with Recurrent Uterine Cancer.” Clin Cancer Res. August 3, 2026. PMID 42132892. https://doi.org/10.1158/1078-0432.CCR-26-0144 (restricted license, CC BY-NC-ND)
36. Borden LE, et al. “MLH1 promoter hypermethylation and associations with survival outcomes: A real-world endometrial cancer molecularly targeted therapy consortium cohort study.” Gynecol Oncol. August 2026. PMID 42468445. https://doi.org/10.1016/j.ygyno.2026.07.008 (subscription access)
37. Yao L, et al. “Immunotherapy response and resistance in endometrial cancer: Integrating molecular subtype, spatial immune states, and pharmacodynamic biomarkers.” Crit Rev Oncol Hematol. August 2026. PMID 42202924. https://doi.org/10.1016/j.critrevonc.2026.105388 (subscription access)
38. Chao A, et al. “Promising response to neoadjuvant pembrolizumab and low-dose chemotherapy in advanced endometrial cancer: A preliminary report.” J Formos Med Assoc. August 2026. PMID 41672816. https://doi.org/10.1016/j.jfma.2026.02.003 (restricted license, CC BY-NC-ND)
39. Cao Y, et al. “Comment on ‘Promising response to neoadjuvant pembrolizumab and low-dose chemotherapy in advanced endometrial cancer: A preliminary report’.” J Formos Med Assoc. August 2026. PMID 41760503. https://doi.org/10.1016/j.jfma.2026.02.027 (restricted license, CC BY-NC-ND)
40. De Tommasi O, et al. “Integrated expression profiling of trophoblast cell-surface antigen 2 (TROP2), folate receptor alpha (FRα), and human epidermal growth factor receptor 2 (HER2) in endometrial Cancer across molecular classes, genomic alterations, and histologic subtypes.” Gynecol Oncol. August 7, 2026. PMID 42567118. https://doi.org/10.1016/j.ygyno.2026.08.002 (subscription access)
41. da Silva Neto AL, et al. “Between biology and benefit: who gains from PARP-immunotherapy in p53-abnormal endometrial cancer?” Int J Gynecol Cancer. August 2026. PMID 42235256. https://doi.org/10.1016/j.ijgc.2026.104747 (subscription access)
42. Barber EL, et al. “Surgical window of opportunity clinical trial of abemaciclib and letrozole for endometrioid adenocarcinoma of the endometrium.” Gynecol Oncol. August 2026. PMID 42447658. https://doi.org/10.1016/j.ygyno.2026.07.001 (subscription access)
43. 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)
44. Casaccia Giordano F, et al. “Hold the line: Local control strategies in oligoprogressive gynecologic cancers during systemic therapy.” Eur J Cancer. August 2026. PMID 42335568. https://doi.org/10.1016/j.ejca.2026.116894 (subscription access)
Keeping your uterus is possible for some early cancers and precancers, and molecular testing is starting to say for whom.
Directly referenced:
45. Catena U, et al. “Fertility-sparing treatment in stage IA grade 2 endometrioid endometrial cancer: Outcomes of a standardized approach.” Gynecol Oncol. August 2026. PMID 42419001. https://doi.org/10.1016/j.ygyno.2026.06.019
46. Jerbaka M, et al. “Fertility-Sparing Management of Atypical Hyperplasia and Endometrial Cancer from the Perspective of Molecular and Hormonal Profiles: A Meta-Analysis-Driven Framework.” Cancers (Basel). August 4, 2026. PMID 42588707. https://doi.org/10.3390/cancers18152490
47. Shcherbatiuk K, et al. “Diagnostic accuracy of phosphatase and tensin homolog loss in differentiating between atypical endometrial hyperplasia/endometrioid intraepithelial neoplasia and non-atypical endometrial hyperplasia: A systematic review and meta-analysis.” Int J Gynaecol Obstet. August 2026. PMID 41742842. https://doi.org/10.1002/ijgo.70901
Additional citations on related topics:
48. Nolin A, et al. “Associations between molecular classification and response to intra-uterine levonorgestrel device therapy in patients with medically managed endometrial cancer and endometrial intra-epithelial neoplasia: a multi-center Endometrial Cancer Molecularly Targeted Therapy (ECMT2) Consortium study.” Int J Gynecol Cancer. August 2026. PMID 42235254. https://doi.org/10.1016/j.ijgc.2026.104727 (subscription access)
49. Mariani C, et al. “Therapy with a levonorgestrel-releasing intra-uterine system in atypical endometrial hyperplasia and low-grade endometrial cancer.” Int J Gynecol Cancer. August 2026. PMID 42235255. https://doi.org/10.1016/j.ijgc.2026.104728 (subscription access)
50. Raffone A, et al. “Prolonged conservative treatment of women with atypical endometrial hyperplasia and early endometrial carcinoma: A systematic review and meta-analysis.” Eur J Obstet Gynecol Reprod Biol. August 2026. PMID 42258906. https://doi.org/10.1016/j.ejogrb.2026.115212 (restricted license, CC BY-NC-ND)
51. Liu Q, et al. “Gonadotropin-releasing hormone agonist plus aromatase inhibitor versus oral progestins for fertility-sparing treatment in early endometrial carcinoma and atypical hyperplasia: interim analysis of a prospective controlled trial.” Int J Gynecol Cancer. August 2026. PMID 42330749. https://doi.org/10.1016/j.ijgc.2026.104718 (subscription access)
52. Jang EB, et al. “Predictive value of primary tumour SUV on F-fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography in patients undergoing fertility-sparing treatment for early endometrial cancer.” Eur J Obstet Gynecol Reprod Biol. August 2026. PMID 42287870. https://doi.org/10.1016/j.ejogrb.2026.115230 (subscription access)
53. Ding S, et al. “MRI-Based Radiomics Model for Predicting Eligibility for Conservative Management of Endometrial Cancer.” Cancer Med. August 2026. PMID 42618514. https://doi.org/10.1002/cam4.72141 (restricted license, CC BY-NC-ND)
The tests used to find, stage and follow endometrial cancer got a careful look, including the ultrasound cutoff used on thousands of women a year.
Directly referenced:
54. Rotenberg O, et al. “Evaluating endometrial thickness for sonographic detection of neoplasia in diverse population of women.” Int J Gynecol Cancer. August 2026. PMID 42247730. https://doi.org/10.1016/j.ijgc.2026.104750
55. Macdonald ER, et al. “Evaluating the utility of circulating cell-free DNA in the context of endometrial cancer: a systematic scoping review.” Int J Gynecol Cancer. August 2026. PMID 42330750. https://doi.org/10.1016/j.ijgc.2026.104767
56. 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:
57. Yu F, et al. “Diagnostic performance of CDO1 and ZSCAN12 methylation in endometrial versus cervical samples for endometrial cancer and atypical hyperplasia: a comparative study.” Ann Med. August 12, 2026. PMID 42584228. https://doi.org/10.1080/07853890.2026.2716939 (open access — DNA-methylation testing on endometrial versus cervical samples)
58. Minareci Y, et al. “MicroRNA-204 and microRNA-652-3p as promising biomarkers for endometrial cancer diagnosis and prognosis.” Rev Assoc Med Bras (1992). August 3, 2026. PMID 42561202. https://doi.org/10.1590/1806-9282.20252283 (open access — serum microRNAs in 150 patients versus 76 controls)
59. Atalay F, et al. “Inflammatory markers and the systemic immune-inflammation index in endometrial carcinoma and hyperplasia: a retrospective cohort study.” J Obstet Gynaecol. August 21, 2026. PMID 42626923. https://doi.org/10.1080/01443615.2026.2705901 (open access — blood-count ratios for distinguishing cancer from hyperplasia)
60. Pulsawat A, et al. “Preoperative Immuno-inflammatory Markers as Predictors of Deep Myometrial Invasion in Endometrial Cancer: A Retrospective Study from Southern Thailand.” Asian Pac J Cancer Prev. August 1, 2026. PMID 42663204. https://doi.org/10.31557/APJCP.2026.27.8.2839 (open access — low-cost markers for predicting deep muscle invasion)
61. Li S, et al. “Incremental prognostic value of a preoperative immune-metabolic-inflammatory score for disease-free survival in endometrial cancer: A retrospective cohort study.” Medicine (Baltimore). August 21, 2026. PMID 42629761. https://doi.org/10.1097/MD.0000000000050354 (open access — a four-part blood score in 853 patients)
62. Wang J, et al. “Preoperative Prediction of Lymphovascular Space Invasion in Endometrial Cancer Using Diffusion MRI-Derived Vessel Density.” Korean J Radiol. August 2026. PMID 42543756. https://doi.org/10.3348/kjr.2026.0116 (open access — MRI-derived vessel density for predicting lymphovascular invasion)
63. Vaz I, et al. “Hidden endometrial cancer due to vaginal obliteration associated with lichen sclerosus/lichen planus.” BMJ Case Rep. August 18, 2026. PMID 42613127. https://doi.org/10.1136/bcr-2026-272712 (open access — vulvovaginal scarring preventing standard examination and delaying diagnosis)
64. Li F, et al. “The value of microvascular flow imaging and color Doppler flow imaging in the differential diagnosis of benign and malignant endometrial lesions.” Clin Radiol. August 2026. PMID 42314358. https://doi.org/10.1016/j.crad.2026.107388 (subscription access)
65. Saleh KA, et al. “Harnessing exosomes for endometrial Cancer: From non-invasive diagnostics to precision therapies.” Clin Chim Acta. August 2026. PMID 42092669. https://doi.org/10.1016/j.cca.2026.121061 (subscription access)
Weight and metabolic health are part of endometrial cancer care, not a side issue.
Directly referenced:
66. Innocenzi C, et al. “Beyond Weight Loss: A Comprehensive Review of Integrated Pharmacotherapy and Metabolic Bariatric Surgery in Endometrial Cancer Care.” Medicina (Kaunas). August 17, 2026. PMID 42654468. https://doi.org/10.3390/medicina62081571
Additional citations on related topics:
67. Kong R, et al. “Correlation of the estimated glucose disposal rate with self-reported endometrial cancer: a cross-sectional study from NHANES 1999-2018.” Gynecol Endocrinol. August 26, 2026. PMID 42647182. https://doi.org/10.1080/09513590.2026.2720976 (open access — insulin-resistance measure and self-reported endometrial cancer)
68. Yen TT, et al. “Adjunctive sodium-glucose cotransporter 2 (SGLT2) inhibitors with progestins and endometrial cancer risk in benign uterine diseases and hyperplasia.” Gynecol Oncol. August 2026. PMID 42385610. https://doi.org/10.1016/j.ygyno.2026.06.023 (subscription access)
69. Raja NP, et al. “GLP-1 Receptor Agonists and Obesity Related Cancers: What We Know So Far.” Curr Oncol Rep. August 26, 2026. PMID 42645635. https://doi.org/10.1007/s11912-026-01825-z (subscription access)
70. Cao Y, et al. “Progress in Molecular Biological Mechanism of Endometrial Cancer Induced by Obesity.” Zhongguo Yi Xue Ke Xue Yuan Xue Bao. August 30, 2026. PMID 42660843. https://doi.org/10.3881/j.issn.1000-503X.16722 (subscription access)
71. Lu S, et al. “Establishment of insulin resistance-related ten-gene signature in endometrial cancer and identification of ACTL8 as a prognostic and immunological biomarker.” Clin Transl Oncol. August 2026. PMID 41670819. https://doi.org/10.1007/s12094-026-04230-x (restricted license, CC BY-NC-ND)
Some of the month’s most useful findings came from asking people with endometrial cancer about their own experience.
Directly referenced:
72. DiSipio T, et al. “Information experiences among women diagnosed with endometrial cancer: a mixed methods study.” Support Care Cancer. August 11, 2026. PMID 42581238. https://doi.org/10.1007/s00520-026-11082-2
73. 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
74. Liu S, et al. “Frailty and an Inflammation-Nutrition Composite for Predicting Postoperative Outcomes in Older Patients Undergoing Endometrial Cancer Surgery.” Clin Interv Aging. August 7, 2026. PMID 42583416. https://doi.org/10.2147/CIA.S609218
Additional citations on related topics:
75. Hsu CD, et al. “Vaginal estrogen therapy utilization and associated outcomes in younger survivors of endometrial cancer.” Menopause. August 1, 2026. PMID 41774009. https://doi.org/10.1097/GME.0000000000002747 (subscription access)
76. Thayer EG, et al. “High rates of venous thromboembolism in endometrial cancer patients requiring systemic therapy: an opportunity for risk assessment and intervention.” Gynecol Oncol. August 29, 2026. PMID 42667794. https://doi.org/10.1016/j.ygyno.2026.08.019 (subscription access)
Rarer uterine cancers behave differently and telling them apart is the first step to treating them right.
Directly referenced:
77. Miyama Y, et al. “Multi-institutional study of mesonephric-like adenocarcinoma: its clinicopathological characteristics and histogenetic association with ectopic endometrium.” Virchows Arch. August 2026. PMID 41160109. https://doi.org/10.1007/s00428-025-04286-0
Additional citations on related topics:
78. Slaager FC, et al. “Intraepithelial serous carcinoma of the endometrium: protocol for a prospective multicentre registry in the Netherlands.” BMJ Open. August 7, 2026. PMID 42567642. https://doi.org/10.1136/bmjopen-2026-120737 (open access — registry protocol on how much surgery this rare non-invasive lesion needs)
79. Zheng Y, et al. “Molecular and clinicopathological characterisation of SMARCA4-deficient uterine tumours: distinguishing features between dedifferentiated/undifferentiated endometrial carcinoma and undifferentiated uterine sarcoma.” Pathology. August 2026. PMID 42321072. https://doi.org/10.1016/j.pathol.2026.03.012 (subscription access)
80. Tieng FYF, et al. “Rescuing a refractory Leiomyosarcoma: ALK-DCTN1 fusion as a gateway to long-term control with Ceritinib.” Gynecol Oncol Rep. August 2026. PMID 42569171. https://doi.org/10.1016/j.gore.2026.102175 (restricted license, CC BY-NC-ND)
81. Nishikawa Y, et al. “Gynecologic Tumors and Precursor Lesions, Including p53-Aberrant Atypical Hyperplasia-like Endometrial Lesions, in Li-Fraumeni Syndrome.” Mod Pathol. August 2026. PMID 42190817. https://doi.org/10.1016/j.modpat.2026.101019 (subscription access)
Epidemiology, access and health disparities research.
Additional citations on related topics:
82. Rotenberg O, et al. “Racial Differences in Sonographic Evaluation in Suspected Cases of Endometrial Neoplasia.” JAMA Netw Open. August 3, 2026. PMID 42550505. https://doi.org/10.1001/jamanetworkopen.2026.27283 (restricted license, CC BY-NC-ND)
83. Suh-Burgmann EJ, et al. “Age and Endometrial Cancer Survival Disparities Among Black and White Insured Patients.” JAMA Netw Open. August 3, 2026. PMID 42599704. https://doi.org/10.1001/jamanetworkopen.2026.29596 (restricted license, CC BY-NC-ND)
84. Weimer A, et al. “Impact of patient neighborhood area deprivation index on prognostic factors and outcomes in endometrioid adenocarcinoma of the endometrium: a retrospective multi-center healthcare network analysis.” Gynecol Oncol Rep. August 2026. PMID 42433624. https://doi.org/10.1016/j.gore.2026.102159 (restricted license, CC BY-NC-ND)
General and basic-science uterine cancer research.
Additional citations on related topics:
85. Jiang H, et al. “A novel tRNA-derived fragment, tRF-19-79MP9PJZ, promotes uterine corpus endometrial carcinoma progression by targeting DSC3.” Hum Cell. August 6, 2026. PMID 42560623. https://doi.org/10.1007/s13577-026-01432-x (open access — a small RNA fragment driving tumor progression in cells and tissue)
86. Zhang J, et al. “Engineered exosomes with RNA-motif short hairpin RNA loading and Rab4-boosted production enable controlled ferroptosis in endometrial carcinoma.” Bioeng Transl Med. August 28, 2026. PMID 42666679. https://doi.org/10.1002/btm2.70163 (open access — laboratory drug-delivery platform triggering tumor cell death in mice)
87. Chen H, et al. “TRIM21 suppresses uterine corpus endometrial carcinoma progression by promoting K48-linked ubiquitination and degradation of SOAT1.” Front Immunol. August 17, 2026. PMID 42676445. https://doi.org/10.3389/fimmu.2026.1863307 (open access — candidate tumor suppressor linking protein turnover to tumor fat metabolism)
88. Anastasiu CV, et al. “Exploring the Possible Role of Endometriosis-Associated Dysbiosis in Endometrial Carcinogenesis.” Medicina (Kaunas). August 17, 2026. PMID 42654474. https://doi.org/10.3390/medicina62081577 (open access — hypothesis-generating review on microbial changes, endometriosis and cancer development)
89. Sun Y, et al. “A preliminary exploration of the mechanism of endometrial cancer development induced by intestinal flora diversity and its metabolites.” Front Cell Infect Microbiol. August 12, 2026. PMID 42656427. https://doi.org/10.3389/fcimb.2026.1815291 (open access — gut bacteria and blood metabolites in 17 patients versus 24 controls)
90. Xu Y, et al. “FABP7 Enhances Endometrial Cancer Cell Migration and Stemness by Activating the Wnt/β-catenin Pathway.” Biochem Genet. August 2026. PMID 41402614. https://doi.org/10.1007/s10528-025-11302-0 (subscription access)
91. Wu J, et al. “FBXW7 Inhibited M2 Macrophage Polarization in Endometrial Cancer by Reducing CCL2 Secretion Through Ubiquitination of MYBL2.” Biochem Genet. August 2026. PMID 41484508. https://doi.org/10.1007/s10528-025-11309-7 (subscription access)
92. Yin M, et al. “DEHP-associated toxic targets in endometrial carcinoma: prognostic value and immunological implications.” Int J Environ Health Res. August 2026. PMID 41616042. https://doi.org/10.1080/09603123.2026.2621066 (subscription access)
93. Yu M, et al. “Characterization of immune landscape and prognostic value of IL-17-related signature in uterine corpus endometrial carcinoma.” Clin Transl Oncol. August 2026. PMID 41661403. https://doi.org/10.1007/s12094-026-04242-7 (subscription access)
94. 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)
95. Yao L, et al. “When death pathways converge: PANoptosis in the evolution and treatment of female tumors.” Crit Rev Oncol Hematol. August 2026. PMID 42144174. https://doi.org/10.1016/j.critrevonc.2026.105380 (subscription access)
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97. Ran Y. “Subtype-specific mechanisms of lipid metabolism in gynecological malignancies and novel targeted intervention strategies.” Oncol Lett. August 4, 2026. PMID 42597907. https://doi.org/10.3892/ol.2026.15800 (restricted license, CC BY-NC-ND)
98. Canbek S, et al. “Genomic landscape of ERCC alterations in breast and gynecological cancers: implications for targeted therapy and VUS reclassification.” Mol Biol Rep. August 21, 2026. PMID 42627456. https://doi.org/10.1007/s11033-026-12640-x (subscription access)
99. He J, et al. “WNK4 restrains endometrial cancer progression by reprogramming macrophage polarization toward an M1-like phenotype.” Mol Biol Rep. August 21, 2026. PMID 42627588. https://doi.org/10.1007/s11033-026-12630-z (subscription access)
100. 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)
101. Korkmaz O, et al. “Stage-dependent expression and nuclear localization of EZH2 in endometrial carcinogenesis: evidence from cell lines and human tissues.” J Mol Histol. August 7, 2026. PMID 42565851. https://doi.org/10.1007/s10735-026-10930-z (subscription access)