Gynecologic oncology最新文献

{"title":"Insurance coverage and access to gynecologic oncology: Where are we now","authors":"Lakeisha Mulugeta-Gordon ,&nbsp;Anna Jo Bodurtha Smith","doi":"10.1016/j.ygyno.2024.11.001","DOIUrl":"10.1016/j.ygyno.2024.11.001","url":null,"abstract":"<div><div>In the United Sates, over 115,000 individuals are diagnosed with a gynecologic cancer annually with access to a gynecologic oncologist and evidence-based treatment remaining a persistent challenge. Coverage decisions by private and public insurance, including Medicaid and Medicare, play key roles in access to care, impacting oncologic outcomes. The expansion of Medicaid insurance under the Affordable Care Act improved early diagnosis, treatment, and survival in gynecologic cancers, but disparities remain for individuals in non-Medicaid expansion states. For individuals with Medicare or private insurance, coverage gaps and high out-of-pocket costs are barriers to cancer care, particularly for novel therapeutic treatments. Efforts to streamline care access, expand clinical trial participation, and reduce administrative burdens continue. Addressing these disparities require improving insurance literacy in patients and clinicians, coordination, and community partnerships to support equitable and comprehensive gynecologic cancer care.</div></div>","PeriodicalId":12853,"journal":{"name":"Gynecologic oncology","volume":"192 ","pages":"Pages 56-58"},"PeriodicalIF":4.5,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142618761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adverse events in the placebo arm of SOLO2/ENGOT-Ov21 maintenance trial of olaparib in recurrent ovarian cancer","authors":"Katherine Elizabeth Francis ,&nbsp;Sandy Simon ,&nbsp;Val Gebski ,&nbsp;Florence Joly ,&nbsp;Jonathan A. Ledermann ,&nbsp;Richard T. Penson ,&nbsp;Amit M. Oza ,&nbsp;Jacob Korach ,&nbsp;Nuria Lainez ,&nbsp;Sabrina Chiara Cecere ,&nbsp;Giulia Tasca ,&nbsp;Martina Gropp-Meier ,&nbsp;Keiichi Fujiwara ,&nbsp;Elizabeth S. Lowe ,&nbsp;Michael Friedlander ,&nbsp;Eric Pujade-Lauraine ,&nbsp;Chee Khoon Lee","doi":"10.1016/j.ygyno.2024.11.004","DOIUrl":"10.1016/j.ygyno.2024.11.004","url":null,"abstract":"<div><h3>Background</h3><div>In women with platinum sensitive recurrent ovarian cancer (PSROC) undergoing maintenance treatment, adverse events (AEs) not attributable to the current treatment are not well understood. We used data from SOLO2/ENGOT-Ov21 to evaluate AEs reported in the placebo arm and to explore their longitudinal trajectories.</div></div><div><h3>Methods</h3><div>SOLO2/ENGOT-Ov21 (<span><span>NCT01874353</span><svg><path></path></svg></span>) randomly assigned 295 PSROC participants with a <em>BRCA1/2</em> mutation to maintenance olaparib tablets (<em>N</em> = 196) or matching placebo (<em>N</em> = 99). For those assigned to placebo, we analyzed the AE (CTCAE v4.0) data including type, grade, time of onset and resolution, and attribution by investigator.</div></div><div><h3>Results</h3><div>Amongst 99 participants who received placebo 788 AEs were reported (95 % reporting ≥1 AE). Twenty-two percent of participants reported at least one grade ≥ 3 AE. Grade ≥ 2 AEs that persisted for over 100 days affected 21 % of participants. Recurring grade ≥ 1 AEs were experienced by 44 % of participants. Study investigators attributed 25 % of all AEs to the placebo treatment, with neutropenia (88 %), nausea (52 %) and thrombocytopenia (50 %) most attributed. Three percent of participants had a dose reduction, 19 % had treatment delays, and 2 % had permanent treatment discontinuation, due to AEs attributed to placebo.</div></div><div><h3>Conclusion</h3><div>Virtually all PSROC participants in the SOLO2/ENGOT-Ov21 experienced one or more AE whilst on placebo. Furthermore, study investigators attributed one quarter of AEs to be related to placebo therapy and dose alterations and treatment changes were made based on these AE. Further work is needed to improve measurement and categorization of AEs in trials of maintenance therapy in PSROC.</div></div>","PeriodicalId":12853,"journal":{"name":"Gynecologic oncology","volume":"192 ","pages":"Pages 50-55"},"PeriodicalIF":4.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142618757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and safety of dostarlimab in combination with chemotherapy in patients with dMMR/MSI-H primary advanced or recurrent endometrial cancer in a phase 3, randomized, placebo-controlled trial (ENGOT-EN6-NSGO/GOG-3031/RUBY)","authors":"Matthew A. Powell ,&nbsp;David Cibula ,&nbsp;David M. O'Malley ,&nbsp;Ingrid Boere ,&nbsp;Mark S. Shahin ,&nbsp;Antonella Savarese ,&nbsp;Dana M. Chase ,&nbsp;Lucy Gilbert ,&nbsp;Destin Black ,&nbsp;Jørn Herrstedt ,&nbsp;Sudarshan Sharma ,&nbsp;Stefan Kommoss ,&nbsp;Michael A. Gold ,&nbsp;Anna M. Thijs ,&nbsp;Kari Ring ,&nbsp;Magnus Frödin Bolling ,&nbsp;Joseph Buscema ,&nbsp;Sarah E. Gill ,&nbsp;Paul Nowicki ,&nbsp;Nicole Nevadunsky ,&nbsp;Mansoor Raza Mirza","doi":"10.1016/j.ygyno.2024.10.022","DOIUrl":"10.1016/j.ygyno.2024.10.022","url":null,"abstract":"<div><h3>Objectives</h3><div>Part 1 of the RUBY trial (NCT03981796) demonstrated improved survival in patients with primary advanced or recurrent endometrial cancer (EC) treated with dostarlimab plus carboplatin-paclitaxel versus placebo plus carboplatin-paclitaxel. Here, we examine additional efficacy and safety data from patients with mismatch repair deficient/microsatellite instability-high (dMMR/MSI-H) EC in the RUBY trial.</div></div><div><h3>Methods</h3><div>Patients were randomized 1:1 to dostarlimab 500 mg or placebo plus carboplatin-paclitaxel every 3 weeks for 6 cycles followed by dostarlimab or placebo every 6 weeks for up to 3 years. In the dMMR/MSI-H population of RUBY Part 1, analysis of progression-free survival by investigator assessment compared with blinded independent central review, sensitivity analyses of the source-verified population compared with the randomized population, and analysis of safety in this population were completed.</div></div><div><h3>Results</h3><div>In total, 118 patients with dMMR/MSI-H were enrolled in the RUBY trial (53, dostarlimab arm; 65, placebo arm). At the first interim analysis, a 72% reduction in the risk of progression or death (<em>P</em> &lt; 0.0001) was seen with dostarlimab plus carboplatin-paclitaxel by investigator assessment per Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST v1.1), which was consistent with blinded independent central review per RECIST v1.1. Likewise, sensitivity analyses of the source-verified dMMR/MSI-H population compared with the randomized dMMR/MSI-H population were consistent for progression-free survival and overall survival. Safety results seen in the dMMR/MSI-H population were similar to those previously reported for the overall population.</div></div><div><h3>Conclusions</h3><div>All primary and secondary efficacy assessments demonstrate the consistent benefit of dostarlimab plus carboplatin-paclitaxel. The improvements seen in survival and the manageable safety profile support the favorable benefit–risk profile for dostarlimab plus carboplatin-paclitaxel in patients with dMMR/MSI-H primary advanced or recurrent EC.</div></div>","PeriodicalId":12853,"journal":{"name":"Gynecologic oncology","volume":"192 ","pages":"Pages 40-49"},"PeriodicalIF":4.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142618760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cost-effectiveness of dostarlimab plus carboplatin-paclitaxel for primary advanced or recurrent endometrial cancer from a US payer perspective","authors":"Robert L. Coleman ,&nbsp;Solomon J. Lubinga ,&nbsp;Qin Shen ,&nbsp;Lydia Walder ,&nbsp;Mark Burton ,&nbsp;Cara Mathews","doi":"10.1016/j.ygyno.2024.10.021","DOIUrl":"10.1016/j.ygyno.2024.10.021","url":null,"abstract":"<div><h3>Objective</h3><div>Dostarlimab in combination with carboplatin-paclitaxel (CP) improves progression-free survival in patients with primary advanced or recurrent endometrial cancer (pA/rEC), including in patients whose cancer is mismatch repair–deficient (dMMR) or microsatellite instability–high (MSI-H). This study examined the cost-effectiveness of dostarlimab plus CP as a first-line treatment in the dMMR/MSI-H and overall populations.</div></div><div><h3>Methods</h3><div>A partitioned survival model with three mutually exclusive health states (progression-free disease, progressed disease, death) was developed using a US base case and a third-party payer perspective. Clinical data were from the RUBY trial and published sources. Costs were from US databases. The primary outcomes were life-years (LYs), quality-adjusted life-years (QALYs), incremental costs, and incremental cost-effectiveness ratios (ICERs). One-way and probabilistic sensitivity analyses were also performed.</div></div><div><h3>Results</h3><div>In the dMMR/MSI-H population, the model predicted gains of 6.9 LYs and 5.4 QALYs with dostarlimab plus CP compared with CP; costs were $307,696 higher with dostarlimab plus CP, resulting in an ICER of $57,151 per QALY gained. In the overall population, gains of 2.0 LYs and 1.5 QALYs were predicted with dostarlimab plus CP compared with CP; costs were $215,876 higher, resulting in an ICER of $143,783 per QALY gained. ICERs were most sensitive to the overall survival hazard ratio. At a willingness-to-pay threshold of $150,000, dostarlimab plus CP had cost-effectiveness probabilities of 100 % and 53.7 % in the dMMR/MSI-H and overall populations, respectively.</div></div><div><h3>Conclusions</h3><div>Dostarlimab plus CP is cost-effective as a treatment for the dMMR/MSI-H and overall populations of US patients with pA/rEC.</div></div>","PeriodicalId":12853,"journal":{"name":"Gynecologic oncology","volume":"192 ","pages":"Pages 24-31"},"PeriodicalIF":4.5,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142618759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of the gut microbiome with outcomes in cervical and endometrial cancer patients treated with pembrolizumab: Insights from the phase II PRIMMO trial","authors":"Emiel A. De Jaeghere ,&nbsp;Hannelore Hamerlinck ,&nbsp;Sandra Tuyaerts ,&nbsp;Lien Lippens ,&nbsp;An M.T. Van Nuffel ,&nbsp;Regina Baiden-Amissah ,&nbsp;Peter Vuylsteke ,&nbsp;Stéphanie Henry ,&nbsp;Xuan Bich Trinh ,&nbsp;Peter A. van Dam ,&nbsp;Sandrine Aspeslagh ,&nbsp;Alex De Caluwé ,&nbsp;Eline Naert ,&nbsp;Diether Lambrechts ,&nbsp;An Hendrix ,&nbsp;Olivier De Wever ,&nbsp;Koen K. Van de Vijver ,&nbsp;Frédéric Amant ,&nbsp;Katrien Vandecasteele ,&nbsp;Bruno Verhasselt ,&nbsp;Hannelore G. Denys","doi":"10.1016/j.ygyno.2024.10.020","DOIUrl":"10.1016/j.ygyno.2024.10.020","url":null,"abstract":"<div><h3>Background</h3><div>The phase II PRIMMO trial investigated a pembrolizumab-based regimen in patients with recurrent and/or metastatic cervical (CC) or endometrial (EC) carcinoma who had at least one prior line of systemic therapy. Here, exploratory studies of the gut microbiome (GM) are presented.</div></div><div><h3>Methods</h3><div>The microbial composition of 77 longitudinal fecal samples obtained from 35 patients (CC, <em>n</em> = 15; EC, <em>n</em> = 20) was characterized using <em>16S rRNA</em> gene sequencing. Analyses included assessment of alpha (Shannon index) and beta diversity (weighted UniFrac), unbiased hierarchical clustering, and linear discriminant analysis effect size. Correlative studies with demographics, disease characteristics, safety, efficacy, and immune monitoring data were performed.</div></div><div><h3>Results</h3><div>Significant enrichment in multiple bacterial taxa was associated with the occurrence or resistance to severe treatment-related adverse events (overall or gastrointestinal toxicity specifically). Consistent differences in GM taxonomic composition before pembrolizumab initiation were observed between patients with favorable efficacy (e.g., enriched with <em>Blautia</em> genus) and those with poor efficacy (e.g., enriched with <em>Enterobacteriaceae</em> family and its higher-level taxa up to the phylum level, as well as <em>Clostridium</em> genus and its <em>Clostridiaceae</em> family). Two naturally occurring GM clusters with distinct bacterial compositions were identified. These clusters showed a more than four-fold differential risk for death (hazard ratio, 4.4 [95 % confidence interval, 1.9 to 10.3], <em>P</em> &lt; 0.001) and were associated with interesting (but non-significant) trends in peripheral immune monitoring data.</div></div><div><h3>Conclusion</h3><div>Although exploratory, this study offers initial insights into the intricate interplay between the GM and clinical outcomes in patients with CC and EC treated with a pembrolizumab-based regimen.</div><div>Trial registration: <span><span>ClinicalTrials.gov</span><svg><path></path></svg></span> (identifier <span><span>NCT03192059</span><svg><path></path></svg></span>) and EudraCT Registry (number 2016–001569-97).</div></div>","PeriodicalId":12853,"journal":{"name":"Gynecologic oncology","volume":"191 ","pages":"Pages 275-286"},"PeriodicalIF":4.5,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hormonal biomarkers remain prognostically relevant within the molecular subgroups in endometrial cancer","authors":"Stephanie W. Vrede ,&nbsp;Willem Jan Van Weelden ,&nbsp;Johan Bulten ,&nbsp;C. Blake Gilks ,&nbsp;Steven Teerenstra ,&nbsp;Jutta Huvila ,&nbsp;Xavier Matias-Guiu ,&nbsp;Antonio Gil-Moreno ,&nbsp;Jasmin Asberger ,&nbsp;Sanne Sweegers ,&nbsp;Louis J.M. van der Putten ,&nbsp;Heidi V.N. Küsters-Vandevelde ,&nbsp;Casper Reijnen ,&nbsp;Eva Colas ,&nbsp;Jitka Hausnerová ,&nbsp;Vit Weinberger ,&nbsp;Marc P.L.M. Snijders ,&nbsp;Petra Vinklerova ,&nbsp;Antonella Ravaggi ,&nbsp;Franco Odicino ,&nbsp;Johanna M.A. Pijnenborg","doi":"10.1016/j.ygyno.2024.10.028","DOIUrl":"10.1016/j.ygyno.2024.10.028","url":null,"abstract":"<div><h3>Objective</h3><div>The prognostic relevance of hormonal biomarkers in endometrial cancer (EC) has been well-established. A refined three-tiered risk model for estrogen receptor (ER)/progesterone receptor (PR) expression was shown to improve prognostication. This has not been evaluated in relation to the molecular subgroups. This study aimed to evaluate the ER/PR expression within the molecular subgroups in EC.</div></div><div><h3>Methods</h3><div>A retrospective multicenter cohort study was performed and data from the European Network for Individualized Treatment centers and Vancouver, Canada were used. ER/PR immunohistochemical expression was grouped as: ER/PR 0–10 %, 20–80 % or 90–100 %. Molecular subgroups were determined with full next-generation sequencing or combined with immunohistochemistry: <em>POLE</em>mut, mismatch repair deficient (MMRd), p53mut and no-specific molecular profile (NSMP).</div></div><div><h3>Results</h3><div>A total of 739 patients were included (median follow-up 5.0 years). Tumors were classified as <em>POLE</em>mut in 9.1 %(<em>N</em> = 67), MMRd in 27.6 %(<em>N</em> = 204), p53mut in 20.8 %(<em>N</em> = 154) and NSMP in 42.5 %(<em>N</em> = 314). Among all molecular subgroups, patients with ER/PR 90–100 % expression revealed the best disease-specific survival (DSS). Within p53mut, PR 90–100 % expression showed a 5-year DSS of 100.0 %. ER expression is prognostic more relevant in MMRd and NSMP tumors while PR expression in p53mut and NSMP tumors. Across all molecular subgroups, PR 0–10 %, p53mut, lympho-vascular space invasion and FIGO stage III-IV remained independently prognostic for reduced DSS Whereas PR 90–100 % and <em>POLE</em>mut remained independently prognostic for improved DSS.</div></div><div><h3>Conclusion</h3><div>We demonstrated that ER/PR expression remain prognostically relevant within the molecular subgroups, and that a three-tiered cutoff refines prognostication. These data support incorporating routine evaluation of ER/PR expression in clinical practice.</div></div>","PeriodicalId":12853,"journal":{"name":"Gynecologic oncology","volume":"192 ","pages":"Pages 15-23"},"PeriodicalIF":4.5,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evolutionary pathways in early-stage, non-myoinvasive endometrioid endometrial cancers of no specific molecular profile","authors":"Sara Moufarrij ,&nbsp;Yulia Lakhman ,&nbsp;Carol Aghajanian ,&nbsp;Nadeem R. Abu-Rustum ,&nbsp;Lora H. Ellenson ,&nbsp;Britta Weigelt ,&nbsp;Amir Momeni-Boroujeni","doi":"10.1016/j.ygyno.2024.10.029","DOIUrl":"10.1016/j.ygyno.2024.10.029","url":null,"abstract":"<div><h3>Objective</h3><div>To characterize the genomic landscape of FIGO 2009 stage IA, non-myometrial invasive endometrioid endometrial cancers (ECs) of no specific molecular profile (NSMP) and define the earliest driver genetic alterations and subsequent tumor evolution.</div></div><div><h3>Methods</h3><div>Early-stage (FIGO 2009 stage IA), non-myoinvasive endometrioid NSMP ECs subjected to clinical tumor-normal targeted sequencing between 2014 and 2022 were identified. ECs were dichotomized into low- and high-volume disease based on gross and histologic measurement using a cutoff of 1.8 cm³. Cancer cell fractions (CCF) of somatic mutations were determined.</div></div><div><h3>Results</h3><div>A total of 171 noninvasive, FIGO 2009 stage I endometrioid ECs of NSMP subtype were identified, of which the majority (<em>n</em> = 139; 81 %) were FIGO grade 1. The median calculated volume of disease was 1.8 cm³ at diagnosis. The ECs had on average 6 pathogenic mutations, affecting known EC cancer-related genes, including <em>PTEN</em> (80 %), <em>ARID1A</em> (52 %), <em>PIK3CA</em> (52 %), <em>CTNNB1</em> (39 %), <em>PIK3R1</em> (37 %), and <em>KRAS</em> (29 %). Genomic alterations did not correlate with tumor volume. <em>PTEN</em> mutations had the highest CCFs. Unsupervised hierarchical clustering based on CCF revealed 4 main groups characterized by: 1. clonal alterations in <em>PTEN</em> accompanied by <em>PIK3CA, PIK3R1,</em> or <em>ARID1A</em> alterations, 2. mutations in <em>PIK3CA</em> co-occurring with <em>ARID1A</em> alterations, 3. <em>KRAS</em> mutations, particularly associated with 1q high-level gain, or 4. <em>AKT1</em> mutations, which uniquely occurred without concurrent <em>PTEN</em>, <em>PIK3CA</em>, or <em>PIK3R1</em> alterations.</div></div><div><h3>Conclusion</h3><div>Stage IA non-myoinvasive NSMP ECs show genomic heterogeneity suggestive of multiple evolutionary pathways. Further studies are warranted to define whether this is a sign of early genomic drift.</div></div>","PeriodicalId":12853,"journal":{"name":"Gynecologic oncology","volume":"192 ","pages":"Pages 8-14"},"PeriodicalIF":4.5,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142593098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What happens after menopause? (WHAM): Impact of risk-reducing salpingo-oophorectomy on depressive and anxiety symptoms at 24 months","authors":"Martha Hickey ,&nbsp;Tuong L. Nguyen ,&nbsp;Efrosinia O. Krejany ,&nbsp;Susan M. Domchek ,&nbsp;Alison Brand ,&nbsp;John L. Hopper ,&nbsp;Hadine Joffe","doi":"10.1016/j.ygyno.2024.10.031","DOIUrl":"10.1016/j.ygyno.2024.10.031","url":null,"abstract":"<div><h3>Objective</h3><div>For women with pathogenic variants in <em>BRCA1</em> and <em>BRCA2,</em> risk-reducing salpingo-oophorectomy (RRSO) at the recommended age causes surgical menopause. We previously reported elevated depressive symptoms at 6 and 12 months and elevated anxiety symptoms at 6 months after RRSO. We now report these outcomes at 24 months, their baseline and 12-month predictors and the effect of Menopausal Hormone Therapy (MHT).</div></div><div><h3>Methods</h3><div>Prospective controlled study of 59 premenopausal women planning RRSO and 91 comparisons who retained their ovaries. Depressive (CES<img>D) and anxiety symptoms (GAD-7) were measured at baseline (before RRSO) and at 12 and 24 months. We used ordinary and logistic multivariable regression to estimate differences between and within groups at 24 months, before and after conditioning on baseline and 12 month measures.</div></div><div><h3>Results</h3><div>Overall, depressive and anxiety symptoms were not elevated above baseline at 24 months and did not differ between RRSO and comparisons, before or after adjusting for previous measures (<em>P</em> &gt; 0.05). Elevated depressive symptoms at 12 months (OR = 24, <em>P</em> &lt; 0.001), and elevated anxiety symptoms at 12 months (OR = 13, <em>P</em> &lt; 0.001), strongly predicted 24 month measures. Elevated depressive symptoms at baseline no longer predicted 24 month symptoms once 12 month symptoms were considered, but elevated baseline anxiety still predicted anxiety at 24 months, even when 12 month anxiety was considered. No association between MHT use and depressive or anxiety symptoms was observed.</div></div><div><h3>Conclusions</h3><div>Depressive and anxiety symptoms are not elevated 24 months after RRSO. However, depressive symptoms at 12 months after RRSO are likely to persist at 24 months.</div></div>","PeriodicalId":12853,"journal":{"name":"Gynecologic oncology","volume":"192 ","pages":"Pages 1-7"},"PeriodicalIF":4.5,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KRAS mutations in endometrial cancers: Possible prognostic and treatment implications","authors":"Karolina A. Kilowski ,&nbsp;Martin F. Dietrich ,&nbsp;Joanne Xiu ,&nbsp;Yasmine Baca ,&nbsp;Andrew Hinton ,&nbsp;Sarfraz Ahmad ,&nbsp;Thomas J. Herzog ,&nbsp;Premal Thaker ,&nbsp;Robert W. Holloway","doi":"10.1016/j.ygyno.2024.10.026","DOIUrl":"10.1016/j.ygyno.2024.10.026","url":null,"abstract":"<div><h3>Background/Objectives</h3><div>Patients with recurrent or metastatic endometrial cancer (EC) have poor prognoses with limited therapeutic options following immunotherapy or immunochemotherapy treatments. Inhibitors of KRAS mutations (KRAS-mut) have shown efficacy in early solid tumor studies, but data in EC are lacking. This study describes the frequency of KRAS-mut relative to other oncogenic alterations in EC to identify genomic characteristics of KRAS-mut tumors that could lead to novel therapeutic options.</div></div><div><h3>Methods</h3><div>A molecular database of 7870 ECs was queried for presence of oncogenic mutations and immunotherapy biomarkers. Comparisons were performed using Fisher-Exact/ChiSquare (<em>p</em>-values) and adjusted for multiple tests by Benjamini-Hochberg (q) and pairwise nonparametric analysis using Wilcoxon Method.</div></div><div><h3>Results</h3><div><em>KRAS-</em>mut is a relatively frequent genotype in EC, detected in 16% of cases. Codon 12 was most frequently mutated, with G12D (31%) and G12V (27%) the most common subtypes. Biomarkers of immunotherapy response co-occur with <em>KRAS-</em>mut. Microsatellite instability-high and tumor mutational burden-high status were observed in 34.1% and 36.5% in <em>KRAS-</em>mut compared to 19.8% and 16.9% in <em>KRAS-</em>WT, respectively (<em>p</em> &lt; 0.05). PD-L1 &gt;1% was detected in 8.4% vs 6.4% of KRAS-mut vs KRAS-WT (<em>p</em> &lt; 0.05). <em>BRCA1/2</em> mutations were detected with similar low frequency (5.9% vs 4.9%) among <em>KRAS-</em>mut and <em>KRAS-</em>WT ECs (<em>p</em> &gt; 0.05). KRAS-mut was inversely associated with Her-2 overexpression (1.8% KRAS-mut vs 13% KRAS-WT. (<em>p</em> &lt; 0.001).</div></div><div><h3>Conclusions</h3><div><em>KRAS-</em>mut represents a genotypically distinct group of ECs. Overlap exists with genomic predictors (TMB-high, MSI-high) of immunotherapy response, suggesting a possible biomarker-driven combination option with immunotherapy. Clinical trials to evaluate these strategies should be developed.</div></div>","PeriodicalId":12853,"journal":{"name":"Gynecologic oncology","volume":"191 ","pages":"Pages 299-306"},"PeriodicalIF":4.5,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disparities in ovarian cancer survival among ethnic Asian American populations, 2006–2020","authors":"Alice W. Lee ,&nbsp;Valerie Poynor ,&nbsp;Sannia Siddiqui","doi":"10.1016/j.ygyno.2024.10.017","DOIUrl":"10.1016/j.ygyno.2024.10.017","url":null,"abstract":"<div><h3>Background</h3><div>Asian Americans have the highest ovarian cancer survival across the major racial groups although it is unclear whether this survival advantage is observed when each Asian ethnic subgroup is examined separately. Disaggregated survival analyses of this heterogeneous population is needed to ensure ethnic-specific disparities are not overlooked.</div></div><div><h3>Methods</h3><div>Data on ovarian cancer cases diagnosed from 2006 through 2020 from the Surveillance, Epidemiology, and End Results (SEER) Program were analyzed. Age-standardized five-year cause-specific survival was calculated for Non-Hispanic Whites and seven Asian ethnic subgroups in the U.S. (Asian Indian/Pakistani, Chinese, Filipino, Hawaiian/Pacific Islander, Japanese, Korean, Vietnamese) by stage and histotype. Multivariable Cox regression analyses using a weighted approach were conducted to calculate average hazard ratios (AHRs) and 95 % confidence intervals (CIs) to quantify the risk of ovarian cancer death comparing each Asian ethnic subgroup to Non-Hispanic Whites.</div></div><div><h3>Results</h3><div>Hawaiian/Pacific Islanders were the only Asian subgroup to show lower five-year cause-specific survival than Non-Hispanic Whites (44.99 % versus 47.90 %, respectively); Asian Indian/Pakistanis showed the highest survival (56.12 %). After adjusting for sociodemographic, tumor, and treatment characteristics, Asian Indian/Pakistani ovarian cancer patients were 17 % less likely to die from their disease whereas Hawaiian/Pacific Islander patients were 28 % more likely to die when compared to Non-Hispanic Whites (AHR = 0.83, 95 % CI 0.75–0.92 and AHR = 1.28, 95 % CI 1.07–1.53, respectively).</div></div><div><h3>Conclusions</h3><div>There are clear ethnic-specific survival disparities among Asian American ovarian cancer patients that are missed when the population is examined as a single group, further highlighting the need for data disaggregation in future ovarian cancer research.</div></div>","PeriodicalId":12853,"journal":{"name":"Gynecologic oncology","volume":"191 ","pages":"Pages 292-298"},"PeriodicalIF":4.5,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}