MYB expression increases progressively in pancreatic cancer, correlating with advancing tumor grade, metastasis, and poor patient survival

The transcription factor MYB plays a pivotal role in regulating cell proliferation, differentiation, and survival. Although it is amplified in a subset of pancreatic cancers, emerging evidence indicates that MYB overexpression may also arise through diverse regulatory mechanisms. We have previously demonstrated multiple oncogenic roles of MYB in pancreatic cancer pathogenesis; however, the temporal dynamics of its dysregulation during tumor progression remain poorly understood. Here, we investigated MYB expression across a spectrum of tissue samples representing normal, precancerous, and malignant stages of the pancreas, as well as matched liver metastases, by performing immunohistochemical analysis. The differential expression of MYB and its correlation with advancing tumor grade and patient survival were assessed using appropriate statistical analyses. We observed negligible expression of MYB in the normal pancreas, and its aberrant expression became noticeable in precancerous lesions, increasing progressively as the disease advanced. A high expression of MYB was also reported in metastatic lesions. Elevated MYB levels were positively correlated with higher tumor grade and significantly associated with reduced survival of pancreatic cancer patients. Interestingly, functional enrichment analyses of genes regulated by MYB overexpression suggested its involvement in key oncogenic programs, including proliferation, survival, epithelial-mesenchymal transition, and metastatic signaling pathways. These findings demonstrate that MYB dysregulation occurs early in pancreatic tumorigenesis and intensifies with disease progression, underscoring its potential as a biomarker for tumor aggressiveness and a potential target for therapeutic intervention.