These are reviewed studies whose abstracts concern Uterine Serous Carcinoma. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Uterine Serous Carcinoma. Most are early lab, animal, or small human studies, and findings often conflict.
4 studies2 human⚠ Conflicting evidenceMechanism (3)
Tracking 4 published studies of Uterine Serous Carcinoma: 2 in humans, 2 reviews/other.
Reported direction across studies: 2 positive, 2 mixed.
Findings conflict — both supportive and negative/mixed results exist (see below). Human evidence is limited.
These counts summarize what the studies reported; they are not a measure of whether anything works for Uterine Serous Carcinoma.
ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical
International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Mar 2025 · Review
uterine serous carcinomauterine carcinosarcoma
This is a narrative review summarizing recent evidence on molecular classification, biomarkers, and new treatment approaches for uterine serous carcinoma and uterine carcinosarcoma. The authors highlight biomarkers such as HER2, TP53, and mismatch repair deficiency/microsatellite instability, discuss circulating tumor DNA and precision-based treatment options, and note survival disparities for non-Hispanic Black and other underserved minority patients. They conclude that continuing to prioritize biomarker-driven therapies and developing novel treatments through clinical trials — integrated with surgery and cytotoxic chemotherapy — is necessary.
Reported effects: proportion_of_cases 15% · proportion_of_deaths 50%
Key findings
- Uterine serous carcinoma and uterine carcinosarcoma are rare but account for a disproportionate share of endometrial cancer deaths.
- These subtypes have a high likelihood of metastasis and multisite recurrence and are biologically distinct from other endometrial cancers.
- The review analyzes the role of biomarkers including HER2, TP53, and mismatch repair deficiency/microsatellite instability and their influence on treatment strategies and surveillance.
- Circulating tumor DNA (ctDNA) is discussed as a potential tool.
- Novel precision-based treatment options are described and the authors call for continued development of biomarker-driven therapies through clinical trials.
- Disparate survival outcomes for non-Hispanic Black and other underserved minority patients are identified, and strategies to improve their outcomes are discussed.
Limitations: Narrative review rather than primary research; no new experimental or trial data presented in the abstract.; Abstract provides no methods, search strategy, or inclusion criteria (potential selection bias).; Rare tumor subtypes mean available evidence is likely limited and heterogeneous (implicit limitation).; No quantitative synthesis (meta-analysis) or new clinical outcome data reported in the abstract..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalReported positiveLimited evidenceTier 3 · early humann = 10
BMC cancer · Dec 2024 · retrospective cohort
Trastuzumab-deruxtecan-t-dxdTrastuzumab-deruxtecanendometrial neoplasmsovarian neoplasmscervical neoplasmsuterine carcinosarcomauterine leiomyosarcomauterine serous carcinomaovarian carcinosarcomahigh-grade serous ovarian carcinomamucinous ovarian carcinomasquamous cervical carcinoma This retrospective single-center study identified 10 patients with HER2-expressing (IHC 2+/3+) recurrent or metastatic gynecological cancers who received trastuzumab deruxtecan (5.4 mg/kg IV every 3 weeks). The cohort had a median progression-free survival of 5.4 months (95% CI 0.8-9.8). Five patients had a partial response, one had stable disease at 12 weeks, and four had disease progression at initial assessment. Clinical benefit was observed mainly in tumors with HER2 IHC 3+.
Reported effects: median PFS 5.4 mo [0.8–9.8], n=10 · partial responses 5, n=10 · +2 more
Key findings
- 10 patients with recurrent/metastatic HER2-expressing gynecological malignancies were treated with T-DXd.
- Histologies included uterine neoplasms (n=5), cervical squamous carcinoma (n=1) and ovarian cancers (n=4).
- Median age was 65.4 years (25th-75th percentile, 58.1-75.2 years).
- HER2 by IHC: 5 patients were 3+ and 5 patients were 2+.
- Median number of prior therapy lines was 4 (range 2-6); 2 uterine serous carcinoma patients were pretreated with trastuzumab and 4 patients had prior immunotherapy.
- Dose: T-DXd 5.4 mg/kg IV every 3 weeks until progression/toxicity.
- Median progression-free survival (PFS) in the cohort was 5.4 months (95% CI 0.8-9.8 months).
- Responses: 5 patients had partial response (including 2 previously treated with trastuzumab), 1 patient had stable disease at 12 weeks, 4 patients had disease progression at initial assessment.
- Most patients who derived clinical benefit had HER2 IHC 3+ expression.
Limitations: Retrospective, single-center design; Very small sample size (n=10); No control or comparator arm; Heterogeneous mix of gynecologic histologies; Heavily pre-treated population limits generalizability; Limited/absent reporting of safety or adverse event data in the abstract; Potential selection and reporting bias inherent to retrospective series.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismReported positiveLimited evidenceTier 3 · early human
Histology and histopathology · Nov 2018 · Review
uterine serous carcinomaendometrial cancerendometrial neoplasms
This is a narrative review linking advanced age to uterine serous carcinoma (USC). The authors summarize evidence that the p53 signature (p53S) is an early indicator of USC and is almost always found in elderly women; they suggest p53S may drive an age-related imbalance between proliferation and apoptosis of endometrial epithelial cells and propose an age-related type of endometrial cancer distinct from the traditional Type II classification.
Key findings
- Uterine serous carcinoma (USC) is closely associated with advanced age.
- The p53 signature (p53S) is considered the earliest indication for carcinogenesis of USC.
- p53 signatures have almost always been found in elderly women.
- p53 signatures are suspected to be responsible for an imbalance between proliferation and apoptosis of endometrial epithelial cells with advanced age.
- Authors propose an age-related type of endometrial cancer instead of the conventional Type II estrogen-independent classification.
Limitations: Narrative review with no new primary data presented in the abstract.; No sample sizes, methods, or systematic review methodology reported in the abstract.; Causal role of p53 signatures is described as 'suspected' and therefore remains speculative based on the abstract.; Proposal of a new age-related classification is not supported by new evidence within the abstract..
Discusses molecular/biomarker (p53) links between aging and uterine serous carcinoma and proposes a classification based on age.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismMixed resultsModerate evidenceTier 3 · early humann = 373
Nature · May 2013 · Integrated genomic, transcriptomic and proteomic characterization
endometrial carcinomauterine serous carcinomaendometrioid tumourovarian serous carcinomabasal-like breast carcinoma
The authors performed integrated genomic, transcriptomic and proteomic analyses of 373 endometrial carcinomas. They identified four molecular subtypes (POLE ultramutated, microsatellite instability hypermutated, copy-number low, and copy-number high) with distinct mutation and copy-number profiles. Uterine serous and about 25% of high-grade endometrioid tumors had many copy-number alterations and frequent TP53 mutations, while most endometrioid tumors had frequent PTEN, CTNNB1, PIK3CA, ARID1A and KRAS mutations and novel ARID5B alterations. The authors note that this genomic classification may affect post-surgical adjuvant treatment decisions for women with aggressive tumors.
Reported effects: sample_size 373, n=373 · proportion_high-grade_endometrioid_with_extensive_copy_number_alterations 25% · +1 more
Key findings
- Integrated analysis of 373 endometrial carcinomas was performed using array- and sequencing-based technologies.
- Uterine serous tumours and ∼25% of high-grade endometrioid tumours had extensive copy number alterations, few DNA methylation changes, low estrogen/progesterone receptor levels, and frequent TP53 mutations.
- Most endometrioid tumours had few copy number alterations or TP53 mutations, but frequent mutations in PTEN, CTNNB1, PIK3CA, ARID1A and KRAS and novel mutations in ARID5B.
- A subset of endometrioid tumours had a markedly increased transversion mutation frequency and newly identified hotspot mutations in POLE.
- Endometrial cancers were classified into four categories: POLE ultramutated, microsatellite instability hypermutated, copy-number low, and copy-number high.
- Uterine serous carcinomas share genomic features with ovarian serous and basal-like breast carcinomas.
Limitations: Observational genomic characterization of tumor samples without interventional or longitudinal clinical trial data.; No clinical outcome or treatment-response data reported in the abstract to validate proposed treatment implications.; Functional consequences of newly identified mutations (e.g., ARID5B, POLE hotspots) are not demonstrated in this report.; Cohort is limited to 373 tumors; subgroup counts and generalizability to all patient populations are not detailed in the abstract..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text