ArticleFunctional & integrative genomics2023
Identification and validation of TME-related signatures to predict prognosis and response to anti-tumor therapies in skin cutaneous melanoma.
Article in Functional & integrative genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Construction of a prognostic risk-scoring model based on SASP-related genes in patients with skin cutaneous melanoma.Discover oncology · 2025Article
- Article
- Construction and Identification of an NLR-Associated Prognostic Signature Revealing the Heterogeneous Immune Response in Skin Cutaneous Melanoma.Clinical, cosmetic and investigational dermatology · 2023Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor microenvironment (TME) dynamically regulates cancer progression and affects clinical outcomes. This study aimed to identify molecular subtypes and construct a prognostic risk model based on TME-related signatures in skin cutaneous melanoma (SKCM) patients. We categorized SKCM patients based on transcriptome data of SKCM from The Cancer Genome Atlas (TCGA) database and 29 TME-related gene signatures. Differentially expressed genes were identified using univariate Cox regression and Lasso regression analysis, which were used for risk model construction. The robustness of this model was validated in independent external cohorts. Genetic landscape alterations, immune characteristics, and responsiveness to immunotherapy/chemotherapy were evaluated. Three TME-related subtypes were identified, and subtype C3 exhibited the most favorable prognosis, had enriched immune-related pathways, and possessed more infiltration of T_cells_CD8, T_cells_CD4_memory_activated, and Macrophages_M1 but a lower TumorPurity, whereas Macrophages_M2 were increased in subtype C1 and subtype C2. Subtype C1 was more sensitive to Cisplatin, subtype C2 was more sensitive to Temozolomide, and subtype C3 was more sensitive to Paclitaxel; 8 TME-related genes (NOTCH3, HEYL, ZNF703, ABCC2, PAEP, CCL8, HAPLN3, and HPDL) were screened for risk model construction. High-risk patients had dismal prognosis with good prediction performance. Moreover, low-risk patients were more sensitive to Paclitaxel and Temozolomide, whereas high-risk patients were more sensitive to Cisplatin. This risk model had robustness in predicting prognosis in SKCM patients. The results facilitate the understanding of TME-related genes in SKCM and provide a TME-related genes-based predictive model in prognosis and direction of personalized options for SKCM patients.
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