ArticleTranslational lung cancer research2026
Major histocompatibility complex II serves as a prognostic biomarker in resectable pulmonary sarcomatoid carcinoma: development of a prediction model.
Article in Translational lung cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Pulmonary sarcomatoid carcinoma (PSC) is a rare pulmonary malignancy, exhibiting a poor outcome even after complete resection. Major histocompatibility complex II (MHC-II) is a critical molecule in priming anti-tumor immunity, while its expression and the prognostic role in PSC have been rarely investigated. This study aimed to evaluate intratumoral MHC-II expression and assess its prognostic value in resected PSC for the development of MHC-II-based prediction models. Methods: In this retrospective study, we enrolled 86 patients with resected PSC. Immunohistochemistry (IHC) was used to evaluate MHC-II expression. Patients were randomly divided into training and validation cohorts. Least absolute shrinkage and selection operator (LASSO) regression was used to select predictors and construct prognostic models for progression-free survival (PFS) and overall survival (OS). Model performance was assessed using the area under the curve (AUC). Additionally, public RNA sequencing data (n=17) from Gene Expression Omnibus (GEO) were used for bioinformatics analysis. Results: We demonstrated positive MHC-II expression on both tumor cells (22.09%) and tumor-infiltrating lymphocytes (TILs) (36.05%). Higher expression of MHC-II on both tumor cells and TILs indicated longer PFS (P=0.005 and P=0.042) and OS. The MHC-II-based prognostic models showed performance in the validation cohort with AUC exceeding 0.70 for both PFS and OS. Bioinformatics analysis suggested that samples with high MHC-II expression had higher infiltration levels of CD4 Conclusions: Our study uncovered the expression of MHC-II and its prognostic role in PSC. High expression of MHC-II might induce an inflamed tumor microenvironment (TME). And anti-PD-1 treatment might be a promising treatment for MHC-II
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