The DNA lesion repair enzyme, O6-methylguanine-DNA methyltransferase (MGMT) is essential for reverting mispaired lesions to maintain genomic stability. While MGMT expression is present in all normal tissues, its expression is heterogeneous in tumors. MGMT promoter hypermethylation and reduced MGMT protein appear to be early events in tumorigenesis and are associated with poor tumor differentiation. Epigenetic silencing may lead to transition mutations in p53, K-ras, and PIK3CA.
The independent prognostic value of MGMT varies in different tumors. Reduced or loss of MGMT expression was correlated with poor outcomes in breast ductal adenocarcinoma, gastric cancers, hepatocellular carcinoma, and lung carcinoma. Approximately 31% of endometrial and 25-37% of lung carcinomas demonstrated loss of MGMT expression. Conversely, MGMT deficiency predicted favorable treatment and survival in glioblastoma and melanoma, while positive MGMT expression associated with poor survival in basal-like breast cancer patients.
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MGMT (EP337)
Rabbit Monoclonal
The DNA lesion repair enzyme, O6-methylguanine-DNA methyltransferase (MGMT) is essential for reverting mispaired lesions to maintain genomic stability. While MGMT expression is present in all normal tissues, its expression is heterogeneous in tumors. MGMT promoter hypermethylation and reduced MGMT protein appear to be early events in tumorigenesis and are associated with poor tumor differentiation. Epigenetic silencing may lead to transition mutations in p53, K-ras, and PIK3CA.
The independent prognostic value of MGMT varies in different tumors. Reduced or loss of MGMT expression was correlated with poor outcomes in breast ductal adenocarcinoma, gastric cancers, hepatocellular carcinoma, and lung carcinoma. Approximately 31% of endometrial and 25-37% of lung carcinomas demonstrated loss of MGMT expression. Conversely, MGMT deficiency predicted favorable treatment and survival in glioblastoma and melanoma, while positive MGMT expression associated with poor survival in basal-like breast cancer patients.
Rabbit Monoclonal
The DNA lesion repair enzyme, O6-methylguanine-DNA methyltransferase (MGMT) is essential for reverting mispaired lesions to maintain genomic stability. While MGMT expression is present in all normal tissues, its expression is heterogeneous in tumors. MGMT promoter hypermethylation and reduced MGMT protein appear to be early events in tumorigenesis and are associated with poor tumor differentiation. Epigenetic silencing may lead to transition mutations in p53, K-ras, and PIK3CA.
The independent prognostic value of MGMT varies in different tumors. Reduced or loss of MGMT expression was correlated with poor outcomes in breast ductal adenocarcinoma, gastric cancers, hepatocellular carcinoma, and lung carcinoma. Approximately 31% of endometrial and 25-37% of lung carcinomas demonstrated loss of MGMT expression. Conversely, MGMT deficiency predicted favorable treatment and survival in glioblastoma and melanoma, while positive MGMT expression associated with poor survival in basal-like breast cancer patients.
