ArticleGynecologic oncology2023
Impact of immune infiltration signatures on prognosis in endometrial carcinoma is dependent on the underlying molecular subtype.
Article in Gynecologic oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- Transcriptomic Evidence of Immune-Tumor Uncoupling Defines a High-Risk State in Uterine Corpus Endometrial Carcinoma.International journal of molecular sciences · 2026Article
- IMPDH1 is a potential immune evasion-related oncoprotein in endometrial cancer.BMC genomic data · 2026Article
- TAMs in the Gynecological Tumor Microenvironment: Insights from Cross-Cancer Studies for Immunotherapy.Cancers · 2026Review
- Genomic and Transcriptomic Analysis of High-Grade Endometrial Carcinoma Reveals Biological Heterogeneity and Molecular Classification Challenges.Cancer research communications · 2026Article
- ATM immunohistochemistry as an effective screening method for POLE variants among endometrial carcinomas lacking mismatch repair deficiency and p53 abnormalities.The journal of pathology. Clinical research · 2026Article
- UnveilingTranslational cancer research · 2025Article
- Impact of molecular and immune signature on endometrial biopsies with atypical hyperplasia with and without concurrent endometroid carcinoma.Gynecologic oncology reports · 2025Article
- The protective role of γδ T cells in endometrial cancer.Cancer immunology, immunotherapy : CII · 2025Article
- Molecular mechanism of tumor-infiltrating immune cells regulating endometrial carcinoma.Genes & diseases · 2025Review
- Unveiling immunogenic characteristics and neoantigens in endometrial cancer with POLE hotspot mutations for improved immunotherapy.Frontiers in immunology · 2025Article
- GGTLC1 knockdown inhibits the progression of endometrial cancer by regulating the TGF-β/Smad signaling pathway.Heliyon · 2024Article
- Body mass index and adiposity influence responses to immune checkpoint inhibition in endometrial cancer.medRxiv : the preprint server for health sciences · 2024Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
objectivesIncreased numbers of tumor infiltrating lymphocytes (TIL) in endometrial cancer (EC) are associated with improved survival, but it is unclear how this prognostic significance relates to the underlying EC molecular subtype. In this explorative hypothesis-generating study, we sought to define the immune signatures associated with the molecular subtypes of EC (i.e., POLE-mutated, microsatellite unstable (MSI-high), copy number (CN)-low, and CN-high) and to determine their correlation with patient outcomes.
methodsRNA-sequencing and molecular subtype data of 232 primary ECs were obtained from The Cancer Genome Atlas. Deconvolution of bulk gene expression data was performed using single sample Gene Set Enrichment Analysis (ssGSEA) and Cell type Identification By Estimating Relative Subsets Of known RNA Transcripts (CIBERSORT). The association of the resultant immune signatures with overall survival was determined across molecular subtypes.
resultsStatistically significant differences in enrichment were identified in 16/30 and 6/23 immune gene sets by ssGSEA and CIBERSORT, respectively. Signature of CD8+ cells in ECs of CN-high molecular subtype was associated with improved overall survival by ssGSEA (p = 0.0108), while CD8 signatures did not appear to be prognostic in MSI-high (p = 0.74) or CN-low EC molecular subtypes (p = 0.793). Of all molecular subtypes, CN-high ECs exhibited the lowest levels of CD8+ T cell infiltration. Consistent with antigen-induced T cell activation and exhaustion, enrichment for immunomodulatory receptors was predominantly observed in ECs of MSI-high and POLE-mutated molecular subtypes.
conclusionsDeconvolution of bulk gene expression data can be used to identify populations of immune infiltrated endometrial cancers with improved survival. These data support the existence of unique mechanisms of immune resistance within molecular subgroups of the disease.
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