These are reviewed studies whose abstracts concern Uterine Leiomyosarcoma. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Uterine Leiomyosarcoma. Most are early lab, animal, or small human studies, and findings often conflict.
ReviewMechanismMixed resultsLimited evidenceTier 4 Β· clinical
International journal of gynecological cancer : official journal of the International Gynecological Cancer Society Β· Jan 2026
uterine leiomyosarcoma
This is a narrative review of the immune environment of uterine leiomyosarcoma and the potential role of immune checkpoint inhibitors. The authors report variable PD-L1 expression, heterogeneous lymphocytic infiltration, and interactions with tumor-associated macrophages, note modest response rates to checkpoint inhibitors in clinical trials, and discuss that dual PD-1/CTLA-4 blockade and chemotherapy-induced immunogenic cell death may enhance immune activation in select patients. They conclude that combinatorial and personalized strategies, improved immune profiling, and macrophage-targeted approaches merit further study.
Studied with: anti-CTLA-4 + anti-PD-1 dual checkpoint blockade, chemotherapy (to induce immunogenic cell death), targeted immunomodulation, macrophage-targeted therapies.
Key findings
- Uterine leiomyosarcoma has a variable tumor immune microenvironment including variable PD-L1 expression and differential lymphocytic infiltration.
- Interactions with tumor-associated macrophages shape immune responses in leiomyosarcoma.
- Clinical trials of immune checkpoint inhibitors in leiomyosarcoma have produced modest response rates.
- Molecular analyses suggest that specific sub-groups of leiomyosarcoma patients may derive greater benefit from checkpoint inhibition.
- Dual-checkpoint blockade combining anti-PD-1 and anti-CTLA-4 has demonstrated enhanced immune activation in select patients.
- Chemotherapy-induced immunogenic cell death has been explored as a complementary approach to immunotherapy.
- Authors recommend innovative combinatorial strategies, improved patient selection, enhanced macrophage-targeted therapies, and optimized immune profiling for future research.
Limitations: Narrative review onlyβno new primary experimental or patient-level data are presented.; Conclusions are based on heterogeneous published studies and molecular analyses rather than definitive randomized trial evidence.; Abstract reports only 'modest response rates' in trials without quantitative pooled estimates or meta-analysis.; Leiomyosarcoma heterogeneity and rarity limit generalizability of existing trial results (as noted by authors)..
AI summary of the abstract, human-reviewed Β· Jun 2026. Describes what this study reported, not medical advice. View on PubMed
Human Β· observationalMechanismReported positiveLimited evidenceTier 3 Β· early humann = 71
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc Β· Nov 2025 Β· Array-based global methylation profiling analysis of tumor samples (71 uterine leiomyosarcoma) compared with several other uterine mesenchymal tumors and soft tissue leiomyosarcoma
uterine leiomyosarcomauterine mesenchymal tumorssoft tissue leiomyosarcoma
Researchers performed array-based global methylation profiling on 71 uterine leiomyosarcoma samples and compared them to other uterine mesenchymal tumors and soft tissue leiomyosarcoma. They found that uLMS have distinct methylation patterns versus other tumor types and that methylation profiling identifies two distinct uLMS subgroups with differing copy number alterations and distinct histologic and clinical behaviors. The authors report this is the first study to describe methylation profiling as a diagnostic tool to differentiate uLMS from its mimics.
Key findings
- uLMS demonstrated distinct methylation patterns differing from all other tumor types.
- Methylation profiling defines 2 distinct subgroups of uLMS with differing copy number alterations.
- The two methylation-defined subgroups exhibit unique histologic and clinical behaviors, supported by differences in methylation pathway analysis.
- This study is the first to report methylation profiling as a useful diagnostic tool in differentiating uLMS from mimics.
Limitations: Observational molecular profiling study without interventional or longitudinal clinical trial data; Sample size limited to 71 uLMS; sizes of comparator tumor groups not reported in abstract; No external validation cohort reported in the abstract; No functional validation experiments described to confirm biological significance of methylation differences; Details on clinical outcome measures, follow-up duration, and statistical metrics are not provided in the abstract.
AI summary of the abstract, human-reviewed Β· Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewReported positiveModerate evidenceTier 4 Β· clinical
The Journal of nutrition Β· Nov 2025 Β· review
colorectal cancerbreast cancerendometrial cancerlung cancer
This review summarizes epidemiologic evidence linking red and processed meat consumption with higher risks of multiple chronic diseases, including colorectal, breast, endometrial, and lung cancers, type 2 diabetes, cardiovascular disease, and all-cause mortality. It reports that processed meats show stronger associations than unprocessed red meat, with dose-response relationships indicating elevated risks even at moderate intakes. The authors describe plausible biological mechanisms (carcinogen formation, inflammation, gut microbiome changes, heme iron, TMAO, and metabolic effects) and note inconsistencies such as short-term randomized trial biomarker findings and modification of risk by overall diet, lifestyle, and genetics. The review concludes that minimizing processed meat and replacing red/processed meats with plant proteins, poultry, or fish is expected to reduce disease risk, and it calls for further research on causality, mechanisms, and population diversity.
Studied with: plant proteins, poultry, fish.
Key findings
- Observational studies and meta-analyses show positive associations between red/processed meat consumption and multiple chronic diseases, including colorectal, breast, endometrial, and lung cancers, type 2 diabetes, cardiovascular disease, and all-cause mortality.
- Dose-response relationships indicate elevated risks even at moderate intakes.
- Processed meats consistently show stronger detrimental associations than unprocessed red meats.
- Mechanistic pathways discussed include carcinogen formation, proinflammatory effects, gut microbiome dysbiosis, heme iron, trimethylamine N-oxide (TMAO), saturated fats, and effects on lipid metabolism and insulin resistance.
- Replacing red/processed meats with plant proteins, poultry, or fish is associated with reduced disease risk according to the review.
- Evidence complexities include inconsistent randomized controlled trial findings on short-term biomarkers and substantial modification of risk by processing, cooking methods, overall diet, lifestyle, and genetic factors.
Limitations: Predominantly observational epidemiologic evidence, which is susceptible to confounding and cannot establish causality.; Inconsistent randomized controlled trial findings limited to short-term biomarkers rather than clinical endpoints.; Heterogeneity introduced by differences in processing methods, cooking techniques, and definitions of processed versus unprocessed meat.; Potential modification of associations by overall diet, lifestyle, and genetic factors, complicating interpretation.; Identified gaps include need for greater mechanistic specificity, more diverse populations, and integrated health-environment assessments..
AI summary of the abstract, human-reviewed Β· Jul 2026. Describes what this study reported, not medical advice. View on PubMed
Human Β· observationalMechanismReported positiveLimited evidenceTier 3 Β· early humann = 6
Frontiers in immunology Β· Aug 2025 Β· Single-cell RNA sequencing (scRNA-seq) of metastatic lesions from a treatment-naΓ―ve uterine leiomyosarcoma patient compared to normal uterine myometrium samples (MMM, n=5); integrated analyses including CNV, pseudotime, cell-cell communication, functional enrichment, and mpIF validation; survival correlations with TCGA-SARC cohort.
uterine leiomyosarcoma
The authors performed single-cell RNA sequencing on metastatic lesions from one treatment-naΓ―ve uterine leiomyosarcoma patient and compared the data to five normal myometrium samples. They found an immunosuppressed tumor microenvironment characterized by exhausted CD8+ T cells, M2-like tumor-associated macrophages, and immature N2 neutrophils enriched in metastatic foci; these features correlated with poorer prognosis in TCGA-SARC analyses. The study also identified cell-cell communication axes (MIF-(CD74+CD44), CXCL8) and candidate biomarkers (EDARADD, CLDN10, TMIGD2) and dysregulated pathways (TGF-beta, angiogenesis, MIF signaling).
Key findings
- The tumor microenvironment showed prominent immunosuppression with exhausted CD8+ T cells, with initial markers (CCR7, MAL) diminishing over time and exhaustion markers (LAG3, HAVCR2, TIGIT) enriched.
- M2-polarized macrophages were mainly composed of M2-like TAMs with tumor-promoting characteristics (CD163, FTH1, FTL, TIMP1) and there was a polarization trajectory from M1 to M2.
- Immature, tumor-promoting N2 neutrophils (CD15+EDARADD+) were enriched in metastatic foci and associated with poor prognosis.
- Cell-cell communication analyses highlighted MIF-(CD74+CD44) interactions between T/B cells and a role for the CXCL8 signaling axis in promoting angiogenesis, TAM polarization, and immunosuppression.
- Constructed a comprehensive single-cell map of ULSA, defined a metastasis-susceptible cell subset (U11-EDARADD), and nominated biomarkers (EDARADD, CLDN10, TMIGD2) and dysregulated pathways (TGF-Ξ², angiogenesis, MIF signaling) as possible targets for future combined-immunotherapy development.
Limitations: Tumor single-cell data derive from a single ULSA patient (metastatic lesions from one individual), limiting generalizability.; Normal comparator samples are limited (MMM, n=5) and cohort sizes are small.; Observational single-cell profiling cannot establish causal relationships between identified cell states/pathways and clinical outcomes or therapy resistance.; Survival associations were assessed using TCGA-SARC correlations (indirect validation) rather than validation in an independent ULSA cohort.; No interventional or functional experiments reported to validate that identified biomarkers/pathways drive immunosuppression or therapy resistance..
AI summary of the abstract, human-reviewed Β· Sep 2026. Describes what this study reported, not medical advice. View on PubMed Β· Full text
Human Β· observationalSupportive careMixed resultsModerate evidenceTier 3 Β· early humann = 267586
Journal of the National Cancer Institute Β· Aug 2025 Β· prospective cohort study
Supportive carecervical cancerHodgkin lymphomaprostate cancerbreast cancercolorectal cancerlung cancerendometrial canceroral cavity and pharynx cancerkidney cancerovarian cancersarcomamelanomaleukemia
Researchers followed participants in three large prospective cohorts for up to 36 years to examine whether a cancer diagnosis was associated with later atherosclerotic cardiovascular disease (ASCVD). They documented 4,334 new ASCVD events among 49,603 incident cancer cases and found that cervical cancer and Hodgkin lymphoma were associated with higher ASCVD risk, prostate cancer with slightly lower risk, and that ASCVD risk trajectories over time varied by cancer type (for example, breast cancer survivors had lower ASCVD risk for the first 7.5 years, then risk increased).
Reported effects: new-onset ASCVD events among incident cancer cases 4334, n=49603 Β· cervical cancer HR 1.56 [1.06β2.29] Β· +6 more
Key findings
- During up to 36 years of follow-up, 4,334 new-onset ASCVD events among 49,603 incident cancer cases were documented.
- Cervical cancer was associated with increased ASCVD incidence (HR = 1.56, 95% CI = 1.06 to 2.29).
- Hodgkin lymphoma was associated with increased ASCVD incidence (HR = 2.80, 95% CI = 1.89 to 4.15).
- Prostate cancer was associated with lower ASCVD incidence (HR = 0.91, 95% CI = 0.85 to 0.97).
- Breast cancer survivors experienced lower ASCVD risk during the first 7.5 years after diagnosis, but risk gradually increased afterward (Pnonlinearity = .01).
- ASCVD risk increased over time among patients with cancers of the colorectum (P = .003), lung (P = .002), and endometrium (P = .04).
- No statistically significant association with ASCVD risk was observed for cancers of the oral cavity and pharynx, kidney, or ovary; sarcoma; melanoma; or leukemia.
Limitations: Observational cohort design cannot establish causality.; Potential for residual confounding despite multivariable adjustment.; Cohorts consist of nurses and health professionals, which may limit generalizability to other populations.; Abstract does not report details on cancer stage or treatments, which could influence ASCVD risk..
AI summary of the abstract, human-reviewed Β· Jun 2026. Describes what this study reported, not medical advice. View on PubMed Β· Full text
Human Β· observationalReported positiveLimited evidenceTier 3 Β· early human
Nature medicine Β· Jul 2025 Β· meta-analysis (Burden of Proof meta-regression)
colorectal cancer
This Burden of Proof meta-regression analyzed associations between processed meat, sugar-sweetened beverages (SSBs), and trans fatty acids (TFAs) and risks of type 2 diabetes, ischemic heart disease (IHD) and colorectal cancer. The authors reported conservative estimates that processed meat intake was associated with at least an 11% increase in type 2 diabetes risk and a 7% increase in colorectal cancer risk; SSBs with at least an 8% increase in type 2 diabetes risk and a 2% increase in IHD risk; and TFAs with at least a 3% increase in IHD risk. The associations were given two-star ratings indicating weak or inconsistent input evidence, and the authors note further research is needed while recommending limiting consumption given disease burden.
Reported effects: average increase in type 2 diabetes risk (processed meat, 0.6-57 g/day) 11% Β· average increase in colorectal cancer risk (processed meat, 0.78-55 g/day) 7% Β· +3 more
Key findings
- Processed meat (0.6-57 g/day) was associated with at least an 11% average increase in type 2 diabetes risk (relative to zero consumption).
- Processed meat (0.78-55 g/day) was associated with at least a 7% average increase in colorectal cancer risk (relative to zero consumption).
- SSB intake (1.5-390 g/day) was associated with at least an 8% average increase in type 2 diabetes risk (relative to zero consumption).
- SSB intake (0-365 g/day) was associated with at least a 2% average increase in ischemic heart disease (IHD) risk (relative to zero consumption).
- TFA consumption (0.25-2.56% of daily energy intake) was associated with at least a 3% average increase in IHD risk (relative to zero consumption).
- Each association received two-star ratings reflecting weak relationships or inconsistent input evidence; authors recommend further research and continuing recommendations to limit consumption given high chronic disease burden.
Limitations: Findings are based on meta-regression of existing studies rather than randomized trials, so causal inference is limited.; The authors rate the associations as two-star, indicating weak or inconsistent input evidence.; Dose-response characterization is described as limited and the results are presented as conservative estimates relative to zero consumption..
AI summary of the abstract, human-reviewed Β· Jul 2026. Describes what this study reported, not medical advice. View on PubMed
Meta-analysisReported positiveStrong evidenceTier 4 Β· clinicaln = 60
GeroScience Β· Jun 2025 Β· meta-analysis of prospective studies
colorectal cancercolon cancerrectal cancer
This meta-analysis pooled 60 prospective studies to evaluate associations between red, processed, and total meat consumption and colorectal, colon, and rectal cancer risk. Higher intake of red, processed, and total meat was each associated with modestly increased hazard ratios for colorectal, colon, and rectal cancer in the pooled analyses.
Reported effects: Red meat - colon cancer HR 1.22 [1.15β1.3] Β· Red meat - colorectal cancer HR 1.15 [1.1β1.21] Β· +7 more
Key findings
- Red meat consumption was associated with increased risk of colon cancer (HR = 1.22, 95% CI 1.15-1.30), colorectal cancer (HR = 1.15, 95% CI 1.10-1.21), and rectal cancer (HR = 1.22, 95% CI 1.07-1.39).
- Processed meat consumption was associated with increased risk of colon cancer (HR = 1.13, 95% CI 1.07-1.20), colorectal cancer (HR = 1.21, 95% CI 1.14-1.28), and rectal cancer (HR = 1.17, 95% CI 1.05-1.30).
- Total meat consumption was associated with increased risk of colon cancer (HR = 1.22, 95% CI 1.11-1.35), colorectal cancer (HR = 1.17, 95% CI 1.12-1.22), and rectal cancer (HR = 1.28, 95% CI 1.10-1.48).
Limitations: Observational prospective studies cannot establish causation; associations may reflect residual confounding.; Potential heterogeneity across included studies (populations, exposure assessment, covariate adjustment) may affect pooled estimates.; Dietary measurement error and misclassification in the original studies may bias results.; Abstract does not report dose-response specifics or uniform exposure definitions across studies..
AI summary of the abstract, published automatically under the strong-evidence tier Β· Jul 2026; an editor has not yet reviewed it. Describes what this study reported, not medical advice. View on PubMed Β· Full text
Human Β· observationalReported positiveLimited evidenceTier 3 Β· early humann = 10
BMC cancer Β· Dec 2024 Β· 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 [0.8β9.8], n=10 Β· partial responses 5, n=10 Β· +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 Β· Jun 2026. Describes what this study reported, not medical advice. View on PubMed Β· Full text
Human Β· observationalSupportive careInconclusiveLimited evidenceTier 3 Β· early humann = 9
Injury Β· Nov 2024 Β· retrospective cohort study
Supportive careuterine leiomyosarcomabone metastasis (appendicular)
This is a retrospective review of nine patients with appendicular bone metastases from uterine leiomyosarcoma treated at a single center between 2004 and 2021. The study compared palliative surgical management versus conservative treatment and found no difference in survival between the groups. Bone metastases occurred a mean of 33.3 months after diagnosis, and six of nine patients died after bone metastasis. The authors recommend individualized assessment before palliative surgery.
Reported effects: cohort_patients_meeting_initial_inclusion 114, n=114 Β· patients_with_appendicular_metastases 9, n=9 Β· +11 more
Key findings
- One hundred fourteen patients diagnosed with uterine leiomyosarcoma and treated at the Department of Oncologic Orthopedics at XXX hospital from 2004 to 2021 met the criteria for inclusion in this retrospective cohort study.
- Notably, the study included nine follow-up patients with at least 2 years of follow-up who developed appendicular skeletal metastases during the follow-up period.
- Of the 9 patients, 3 had humeral metastases, 2 had femoral metastases, 1 had femoral and diffuse pelvic metastases, and the other 3 had pelvic metastases.
- Bone metastases occurred at a mean of 33.3 ± 32.4 months (range 3 - 108) after the diagnosis.
- After bone metastasis, 6 patients died after an average of 40.3 ± 26.7 months (range 12-84 months).
- Surgical interventions included: 1 patient with a pathologic fracture in the proximal humerus underwent resection arthroplasty, 1 patient with metastases in the proximal femur underwent resection arthroplasty, 2 patients with metastases to the femoral shaft underwent curettage-cementation (C&C) and intramedullary nailing, and 1 patient with persistent pelvic pain underwent C&C. No surgery was performed in the other patients.
- Conclusion reported: survival did not differ between palliative surgery and conservative treatment after appendicular bone metastases.
Limitations: Retrospective, single-center design; Very small analytic sample (n=9) of patients with appendicular metastases; Potential selection bias (excluded patients with only vertebral metastases); No randomized allocation to surgical versus conservative management; Abstract provides no statistical test results or p-values to support the stated comparison; Level IV evidence.
AI summary of the abstract, human-reviewed Β· Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Human Β· observationalMechanismReported positiveLimited evidenceTier 3 Β· early humann = 32
Anticancer research Β· Aug 2024
uterine leiomyosarcoma
The authors analyzed Hippo pathway components (YAP1 and TAZ by immunohistochemistry and YAP1 by FISH) in tumor samples from 32 patients with uterine leiomyosarcoma. They found Hippo signaling dysregulation in 20/32 patients (62.5%), nuclear YAP1 expression in 17/32 (53.1%), and YAP1 amplification in 8/32 (25%). The study reports a trend suggesting Hippo pathway deregulation is a positive prognostic factor for overall survival.
Reported effects: Hippo signaling dysregulation 62.5%, n=32 Β· Nuclear YAP1 expression (IHC) 53.1%, n=32 Β· +1 more
Key findings
- Hippo signaling was found to be dysregulated in 20 (62.5%) patients with uLMS.
- Nuclear expression of YAP1 was detected in 17 (53.1%) of the 32 patients with immunohistochemistry.
- YAP1 amplification was found in 8 (25%) patients.
- Regarding OS the authors detected a trend of Hippo deregulation, designating it as a positive prognostic factor.
Limitations: Small sample size (n=32).; Observational, tissue-based study without reported statistical measures (no p-values, HRs, CIs provided in abstract).; Abstract does not report results for TAZ despite stating it was analyzed.; No details on multivariate analysis or adjustment for confounders are provided in the abstract.; Prognostic finding described as a 'trend' with no quantitative survival data in the abstract..
AI summary of the abstract, human-reviewed Β· Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewMechanismInconclusiveLimited evidenceTier 4 Β· clinical
Yi chuan = Hereditas Β· Aug 2024 Β· review
uterine leiomyosarcoma
This article is a review of the molecular pathology of uterine leiomyosarcoma (uLMS). The authors summarize molecular genetic features, epigenetic variants, experimental models, and clinical research progress, and note that understanding of uLMS pathogenesis is inadequate and disease models are limited, which hinders development of effective therapies.
Key findings
- uLMS is an aggressive malignant soft-tissue tumor arising from the myometrium that is difficult to distinguish from benign leiomyoma in early stages and has a poor prognosis.
- Current studies of uLMS pathogenesis and disease biology are inadequate.
- uLMS disease models are very limited, which hinders development of effective therapeutics.
- The review systematically summarizes molecular genetic features, epigenetic alterations, experimental models, and clinical research progress, and discusses directions including tumor evolution, the tumor microenvironment, and therapy development.
Limitations: This publication is a review and does not present new primary experimental or clinical data.; Abstract does not describe review methods in detail (e.g., search strategy, inclusion criteria).; Field-level limitations noted by the authors include inadequate pathogenesis studies and limited disease models, which constrain conclusions about therapeutic development..
AI summary of the abstract, human-reviewed Β· Jun 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewMechanismMixed resultsLimited evidenceTier 4 Β· clinical
Cells Β· Jun 2024
uterine leiomyosarcoma
This is a narrative review summarizing current knowledge about uterine leiomyosarcoma (uLMS), including its poor prognosis and high rates of recurrence and metastasis. The authors discuss multiple biological pathways implicated in uLMS (DNA repair, immune checkpoints, protein kinases, hedgehog), the emerging roles of epigenetics and the epitranscriptome, biomarkers and diagnostic approaches (including AI and shear wave elastography), current medical management, and ongoing clinical trials. The abstract notes that drugs targeting abnormal pathway functions have been reported to improve survival but that chemotherapy resistance remains a major challenge.
Key findings
- uLMS has a poor prognosis with high rates of recurrence and metastasis; five-year survival reported between 25 and 76%, and survival approaches 10-15% for patients with metastatic disease at initial diagnosis.
- Multiple biological pathways are implicated in uLMS pathogenesis, including DNA repair defects, immune checkpoint pathways, protein kinases/intracellular signaling, and the hedgehog pathway.
- The review states that drugs that block abnormal functions of these pathways have been reported to remarkably improve survival in uLMS patients.
- Chemotherapy resistance remains a major unmet need, motivating the search for novel drugs that effectively target these pathways.
- The authors review emerging roles of epigenetics and the epitranscriptome, as well as serum markers, AI/machine learning approaches, shear wave elastography, current management options, and ongoing clinical trials.
Limitations: Narrative review rather than primary research β no original patient-level data presented.; Abstract does not state systematic review methods or a structured literature search, so selection bias in included literature is possible.; Broad scope synthesizes preclinical, early-phase, and clinical data together, which may mix evidence levels.; Survival ranges reported are wide and drawn from the literature rather than newly generated cohort data..
AI summary of the abstract, human-reviewed Β· Jun 2026. Describes what this study reported, not medical advice. View on PubMed Β· Full text