{"paper_id":"53669bd2-cf9e-4946-ab67-7f9e7c978f76","body_text":"REVIEW \nHormone Replacement Therapy After Endometrial Cancer: Current \nEvidence and Treatment Recommendations \nUrsula Gobrecht-Keller1\n, Marcus Vetter2,3a \n1 Gynaecological Endocrinology and Reproductive Medicine, Gynaecology Clinic, University Hospital Basel, Basel, Switzerland, 2 Cancer Center Baselland, \nCantonal Hospital Baselland, Liestal, Switzerland, 3 Center of Oncology and Hematology, Cantonal Hospital Baselland, Liestal, Switzerland \nKeywords: endometrial cancer, hormone replacement therapy, menopause, estrogen \nhttps://doi.org/10.36000/HBT.OH.2026.27.203 \nhealthbook TIMES Oncology Hematology \nVol. 27, Issue 1, 2026 \nEndometrial cancer is the most prevalent gynecologic malignancy in developed \ncountries, with an increasing incidence driven primarily by rising obesity and \naging populations. While survival rates are high, particularly for early-stage, low-\ngrade disease, many endometrial cancer survivors experience significant \nmenopausal symptoms due to the definitive surgical treatments. Hormone \nreplacement therapy (HRT) remains the most effective treatment for vasomotor \nand genitourinary symptoms of menopause; however, its use in women with \nendometrial cancer has been met with caution. This review synthesizes the \ncurrent evidence, evaluates risk stratification models and offers a practical, \npatient-centered approach to the use of HRT in endometrial cancer survivors. \nPEER REVIEWED ARTICLE \nPeer reviewers:   \nProf. Andreas Günthert, Gynecological Tumor Center St. Anna, Lucerne, \nSwitzerland \nDr Eleftherios Pierre Samartzis, Gynecological Tumor Center, University \nHospital Zurich, Zurich, Switzerland \nReceived on December 15, 2025; accepted after peer review on February 23, \n2026; published online on February 25, 2026. \nIntroduction  \nEndometrial cancer is the sixth most common cancer among women globally \nand the most frequently diagnosed gynecological malignancy in high-income \ncountries.1 In 2022, an estimated 420,000 new cases were reported \nworldwide, along with approximately 97,000 deaths. The global incidence \nof endometrial cancer is steadily rising, largely driven by the increasing \nCorresponding author: Corresponding author: \nProf. Dr Marcus Vetter \nCancer Center Baselland \nMedical University Clinic \nCantonal Hospital Baselland \nRheinstrasse 26 \n4410 Liestal \nSwitzerland \nEmail: marcus.vetter@ksbl.ch \na \nGobrecht-Keller U, Vetter M. Hormone Replacement Therapy After Endometrial Cancer:\nCurrent Evidence and Treatment Recommendations. healthbook TIMES Onco Hema.\n2026;27(1):32-37. doi:10.36000/HBT.OH.2026.27.203\n\nprevalence of obesity and the aging population.2,3 While Type I \nendometrioid carcinomas that are estrogen- and adiposity-associated remain \nthe largest contributor to overall disease incidence, multiple population-based \nregistries have reported steep relative increases in Type II high-risk, relatively \nhormone-independent non-endometrioid histologies in the United States and \nin parts of Europe.4‑6 Endometrial cancer typically affects postmenopausal \nwomen, with a median age at diagnosis of 65 years.7 In most cases, abnormal \nvaginal bleeding facilitates early detection, enabling diagnosis before the \ndisease extends beyond the uterus in approximately 75% of patients.8,9 The \nprognosis is generally favorable, with an overall 5-year survival rate of 86%, \nwhich increases to 97% when the disease is confined to the uterus. In \nSwitzerland, the 5-year relative survival rate reported between 2000 and \n2009 was 75.2%.10 The standard treatment for early-stage endometrial cancer \nis total hysterectomy with bilateral salpingo-oophorectomy (BSO), typically \nperformed via a minimally invasive laparoscopic approach, resulting in \nsurgical menopause in premenopausal women who represent roughly 25% of \ncases.2,9 In addition to hysterectomy and BSO, current guidelines from the \nEuropean Society of Gynaecological Oncology (ESGO)/European Society \nfor Radiotherapy and Oncology (ESTRO)/European Society of Pathology \n(ESP),2 as well as the National Comprehensive Cancer Network (NCCN),11 \nrecommend sentinel lymph node mapping as part of standard surgical staging \nin early-stage endometrial cancer. \nMenopausal symptoms, such as hot flashes, night sweats, sleep disturbances, \nmood changes, vaginal atrophy and sexual dysfunction, can significantly \nimpact quality of life (QoL). In women who have undergone treatment \nfor endometrial cancer, these symptoms may be more severe than those \nexperienced during natural menopause.12 Hormone replacement therapy \n(HRT), using either estrogen alone or in combination with progestin, \nremains the most effective treatment for alleviating menopausal symptoms. \nHowever, concerns regarding the potential risk of cancer recurrence have \nlimited its use among endometrial cancer survivors. This review article \nsummarizes the current evidence on the oncologic safety of HRT in this \npopulation and provides recommendations regarding its appropriate use in \npatients with endometrial cancer. \nEndometrial cancer: Background and classification      \nTraditionally, endometrial cancer has been classified into two broad types \nbased on histopathological features and hormonal responsiveness.9,13 Type \nI cancers are predominantly endometrioid adenocarcinomas, which are \nestrogen-dependent, generally low-grade and most often diagnosed at an early \nstage. These tumors typically arise in the setting of unopposed estrogen \nexposure, often related to obesity, metabolic syndrome or chronic \nanovulation, and are associated with a favorable prognosis. In contrast, Type \nII cancers, which include serous carcinoma, clear cell carcinoma and \nHormone Replacement Therapy After Endometrial Cancer: Current Evidence and Treatment Recommendations\nhealthbook TIMES Oncology Hematology 33\n\ncarcinosarcoma, are not clearly hormone-driven, exhibit high-grade histologic \nfeatures and tend to behave more aggressively with a higher risk of recurrence \nand metastasis. They are also more likely to be diagnosed at an advanced \nstage and are associated with significantly worse outcomes. While stage IA \nendometrioid tumors are associated with 5-year survival rates of >90%, \npatients with high-risk histologic subtypes often have survival rates below \n50%.2,7 Reflecting the advances in understanding tumor biology, the \nInternational Federation of Gynecology and Obstetrics (FIGO) recently \nupdated its staging criteria to incorporate both histologic and molecular \nfeatures.13 The updated ESGO/ESTRO/ESP clinical guidelines2 incorporate \nthe new approach through an integrated classification model that combines \nhistotype, tumor grade, invasion pattern, lymphovascular space invasion and \nkey molecular alterations, enabling individualized treatment planning and \nimproved prognostication. \nRisks of HRT in endometrial cancer: The Women’s Health          \nInitiative trial   \nThe use of HRT in endometrial cancer survivors has long been a subject of \ndebate due to concerns regarding the potential for hormone-driven tumor \nrecurrence. Traditionally, HRT was avoided following endometrial cancer \ntreatment, largely due to evidence from the general population showing that \nboth tamoxifen and unopposed estrogen are associated with an increased \nrisk of endometrial hyperplasia and carcinoma14‑17 due to stimulation of \nthe mitotic activity of the endometrium, which potentially increases its \nsusceptibility to malignant transformation.18,19 These findings led to the \nassumption that any estrogen exposure in women previously treated for \nendometrial cancer could stimulate residual malignant cells and increase the \nrisk of recurrence, even though adding progestin can mitigate this effect. \nThe Women’s Health Initiative (WHI) trial evaluated the safety of HRT in \npostmenopausal women with an intact uterus.20 A total of 16,608 patients \nreceived conjugated equine estrogens (0.625 mg/day) plus \nmedroxyprogesterone acetate (2.5 mg/day) (n=8,506) or placebo (n=8,102). \nThe primary endpoint was coronary heart disease (CHD), including nonfatal \nmyocardial infarction and CHD death, with invasive breast cancer as the \nprimary adverse outcome. The study demonstrated an increased incidence of \nCHD (HR: 1.29 [95% CI: 1.02–1.63]) and breast cancer (HR: 1.26 [95% CI: \n1.00–1.59]) versus placebo at an average follow-up of 5.2 years. The estrogen \nplus progestin arm of the WHI study was prematurely closed because the \noverall risks exceeded the benefits. Notably, these risks were not observed in \nthe latter-reported estrogen-alone component of the study in postmenopausal \nwomen with prior hysterectomy (n=10,739) (CHD, HR: 0.91 [95% CI: \n0.75–1.12]; breast cancer, HR: 0.77 [95% CI: 0.59–1.01]), albeit a higher \nrisk of stroke (HR: 1.39 [95% CI: 1.10–1.77]) was noted.21 The results also \nsuggested that estrogen alone had advantages over estrogen plus progestin. \nImportantly, there were fewer endometrial cancers in the combined HRT arm \nHormone Replacement Therapy After Endometrial Cancer: Current Evidence and Treatment Recommendations\nhealthbook TIMES Oncology Hematology 34\n\ncompared with the placebo arm (yearly incidence, 0.06% vs 0.10%; HR: 0.65 \n[95% CI: 0.48–0.89]; p=0.007) and statistically nonsignificant reduction in \ndeaths from endometrial cancer in the HRT arm (5 vs 11 deaths, HR: 0.42 \n[95% CI: 0.15–1.22]) after a median cumulative follow-up of 13 years.22 \nLong-term follow-up data of the trial (mean, 10.7 years) in women receiving \nunopposed estrogen (median use, 5.9 years) indicated no differences in the \npostintervention risk of stroke (0.36% vs 0.41% with placebo, HR: 0.89 [95% \nCI: 0.64–1.24]), while the breast cancer reduction persisted overall (HR: 0.77 \n[95% CI: 0.62–0.95]) and total cancer incidence post-intervention did not \ndiffer significantly (HR: 0.93 [95% CI: 0.77–1.13]).23 Nevertheless, HRT in \nendometrial cancer survivors was historically restricted to patients with severe \nvasomotor symptoms or urogenital atrophy due to concerns of occult disease. \nRecent evidence of HRT safety in endometrial cancer survivors          \nMore recent evidence challenged the concept of avoiding HRT following \nendometrial cancer treatment, indicating no increased risk of cancer \nrecurrence, particularly in women with low-risk disease who have undergone \ncomplete surgical treatment. The data from key studies investigating the \nsafety of HRT in women with endometrial cancer are summarized below. \nThe randomized, double-blind GOG 137 trial performed by the Gynecologic \nOncology Group evaluated the effect of estrogen replacement therapy versus \nplacebo on recurrence rate and survival in women who have undergone \nhysterectomy for stage I–IIB endometrial carcinoma.24 Enrollment dropped \nsharply following the publication of the initial WHI results, although patients \nwere receiving estrogen alone and not estrogen plus progesterone. Ultimately, \nthe trial was stopped prematurely with 1,236 eligible patients enrolled, as it \nbecame evident that reaching the planned accrual target of 2,108 patients was \nno longer feasible. \nAt a median follow-up of 35.7 months, recurrence rates in the overall \npopulation were low and 3-year progression-free survival (PFS) rate was \n94.3% in the HRT group and 95.6% in the placebo group.24 The trial showed \nno significant difference in recurrence risk between the HRT and placebo \narms (relative risk [RR]: 1.27 [80% CI: 0.916–1.77]). Although the study did \nnot enroll a sufficient number of high-risk patients and could not conclusively \nconfirm or refute the safety of HRT in terms of recurrence risk, it did \ndemonstrate a low incidence of recurrence and new malignancies, thereby \ncontributing to the evidence base for evaluating the overall risk–benefit \nprofile of HRT in patients with low-risk endometrial cancer. Of note, a \nretrospective analysis of the trial data showed a racial disparity in the HRT \narm, with increased risk of recurrence among Black versus White patients \nwho continued to receive HRT following primary treatment (RR: 11.2 [95% \nCI: 2.86–43.59]; p=0.0005).25 \nHormone Replacement Therapy After Endometrial Cancer: Current Evidence and Treatment Recommendations\nhealthbook TIMES Oncology Hematology 35\n\nA prospective case-control study by Ayhan et al. evaluating the safety of \nimmediate postoperative HRT in endometrial cancer survivors included 50 \nwomen with stage I or II endometrioid-type endometrial cancer who received \nHRT initiated 4–8 weeks after surgery and 52 matched controls who did \nnot receive HRT.26 The average duration of HRT was 49.1 months and \nmost patients continued therapy for ≥24 months. The study demonstrated \nno recurrences in the HRT group during follow-up. In the control group, \none pelvic recurrence occurred at 12 months, resulting in death despite \nchemotherapy, and one death due to intercurrent disease at 21 months \npost surgery. Adverse effects of HRT were minimal, with seven patients \ndiscontinued the treatment, among them only two within the first 24 \nmonths. While the study was non-randomized and had a limited sample size, \nthe data demonstrated that immediate postoperative use of continuous HRT \ndid not increase the risk of recurrence or death in women with early-stage, \nlow-risk endometrial cancer. \nSeveral systematic reviews aimed to evaluate the safety and effectiveness of \nHRT in women treated for endometrial cancer. Edey et al.27 identified \nGOG 13724 as the only randomized controlled trial that met the inclusion \ncriteria for assessing HRT in this patient population, based on searches of \nthe Cochrane Register of Controlled Trials, MEDLINE and Embase. Di \nDonato et al. screened 1,332 abstracts and included seven eligible studies \nin the analysis, among them four retrospective series, one prospective study, \none randomized controlled trial and one population-based study.28 Overall, \nacross predominantly stage I–II cohorts, HRT use was not associated with \na statistically significant increase in recurrence compared with controls. An \nimportant limitation was selection bias, as HRT was preferentially prescribed \nto younger women with low-risk, early-stage disease. A more recent meta-\nanalysis included both randomized and observational studies, comprising 10 \npapers published between 1986 and 2021.29 Of these, two reported data \nfrom randomized clinical trials, five were non-randomized cohort studies and \nthree were case-control studies.24‑26,30‑34 The total sample included 7,944 \npatients, including 1,801 treated with HRT and 6,015 controls. Based on \nfour studies that allowed time-dependent analysis, the study indicated no \nsignificant difference in disease-free survival between women treated with \nHRT and those not treated (pooled HR: 0.90 (95% CI: 0.28–2.87). However, \nsignificantly increased risk of recurrence was reported among Black American \nwomen treated with continuous estrogen (HR: 7.58 (95% CI: 1.96–29.31),29 \nconfirming the findings of the GOG 137 trial.25 A pooled odds ratio (OR) of \n0.63 (95% CI: 0.48–0.83) across all included studies indicated a significantly \nreduced risk of recurrence among endometrial cancer survivors treated with \nHRT. Combined estrogen and progestin therapy, particularly when \nadministered in cyclic regimens, appeared to be the most favorable for \nreducing the recurrence risk. The results of this study are summarized in \nFigure 1 . \nHormone Replacement Therapy After Endometrial Cancer: Current Evidence and Treatment Recommendations\nhealthbook TIMES Oncology Hematology 36\n\nFigure 1. Forest plot of hazard ratio (HR) meta-analysis (A) and odds ratio (OR) (B) meta-analysis for disease-free \nsurvival/recurrence risk showing a pooled random effect model and subgroup analysis by ethnicity in endometrial \ncancer patients with or without hormone replacement therapy (HRT). \nAdapted from Londero et al. 2021.29 \nReuse of the image is permitted under the terms of the Creative Commons Attribution (CC BY) 4.0 International License. Copyright \n© Authors or their employers. Published in J Clin Med. \nTaken together, the existing evidence suggests that HRT appears safe in \nwomen with low-grade, early-stage endometrial cancer after hysterectomy. \nHowever, since most available data are derived from surgically treated stage \nI cohorts with limited use of adjuvant radiotherapy or systemic therapy, the \noncologic safety of HRT in women receiving adjuvant treatment remains \ninsufficiently studied, warranting a cautious approach. Therapy initiation \nshould be tailored to the patient’s needs and undertaken following careful \ndiscussion with the patient regarding its risks and benefits. As molecular \nclassification is increasingly incorporated into prognostic risk stratification \nand treatment planning, it may further refine individualized counselling \nregarding the use of HRT after endometrial cancer. While clinical evidence \nremains limited, this approach may become relevant for polymerase epsilon \n(POLE)-mutated, mismatch repair (MMR)-deficient, no specific molecular \nprofile (NSMP) and p53-abnormal tumors. Specifically, the excellent \nprognosis of POLE-mutated tumors could support a more permissive \napproach, whereas p53-abnormal or serous-like disease may justify greater \ncaution with systemic HRT. \nBeyond HRT safety, the potential protective role of progestins after \nhysterectomy remains a relevant clinical question. In healthy postmenopausal \nwomen, continuous combined estrogen–progestin therapy has been \nassociated with a reduced risk of developing endometrial cancer, supporting \nHormone Replacement Therapy After Endometrial Cancer: Current Evidence and Treatment Recommendations\nhealthbook TIMES Oncology Hematology 37\n\na biologically plausible antiproliferative effect of progestins on residual \nendometrial tissue.35 Consistent with this rationale, a systematic review by \nShim et al. reported an inverse association between recurrence risk and \nthe use of combined estrogen–progestin therapy compared with estrogen \nmonotherapy in endometrial cancer survivors, suggesting a possible protective \neffect.36 Moreover, in selected young women with atypical hyperplasia or \nwell-differentiated endometrioid endometrial cancer who desire fertility \npreservation, high-dose oral progestins or levonorgestrel-releasing intrauterine \ndevices are established therapeutic options until endometrial normalization \nis achieved, further underscoring the antitumor activity of progestins in \nhormonally driven disease.2 \nHowever, these potential benefits must be balanced against important safety \nconsiderations. Progestin-containing regimens are associated with an \nincreased risk of breast cancer compared with estrogen-only therapy, and \nmay exert unfavorable metabolic and cardiovascular effects.37,38 This is \nparticularly relevant in women with hypertension, diabetes mellitus, \nmetabolic syndrome, polycystic ovary syndrome or obesity, which are highly \nprevalent among patients with endometrial cancer, thereby limiting the \nroutine use of progestins after hysterectomy and reinforcing the need for \nindividualized risk–benefit assessment. \nRecommendations for the use of HRT in women with          \nendometrial cancer   \nChoice of HRT regimen     \nThe choice of HRT in endometrial cancer survivors depends on surgical \nhistory, symptom profile, comorbidities and oncologic risk. Swiss clinical \npractice is aligned with the ESGO-ESTRO-ESP guidelines for the \nmanagement of endometrial carcinoma,2 while substance- and route-specific \nrecommendations for menopausal HRT follow the European Menopause \nand Andropause Society (EMAS) guidelines.39 In addition to treating \nmenopausal symptoms, the decision for or against HRT should include a \ndiscussion of other long-term benefits of HRT with the patient. In women \nunder 60 years of age using HRT, the absolute risks for overall mortality, \nfractures, diabetes mellitus (estrogen-progesterone therapy and estrogen-only \ntherapy) and breast cancer (estrogen therapy) are reduced. This is especially \nimportant in women with endometrial cancer who often have a higher risk \nof these diseases due to obesity and already existing unfavorable metabolic \nprofile. \nIn patients who have undergone total hysterectomy for low-grade early-\nstage endometrial cancer and whose menopausal symptoms significantly \ncompromise their QoL, estrogen-only replacement therapy at the lowest \neffective dose could be considered.11,12,40,41 Common formulations based on \nearly studies include oral 17β-estradiol (E2) starting at a dose of 1 mg/day \nHormone Replacement Therapy After Endometrial Cancer: Current Evidence and Treatment Recommendations\nhealthbook TIMES Oncology Hematology 38\n\nor conjugated equine estrogen (CEE) at 0.625 mg/day (not available/used \nin Switzerland).42‑44 Alternatively, transdermal estradiol patches delivering \n25 (low dose) to 100 µg/day (high dose), estradiol gel or spray are also \nwidely used. Transdermal administration is often favored in women with \ncardiovascular risk factors because it is associated with a lower risk of venous \nthromboembolism, stroke and cardiovascular events due to avoiding first-pass \nhepatic metabolism, which results in fewer adverse effects on coagulation and \ninflammatory markers.40,43,45 \nFor patients experiencing isolated genitourinary syndrome of menopause \n(GSM) with persistent symptoms, low-dose local estrogen therapy delivered \nvia cream, pessary or intravaginal ring may be considered due to its minimal \nsystemic absorption and endometrial safety profile.46‑49 This approach is \nsupported by both the EMAS and Swiss expert recommendations and is \nappropriate when vasomotor symptoms are absent and GSM remains the \npredominant clinical concern. \nTiming of HRT administration     \nThe initiation of systemic HRT is generally delayed until 6–12 months after \nthe completion of cancer treatment, allowing for confirmation of disease \nremission.11 This cautious approach aligns with clinical consensus to reduce \nthe risk of stimulating residual or occult disease. Therapy should be initiated \nat the lowest effective dose and reassessed annually. Monitoring includes \nregular clinical evaluation and adjustment of therapy based on symptom \ncontrol and emerging health risks. \nWho should avoid HRT?     \nHRT is contraindicated in patients with active or recurrent disease and \nin those with high-risk histologic subtypes such as serous, clear cell or \ncarcinosarcoma or with advanced-stage disease (FIGO stage III or IV).11,\n12,40 While data are lacking for these populations, there is a theoretical \nconcern regarding the potential for hormone-driven recurrence. In addition, \ncontraindications unrelated to cancer, including a personal history of \nthromboembolism, active liver disease or estrogen-sensitive comorbidities, \nshould be carefully considered in line with general menopause management \nguidelines. \nAlternative non-hormonal options    \nFor women who are ineligible for or who decline HRT, non-hormonal \ntherapies should be considered.12,40 Vasomotor symptoms can be managed \nwith selective serotonin or norepinephrine reuptake inhibitors, such as \nescitalopram or venlafaxine, or with alternatives, such as gabapentin and \noxybutynin. Genitourinary symptoms may respond to non-hormonal vaginal \nmoisturizers and lubricants or newer interventions, such as vaginal laser \ntherapy, although the latter requires further validation. \nHormone Replacement Therapy After Endometrial Cancer: Current Evidence and Treatment Recommendations\nhealthbook TIMES Oncology Hematology 39\n\nIn addition to established non-hormonal therapies, novel agents targeting \nneurokinin-3 (NK3) and neurokonin-1 (NK1) receptors have recently \nemerged as effective options for vasomotor symptom control. NK3 receptor \nantagonists, such as fezolinetant, and NK1/NK3 receptor antagonists, such \nas elinzanetant, reduce hot flashes by modulating hypothalamic \nthermoregulatory pathways without direct estrogenic or progestogenic \nactivity.50 Fezolinetant has demonstrated significant efficacy in reducing the \nfrequency and severity of vasomotor symptoms and is approved in several \nEuropean countries, including Switzerland.51‑53 These agents represent a \nparticularly attractive option for endometrial cancer survivors in whom \nsystemic HRT is contraindicated or declined, although long-term safety data \nin oncology populations remain limited. \nSpecial considerations   \nIn women with Lynch syndrome (hereditary non-polyposis colorectal cancer) \nundergoing risk-reducing hysterectomy with BSO at a young age (35–45 \nyears), the management of premature menopause is a common indication \nfor HRT. In this setting, systemic estrogen-only therapy can be offered after \npremenopausal BSO.2,54 \nPatient counseling and long-term follow-up      \nEffective counseling is essential given the limited data from large randomized \ncontrolled trials in this population. Clinicians should provide a balanced \ndiscussion of the known benefits and theoretical risks of HRT,9 tailoring \nrecommendations based on cancer characteristics, symptom severity, patient \npreference and overall comorbidity profile. Long-term follow-up with a \ngynecologic oncologist is recommended and should include regular physical \nexaminations, imaging as clinically indicated and ongoing evaluation of \nsymptom control and treatment tolerability. \nConclusions  \nHormone replacement therapy can be safely offered to carefully selected \nsurvivors of early-stage, low-risk endometrial cancer who suffer from \nsignificant menopausal symptoms. Current evidence, primarily from \nobservational studies, supports the oncologic safety of estrogen-only regimens \nin this population. For women with advanced-stage or high-risk histologic \nsubtypes, the absence of robust data continues to warrant a cautious \napproach. In all cases, treatment decisions should be guided by individualized \nrisk assessment, symptom burden and patient preference, supported by \nongoing follow-up within a multidisciplinary framework. Molecular risk \nstratification is likely to become increasingly relevant for individualized \ncounseling and recommendations regarding HRT after endometrial cancer. \nFigure 2  summarizes the current state of evidence and outlines a practical \napproach to HRT use in endometrial cancer survivors. \nHormone Replacement Therapy After Endometrial Cancer: Current Evidence and Treatment Recommendations\nhealthbook TIMES Oncology Hematology 40\n\nFigure 2. Hormone replacement therapy (HRT) in endometrial cancer (EC) survivors. \nESGO, European Society of Gynaecological Oncology; ESP, European Society of Pathology; ESTRO, European Society for \nRadiotherapy and Oncology. \nConflict of interest    \nMarcus Vetter received honoraria for consultancy from GSK, Roche, \nNovartis, ExactSciences, Pfizer, Stemline, AbbVie and ASC Oncology. Ursula \nGobrecht-Keller received honoraria for consultancy from Astellas, Bayer and \nGedeon Richter. These funding entities did not play a role in the \ndevelopment of the manuscript and did not influence its content in any way. \nFunding  \nThe authors declared that no financial support was received from any \norganization for the submitted work. \nAuthor contributions   \nBoth authors contributed to and approved the final manuscript. \nSubmitted: December 15, 2025 CEST. Accepted: February 23, 2026 CEST. Published: February 25, 2026 CEST. \nThis is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 \nInternational License (CCBY-NC-SA-4.0). View this license's legal deed at https://creativecommons.org/\nlicenses/by-nc-sa/4.0 and legal code at https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode for \nmore information. \nHormone Replacement Therapy After Endometrial Cancer: Current Evidence and Treatment Recommendations\nhealthbook TIMES Oncology Hematology 41\n\nreferences \n1. Bray F, Laversanne M, Sung H, et al. Global cancer statistics 2022: GLOBOCAN estimates of \nincidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. \n2024;74(3):229-263. doi:10.3322/caac.21834 \n2. Concin N, Matias-Guiu X, Cibula D, et al. ESGO-ESTRO-ESP guidelines for the \nmanagement of patients with endometrial carcinoma: update 2025. Lancet Oncol. \n2025;26(8):e423-e435. doi:10.1016/s1470-2045(25)00167-6 \n3. 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Updates in gynecologic care for individuals with lynch syndrome. \nFront Oncol. 2023;13:1127683. doi:10.3389/fonc.2023.1127683 \nHormone Replacement Therapy After Endometrial Cancer: Current Evidence and Treatment Recommendations\nhealthbook TIMES Oncology Hematology 45","source_license":"CC0","license_restricted":false}