Abstract
Objective:
Mismatch repair deficiency (dMMR), high microsatellite instability (MSI-H), and high tumor mutation burden (TMB-H) are predictive and prognostic biomarkers in endometrial cancer. We aimed to characterize the racial/ethnic distribution of molecular markers and the clinical characteristics among endometrial cancer patients with TMB-H and MSI-H/dMMR.
Methods:
The Endometrial Cancer Molecularly Targeted Therapy Consortium is a centrally verified clinical and molecular repository. Patients with endometrial cancer who underwent tumor profiling were included. TMB-H was defined as ≥10–12 mutations per megabase. MSI-H was determined by next-generation sequencing or polymerase chain reaction, and dMMR by loss of MLH1, MSH2, MSH6, or PMS2 on immunohistochemistry. Tumor biomarker positivity was defined as TMB-H and/or MSI-H/dMMR. Overall survival was assessed using Kaplan-Meier and Cox proportional hazard models.
Results:
Among 742 patients, 22% (n=164) were biomarker positive: 12% (n=87) had both TMB-H and MSI-H/dMMR, 8% (n=63) had MSI-H/dMMR alone, and 2% (n=14) had 14 TMB-H alone. Only 9% of non-Hispanic Black patients had biomarker positive tumors compared to 26% of patients from other racial/ethnic groups. Pathogenic POLE mutations were rare (<1%, n=5). Patients with TMB-H had a higher proportion of high-risk histologies (43%) than those with MSI-H/dMMR (24%). Biomarker positive tumors were associated with a lower risk of death compared to biomarker negative tumors (aHR 0.63, 95% CI: 0.46, 0.88).
Conclusion:
Less than 10% of non-Hispanic Black patients with endometrial cancer had TMB-H and/or MSI-H/dMMR, and biomarker positivity was associated with improved survival. Prospective studies are necessary to elucidate how these molecular differences impact treatment and outcomes.
Keywords: Endometrial cancer; Tumor mutational burden; microsatellite instability; mismatch, repair deficiency
Introduction
High microsatellite instability (MSI-H) and mismatch repair deficiency (dMMR) are predictive and prognostic biomarkers for patients with advanced and recurrent endometrial cancer. Patients with dMMR tumors, particularly those in high-intermediate risk subgroups, experience higher recurrence rates and decreased recurrence-free survival compared to those with mismatch repair proficiency (pMMR) and TP53 wild-type tumors [1]. Tumors harboring high mutational burdens due to abnormal DNA repair pathways may express cancer-associated antigens that enhance responsiveness to immune checkpoint inhibitors (ICI), which activate patients’ immune systems against their cancers [2, 3].
Patients with MSI-H/dMMR tumors have improved outcomes with ICI therapy compared to those with pMMR tumors. Recent phase III randomized trials leading to FDA approvals have demonstrated that combining ICI with chemotherapy, followed by maintenance ICI, significantly prolongs progression-free survival (PFS) for patients with advanced or recurrent endometrial cancer, especially in MSI-H/dMMR cases [4–6]. In the recurrent setting, phase II studies reported enhanced response to single-agent ICI among patients with MSI-H/dMMR or high tumor mutational burden (TMB-H) tumors [7–10].
Multiple drivers of TMB-H have been identified, including pathogenic POLE mutations, MSI-H/dMMR, and other markers of genomic instability. Notably, the overlap between TMB and MSI varies: 70–83% of MSI-H tumors exhibit TMB-H, whereas only 16–27% of TMB-H tumors are MSI-H, when assessed by commercial next-generation sequencing (NGS) platforms [2, 11, 12]. Recent studies in endometrial cancer demonstrated lower rates of TMB-H and dMMR in Black patients compared to non-Black patients [13, 14]. The objective of this study was to compare racial and ethnic differences, clinical and molecular characteristics, and outcomes among endometrial cancer patients with TMB-H and/or MSI-H/dMMR, utilizing data from the multi-institutional Endometrial Cancer Molecularly Targeted Therapy Consortium (ECMT2).
Methods
The ECMT2 is a prospective and retrospective data repository comprising patients with histologically confirmed endometrial cancer from 22 U.S. institutions [15]. The consortium centrally verifies clinical and molecular data, which are entered in the deidentified database by study personnel at each institution. The database contains demographic information, including race and ethnicity; tumor characteristics such as stage, grade, and histology; treatment details and outcomes, and molecular characteristics such as genomic alterations, protein expressions, and microsatellite instability. This study was approved by the lead institution’s Institutional Review Board (IRB) on March 5, 2020 (IRB Reference Number: Pro00103465). Participants were enrolled retrospectively and prospectively, with consent waived or required per each site’s IRB.
For this retrospective descriptive ECMT2 substudy, data from thirteen participating institutions were included. Data were abstracted and committed to the ECMT2 database between March 2020 and September 2022. Eligible patients underwent comprehensive molecular genomic profiling of tumors at the treating physician’s discretion. All epithelial histologies were included, and pre-invasive disease was excluded. Patients who did not undergo TMB testing or had an unknown TMB status were excluded. All included patients underwent MSI testing by NGS or by polymerase chain reaction (PCR), MMR testing by immunohistochemistry (IHC), or both.
TMB-H was defined as a mutational burden greater than 10 mutations per megabase (FoundationOne, Foundation Medicine, Inc., Cambridge, MA, USA) or greater than 12 mutations per megabase (Caris Life Sciences, Phoenix, AZ, USA). MSI-H was assessed by validated NGS methods or PCR assays with two of five altered or unstable markers [12, 16, 17]. DMMR was defined as the loss of staining of MSH2, MSH6, PMS2, or MLH1 by institutional IHC. Due to the established correlation between MSI-H and dMMR, these molecular signatures were grouped together for analysis [18, 19]. Patients were classified as biomarker positive if tumors demonstrated any of these markers (e.g., TMB-H and/or MSI-H/dMMR), and biomarker negative if none of these markers were present. POLE mutations were extracted from the tumor sequencing reports and verified by a molecular pathologist to determine pathogenicity.
Descriptive statistics summarized patient demographics and clinical characteristics by molecular profile group, using counts and percentages for categorical data and the median and interquartile range (IQR) for ordered or continuous measures. Overall survival was defined as the time from diagnosis to death from any cause, or censored at last known follow-up if the patient was alive. Survival was summarized using Kaplan-Meier methods, and comparisons between biomarker groups and by race and ethnicity were made using Cox proportional hazards models. Hazard ratio (HR) and associated 95% confidence intervals (CI) were estimated, adjusting for potential confounders, including age at diagnosis, which was categorized as less than 60 years, 60–69 years, 70–79 years, and 80 years and older, severe comorbidities as measured by a Charlson Comorbidity Index score of five and above, and histology (endometrioid histology vs. others). Immunotherapy receipt was not included in this multivariate model as it is a mediator in the direct causal pathway between factors of interest and survival. Data management and analyses were conducted in STATA version 18 (College Station, TX).
Results
From March 2020 to September 2022, 3,332 patients were entered into the consortium database. Of these, 941 underwent tumor testing, and 742 patients had known TMB and MSI/MMR status and were included in the analysis. Tumor testing was performed primarily using Foundation One (n=542, 73%), followed by Caris (n=143, 19%), both platforms (n=3, <1%), or other technologies (n=54, 7%). Seventy percent of the data included in this study were centrally verified.
The median age at diagnosis was 70 years (IQR: 64, 75). The majority of patients identified as non-Hispanic White (65%, n=483) or non-Hispanic Black (22%, n=161). Additional racial and ethnic groups included Asian Americans, Native Hawaiian or Native Americans, Hispanic, or those identifying as another or unspecified race/ethnicity, comprising 3%, 1%, 4%, and 4% of the cohort, respectively. The majority of patients (86%, n=644) had advanced-stage or recurrent endometrial cancer. Over half (55%, n=406) had non-endometrioid histology (Table 1). Severe comorbidity, as measured by the Charlson Comorbidity Index, was observed in 69% (n=515).
Table 1.
Characteristics across molecular markers
| Biomarker Positive Type | Biomarker Positive (Any)* | Biomarker Negative | Total | |||
|---|---|---|---|---|---|---|
| MSI-H/dMMR & TMB-H (N= 87) | MSI-H/dMMR only (N=63) | TMB-H only (N=14) | N=164 | N=578 | N=742 | |
| Age (Median, IQR) ^ | 69 (62,74) | 67 (61,74) | 67 (57,74) | 68 (62, 74) | 70 (64,75) | 70 (64,75) |
| Body mass index in kg/m2 (Median, IQR) ^ | 31 (27,38) | 32 (27,40) | 28 (25,35) | 31 (26, 38) | 31 (26,37) | 31 (26,38) |
| Race and ethnicity (n, %) | ||||||
| Asian (Non-Hispanic) | 3 (3) | 3 (5) | 0 (0) | 6 (4) | 17 (3) | 23 (3) |
| Hispanic | 4 (5) | 5 (8) | 1 (7) | 10 (6) | 22 (4) | 32 (4) |
| Native Hawaiian or Native American (Non-Hispanic) | 2 (2) | 3 (5) | 0 (0) | 5 (3) | 6 (1) | 11 (1) |
| Non-Hispanic Black | 6 (78) | 5 (8) | 4 (29) | 15 (9) | 146 (25) | 161 (22) |
| Non-Hispanic White | 66 (76) | 45 (71) | 9 (64) | 120 (73) | 363 (63) | 483 (65) |
| Other race or not available | 6 (7) | 2 (3) | 0 (0) | 8 (5) | 24 (4) | 32 (4) |
| Charlson Comorbidity Index (Median, IQR) ^ | 8 (7, 9) | 7 (5, 9) | 7.5 (6, 10) | 8 (6, 9) | 8 (6, 9) | 8 (6, 9) |
| Stage | ||||||
| I-II | 13 (15) | 10 (16) | 5 (36) | 28 (17) | 70 (12) | 98 (13) |
| III-IV | 26 (30) | 16 (25) | 3 (21) | 45 (27) | 151 (26) | 196 (26) |
| Recurrent# | 48 (55) | 37 (58) | 6 (43) | 91 (55) | 357 (62) | 448 (60) |
| Histology (n, %) | ||||||
| Endometrioid | 74 (85) | 48 (76) | 8 (57) | 130 (79) | 206 (36) | 336 (45) |
| Serous | 1 (1) | 2 (3) | 1 (7) | 4 (2) | 165 (29) | 169 (23) |
| Clear cell | 1 (1) | 1 (2) | 0 (0) | 2 (1) | 31 (5) | 33 (4) |
| Carcinosarcoma | 2 (2) | 3 (5) | 2 (14) | 7 (4) | 81 (14) | 88 (12) |
| Mixed | 3 (3) | 7 (11) | 2 (14) | 12 (7) | 67 (12) | 37 (5) |
| Other | 6 (7) | 2 (3) | 1 (7) | 9 (5) | 28 (5) | 79 (11) |
MSI-H: high microsatellite instability, dMMR: mismatch repair deficiency, TMB-H: high tumor mutational burden
IQR: Interquartile range
Biomarker Positive (Any) includes MSI-H/dMMR and TMB-H, MSI-H/dMMR only, and TMB-H only
Missing data: Age (n=1); BMI (n=109); Charlson co-morbidity index (n=35)
Patients with recurrent disease may have had stage I-IV at the time of initial diagnosis
One hundred sixty-four patients (22%) had biomarker positive tumors (i.e., had at least one of the following markers: TMB-H, MSI-H, or dMMR). Among these, 87 patients (12%) exhibited both TMB-H and MSI-H/dMMR; 63 patients (8%) had MSI-H or dMMR only, and 14 patients (2%) had TMB-H only. The remaining 578 patients (78%) were biomarker negative, lacking all three markers (Figure 1). Biomarker status was associated with both race/ethnicity and tumor histology (Table 1). Of the biomarker positive group, the majority were non-Hispanic White (n=120, 73%). Within the MSI-H/dMMR-only subgroup, 8% (n=5) were Hispanic, 8% (n=5) were non-Hispanic Black, and 71% (n=45) were non-Hispanic White. In contrast, in the TMB-H only group, 7% (n=1) were Hispanic, 29% (n=4) were non-Hispanic Black, and 64% (n=9) were non-Hispanic White. Among the biomarker negative patients, 25% (n=146) were non-Hispanic Black, and 63% (n=363) were non-Hispanic White (Figure 2).
Figure 1. Biomarker classifications of overall cohort.
Figure 2. Biomarker distributions by race and ethnic groups .
Non-Hispanic Black patients were less likely to have tumors characterized as biomarker positive (i.e., TMB-H and/or MSI-H/dMMR) compared to patients of other races and ethnicities [9% (15/161) vs. 26% (149/581); difference: 17%, 95% CI: 11%, 23%]. Additionally, the frequency of MSI-H or dMMR-only tumors (without TMB-H) was lower among non-Hispanic Black patients compared to patients of other races and ethnicities [3% (5/161) vs. 10% (58/581); difference: 7%, 95% CI: 3%, 11%]. Of the 63 patients with MSI-H/dMMR-only tumors, 8% (n=5) were non-Hispanic Black, while among the 14 TMB-H only patients, 29% (n=4) were non-Hispanic Black (difference: 21%, 95% CI: −0.4%, 46%).
Seventy-nine percent (130/164) and 76% (48/63) of patients with biomarker positive tumors and MSI-H/dMMR only tumors were diagnosed with endometrioid histology, respectively. In contrast, patients whose tumors had TMB-H alone had a lower frequency of endometrioid histology (57%, 8/14), while 43% (6/14) had non-endometrioid subtypes. Biomarker negative tumors were predominantly non-endometrioid, with only 36% (206/578) classified as endometrioid and 64% (372/578) as non-endometrioid histologies (Table 1). Of the 164 patients who were biomarker positive, only 72 (44%) received immunotherapy. Fewer non-Hispanic Black patients received immunotherapy compared to those of other races and ethnicity [27% (4/15) vs. 46% (68/149; difference: 19%, 95% CI: −5%, 43%].
Pathogenic POLE mutations were identified in 13 patients (2%) via NGS. Of these patients, only 5 of 13 were confirmed to have pathogenic mutations in the exonuclease domain, while the remaining eight represented variants of uncertain significance or germline polymorphisms. Among the five patients with pathogenic POLE mutations, four had TMB-H alone tumors without MSI-H/dMMR, and one was biomarker negative. One patient identified as non-Hispanic Black, and four patients as non-Hispanic White. Two patients remained recurrence-free, one had persistent disease, and two had unknown recurrence status. Of the eight patients with non-pathogenic POLE mutations, two had both MSI-H/dMMR and TMB-H, two had MSI-H/dMMR alone, and four were biomarker negative. Three patients recurred, one had persistent disease, and four never recurred.
Overall survival data were available for 739 patients, among whom 337 deaths occurred. The median follow-up time was 31 months (IQR: 15, 54), and the median overall survival across all patients was 57 months (95% CI: 50, 66). Patients with biomarker negative tumors had shorter median overall survival of 50 months (95% CI: 45, 59) compared to 100 months (95% CI: 65, upper bound not reached; unadjusted HR 0.52, 95% CI: 0.38, 0.71) for patients with biomarker positive tumors (Figure 3). After excluding patients with missing confounder data, 706 were included in the Cox model estimates, with 325 deaths observed. After adjusting for age, severe comorbidity, and histology, TMB-H and/or MSI-H/dMMR biomarker status was associated with a lower risk of death from any cause (adjusted HR [aHR] 0.63, 95% CI: 0.46, 0.88).
Figure 3. Overall survival by biomarker status.
When stratified by race and ethnicity, non-Hispanic Black patients with biomarker negative tumors had worse unadjusted median overall survival compared to biomarker negative patients of other races/ethnicities (33 months, (95% CI: 29, 49) vs. 56 months, (95% CI: 47, 70), Figure 4]. After adjusting for age, severe comorbidity, and histology, biomarker negative patients identifying as races/ethnicities other than non-Hispanic Black demonstrated a lower risk of mortality compared to their non-Hispanic Black counterparts (aHR 0.75, 95% CI: 0.57, 0.98). Similarly, biomarker positive patients with other races/ethnicities had a lower risk of death compared to biomarker negative patients who identified as non-Hispanic Black (aHR: 0.50, 95% CI: 0.34, 0.75), while biomarker positive non-Hispanic Black patients showed a comparable but less precise risk reduction (aHR: 0.49, 95% CI: 0.18, 1.35). In a sensitivity analysis including immunotherapy receipt in the survival models, there were no differences in the survival estimates (Supplemental Tables 1-2).
Figure 4. Overall survival stratified by race and biomarker status.
Discussion
In this multi-institutional, real-world cohort of patients with endometrial cancer who underwent comprehensive tumor molecular profiling, 22% had MSI-H/dMMR and/or TMB-H tumors (biomarker positive); 12% had both TMB-H and MSI-H/dMMR tumors, 8% had tumors with MSI-H/dMMR alone without TMB-H, and 2% had tumors with TMB-H alone without MSI-H/dMMR. Biomarker positivity differed by race/ethnicity; 9% of non-Hispanic Black patients demonstrated biomarker positive tumors compared to 26% of patients from other racial/ethnic groups. Patients with TMB-H alone tumors had higher-risk histologies compared to patients with MSI-H/dMMR alone. TMB-H and/or MSI-H/dMMR markers were associated with improved survival compared to those with biomarker negative tumors. The survival benefit persisted even after controlling for age, severe comorbidities, and histology. Immunotherapy receipt was not included in this multivariate model as it is a mediator in the direct causal pathway between factors of interest and survival. In a sensitivity analysis including immunotherapy receipt in the model, there were no differences in the survival estimates (Supplemental Tables 1-2).
Patients of diverse backgrounds are less likely to have MSI-H/dMMR biomarkers, as established in previous publications and confirmed in our study. In the current study, there were fewer non-White patients in the MSI-H/dMMR cohort and more non-White patients in the TMB-H alone and biomarker-negative cohorts. A single-institution molecular analysis showed that Black patients were less likely to have tumors with MSI-H compared to White patients (14% vs. 25%) [14]. Because the POLE and dMMR molecular subgroups of endometrial cancer have improved clinical outcomes or responses to immunotherapy, these biomarker differences may suggest a potential molecular rationale for disparities in outcomes.
Yet, disparities in endometrial cancer are multifactorial and complex. Prior studies have demonstrated that Black patients are more likely to be diagnosed with non-endometrioid cancers, present at more advanced stages, experience worse survival, and are less likely to receive guideline concordant cancer care [20–23]. We found that even among biomarker negative patients, non-Hispanic Black patients experienced poorer survival outcomes relative to patients of other racial backgrounds. These findings indicate that systemic factors beyond molecular markers contribute to observed differences in outcomes. Importantly, these disparities are not rooted in inherent biologic differences, as race is a social construct. Instead, race serves as a proxy of a range of non-biologic factors, such as social determinants of health (i.e., socioeconomic status, access to care, etc) and impacts of structural racism and poverty [24].
In addition, POLE mutation interpretation remains clinically complex. Retrospective data suggest that POLE mutations occur in <1% of Black endometrial cancer patients compared to 6% of Asian and 5% of White patients [25]. In our study, only one of five pathogenic POLE mutations was identified in a non-Hispanic Black patient. Notably, four of five patients with pathogenic POLE mutations exhibited TMB-H. Though 13 patients had tumors classified as POLE-mutated, fewer than half harbored confirmed pathogenic exonuclease domain mutations and required molecular oncology consultation to discern true hotspot mutations, highlighting the complexity of the interpretations and risks of misclassification in the real world. In addition, reports of POLE associations with improved prognosis have not been validated in diverse populations.
Biomarker testing may be less reliable and generalizable in diverse patient populations. Tumor-only sequencing can overestimate TMB due to false-positive germline variants, particularly for non-White patients who are underrepresented in reference panels [26]. Germline subtraction TMB— calculated by comparing the tumor mutations with matched normal germline DNA — may minimize the impact of TMB overestimations in diverse populations [27]. However, this methodology has not yet been prospectively validated. The tissue-agnostic FDA threshold of TMB-H of ten mutations per megabase, while allowing for clinical utility optimization and trial standardization, is derived from predominantly White populations and can vary depending on the assay utilized [8, 26]. Some studies suggest that the cutoff value for TMB-H may differ in non-White populations, which may impact ICI eligibility [14, 28]. Increasing diverse representation in trials and molecular databases is imperative to ensure equity in biomarker validation and development.
A strength of this analysis is the ECMT2, a real-world, multi-institutional consortium representing diverse practices from thirteen U.S. institutions, with 70% central data verification. However, the data are limited by the institutions participating in the consortium, which were mostly academic medical centers; therefore, practices may not represent community hospitals or private practices. The majority of the patients in the study had advanced or recurrent endometrial cancers, potentially underrepresenting molecular subtypes and their outcomes in early-stage disease. Though a third of the patients in this study were non-White, Hispanic representation remained low (4%). All patients in the study had access to and underwent NGS, which may not reflect real-world tumor testing disparities, particularly among underserved populations. Additional constraints include small biomarker subgroup sizes and heterogeneity in treatment patterns. Finally, challenges in biomarker interpretation included varying thresholds across multiple diagnostic assays and non-standardized MSI testing approaches (PCR or NGS per institutional protocol), introducing categorization variability [29].
In conclusion, this real-world multi-institutional analysis of patients with endometrial cancer who underwent tumor testing revealed distinct biomarker groups: 8% were MSI-H/dMMR and did not have TMB-H tumors, and 2% were TMB-H and did not demonstrate MSI-H/dMMR. Overall, 22% of patients with endometrial cancers had tumors that were either TMB-H and/or MSI/dMMR. Less than 10% of non-Hispanic Black patients had TMB-H and/or MSI-H/dMMR, compared to approximately 25% of those of other racial/ethnic groups. Non-Hispanic Black patients were more likely to have cancers exhibiting TMB-H alone without MSI-H/dMMR, and patients with TMB-H-only tumors had higher-risk histologies. Patients with biomarker positive tumors had improved survival compared to patients with biomarker negative tumors. These findings suggest that molecular differences may be at least partly responsible for varying outcomes, but disparities related to structural racism and social determinants of health cannot be overlooked as non-Hispanic Black patients without markers had worse survival. Increasing diverse representation is needed in translational and clinical studies to understand the tumoral and molecular differences and outcomes.
Supplementary Material
Highlights.
22% of patients with endometrial cancers had tumors that were either TMB-H and/or MSI-H
8% of endometrial cancer tumors had MSI-H/dMMR without TMB-H, and 2% had TMB-H without MSI-H/dMMR
Non-Hispanic Black patients were less likely to have biomarker positive tumors (TMB-H and/or MSI-H/dMMR tumors)
TMB-H and/or MSI-H/dMMR was associated with improved survival compared to those that were biomarker negative
Acknowledgments
Dr. Angeles Secord reports grants or contracts for clinical trial grants to the institution from AbbVie, Aravive, Astra Zeneca, Clovis, Eisai, Ellipses, GSK, I-MAB Biopharma, Immunogen, Karyopharm, Merck, Mersana, Myriad, Oncoquest/Canaria Bio, Roche/Genentech, Seagen Inc., VBL Therapeutics, and Zentalis. She reports royalties or licenses from UpToDate, and payments or honoraria from Curio Science, ASCO, Research to Practice; GOG Foundation, Clinical HMP Global Great Debates, and Clinical Education Alliance. She reports support for attending meetings from GOG Foundation, NRG Oncology, and Society of Gynecologic Oncology. She participated on a Data Safety Monitoring or Advisory Board for Astra Zeneca, Clovis, Gilead, GSK, Imvax, Merck, Mersana, Natera, and Oncoquest/CanariaBio, GOG Foundation, and Abbvie/Immunogen. She serves in a leadership or fiduciary role in GOG Foundation Board of Directors, NRG Committee Vice Chair, SGO Board of Directors, FWC Board of Directors, AAOGF Board of Trustees, AGOS Council, and holds stock or options from Amgen and Johnson and Johnson.
Dr. Erinn Hade reports support from NIH CTSA UL1 TR001445 and has participated in the Data Safety Monitoring Board of NYU CTSI.
Dr. Amanda Jackson received consulting fees from Ethicon and Auris, and payment or honoraria from OncLive, and participated in the AstraZeneca Advisory Board.
Dr. Floor Backes received grants for investigator-initiated studies paid to the institution from Merck, Eisai, Immunogen, Clovis, Natera, Tempus, and AstraZeneca. She also received personal fees from UpToDate. She received consulting fees from advisory boards from Merck, Clovis, Immunogen, Eisai, AstraZeneca, GSK, Myriad, BioNTech, Daiichi Sankyo, EMD Serono. She received payment or honoraria from Clinical Educational Concepts, Clinical Care Options, Medscape/WebMD, Med Learning, I3Health, CMR institute, Global Learning Initiative/Prova, OncLive, Targeted Oncology, Research to Practice, GOG Foundation. She received support for attending meetings from GSK and BioNTech. She serves in a leadership or fiduciary role in SGO, NRG Oncology Developmental Therapeutics Committee, and IGCS Education 360.
Dr. Premal Thacker received consulting fees from Imunon, and received support for meetings from GSK. She participated in a Data Safety Monitoring Board or Advisory Board for Iovance, AstraZeneca, Clovis Oncology, GSK, Seagen, Agenus, Relacorilant, Immunogen, Mersana, Novocure, Zentalis, Merck, Imunon, and Caris. She reports stock or options from Imunon.
Dr. Rebecca Arend reports research contracts from Abbvie, GSK, Exelixis, LifeNet, Artera, Champions, Tempus. She received consulting fees from AstraZeneca. She participated on a Data Safety Monitoring Board or Advisory Board for Merck.
Dr. Jason Wright reports institutional grants from Merck. He received royalties or licenses from UpToDate. He reports payment for expert testimony from medicolegal consulting. He serves as a Journal Editor for ACOG.
Dr. Bradley Corr reports grants or contracts to the institution from Abbvie. He reports payment or honorarium from Tempus and Topline Bio. She participated in a Data Safety Monitoring or Advisory Board for BioNTech, GSK, Merck, Gilead, AbbVie, and Zentalis.
Dr. Emily Ko reports support from the NCI Hopkins-Penn Ovarian SPORE. She received grants or contracts from Tesaro and Faeth for institutional research support. She received grants from the Winn Diversity in Clinical Trials from BMS and OCRA/GSK. She received payments or honoraria from Brigham and Women’s Hospital and VCU. She serves in a leadership or fiduciary role in SGO Health Policy and Socioeconomic Committee.
Dr. Gottfried Konecny reports payments or honoraria from Immunogen, Abbvie, Merck, and AstraZeneca. He received support for attending meetings from TORL Biotherapeutics. He participated on a Data Safety Monitoring Board or Advisory Board for the GOG Foundation.
Dr. Victoria Bae-Jump reports grants /contracts and drugs from Chimerix, Genentech, and Merck for investigator-initiated trials. She participated in a Data Safety Monitoring Board for Gilead.
Dr. Kari Hacker reports stock options from Strata Oncology.
Dr. Bhavana Pothuri reports grants or contracts from Abbvie, DualityBio, Cybrexa, Daiichi Sankyo, Tesaro/GSK, Merck, AstraZeneca, Karyopharm Therapeutics, Clovis, Roche/Genentech, Mersana, Genmab, Celsion/Immunon, OnCusp, Incyte, Toray, VBL Therapeutics, Loxo/Lily, Agenus, Seagen, NRG Oncology, Daiichi Sankyo, Xencor, Imab, Takeda, Onconova, Celgene, Sutro Biopharma, Alkermes, Immunogen, Eisai, Acrivon, and Pfizer. She reports consulting/advisory board fees from Abbvie, Corcept, GSK, AstraZeneca, Duality Bio, Immunogen, GOG Foundation, SeaGen, Oncusp, Eisai, Signatera, Karyopharm, Celsion, Sutro Biopharma, Imvax Inc, Incyte Corporation, InxMed, Onconova Therapeutics, Pfizer, R Pharm, Regeneron, Toray, Mersana, Loxo/Lily, Tesaro/GSK, Merck, Nuvation, BioNTech, Beigene, Daiichi Sankyo. She served in a leadership or fiduciary role for SGO Board of Directors, GOG Partners, and NYOB Society.
Footnotes
Conflict of interest:
All other authors report no conflicts of interest.
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