![]() MUC16 expression correlates with disease progression and metastasis, such as pancreatic cancer, colorectal cancer, and gastric adenocarcinoma. It is found on the surface of many ovarian cancer cells. Furthermore, titin (TTN), TP53, KRAS proto-oncogene and GTPase (KRAS), epidermal growth factor receptor, Kelch-like ECH-associated protein (KEAP1) have significant relevance with the carcinogenesis and prognosis in LUAD patients.Ĭarcinoma antigen-125 (CA125), also known as mucin 16 (MUC16), is a glycoprotein from the mucin family. This includes the CUB and Sushi multiple domains protein 3 (CSMD3) mutations in ovarian cancer, the mucin 4 mutations in colon cancer, ryanodine receptor 2 in breast cancer, tumor protein P53 (TP53) in prostate cancer and hepatocellular carcinoma, etc. Several genetic variants have been reported to affect the relative risk of different cancers. Identifying the driver mutations in the tumor cells of a cancer patient is crucial in precision cancer treatment. Recent studies have depicted that TMB was significantly positively associated with immune checkpoint blockade across 27 cancer types. A non-synonymous somatic mutation can contribute to cancer development and cause the immune system to mount an antitumor response to the tumor. Tumor mutation burden (TMB) depicts the total number of somatic mutations on a cancer genome per megabase. Therefore, identifying the predictive biomarkers for ICI response can help explore strategies for tumor immunotherapy. This is due to that more than one-half of patients are either insensitive or relapse after a response period, seriously limiting ICI effectiveness. However only a subset of LUAD patients could benefit from ICI treatment. Even though cancer immunotherapy provides new treatment options by integrating conventional and targeted therapies, such as immune checkpoint inhibitors (ICIs), which can block the inhibitory programmed cell death protein 1 and programmed death ligand 1 (PD-1/PD-L1) immune checkpoint axis and has a prominent and durable response in some LUAD patients. Lung adenocarcinoma (LUAD) is makes up approximately half of all lung cancers. Lung cancer ranks among the top ten causes of cancer-related deaths in both men and women. Our project developed a robust risk signature depending on the MUC16 status and provided novel insights for individualized treatment options for LUAD patients. Moreover, the nomogram using the IPM and clinical prognostic factors also predicted the overall survival and clinical utility. Elevated expressions of PD-L1, LAG3, PDCD1, and SIGLEC15, and most of the T-effector and interferon-γ gene signatures, were depicted in the high-risk group. The univariate and multivariate Cox regression analyses demonstrated that the IPM was an independent prognostic indicator for LUAD patients. Based on 436 patients with LUAD, an IPM was established and validated to differentiate patients with a low or high risk of poor survival. MUC16 was frequently mutated in LUAD, with a mutational frequency of 43.4%, significantly associated with higher TMB and better clinical prognosis. Later, the IPM effect on the prognosis and immunotherapy of LUAD was comprehensively evaluated. ![]() An immune prognostic model (IPM) was developed based on immune-related genes that could be differentially expressed between MUC16 MUT and MUC16 WT LUAD patients. All the data were obtained from the cancer genome atlas database to assess the prognostic value and potential mechanism of MUC16 in LUAD. However, whether MUC16 mutations are associated with TMB and tumor-infiltrating immune cells in LUAD is not fully elucidated. It is known that the mucin 16 (MUC16) mutation is the most common and affects the progression and prognosis of several cancers. Immunotherapy is a promising candidate for LUAD, and tumor mutation burden (TMB) could be a new biomarker to monitor the response of cancer patients to immunotherapy. Lung adenocarcinoma (LUAD) is a non-small-cell lung cancer and is the leading cause of cancer-related deaths worldwide.
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