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Gene expression programs in tumor cells refer to the coordinated regulation of sets of genes that collectively determine a cell's phenotype, state, and functional behavior within a malignancy. These programs, often identified through advanced single-cell transcriptomics, encompass critical biological processes such as the cell cycle, hypoxia response, and epithelial-to-mesenchymal transition (EMT), which collectively drive tumor progression, metastasis, and drug resistance (Gavish et al., 2023, Nature). While not a single molecular target like a receptor or enzyme, these programs represent the functional output of complex signaling and epigenetic networks that characterize the heterogeneity of cancer. Therapeutic strategies often aim to disrupt these programs by targeting master regulators, such as transcription factors or chromatin-modifying enzymes (e.g., HDACs or BET proteins), to shift tumor cells toward less aggressive states or induce programmed cell death (Barkley et al., 2022, Nature Genetics). Understanding and targeting these coordinated transcriptional outputs is a major focus of precision oncology and the development of combination therapies designed to overcome cellular plasticity.
Modulation of transcriptional networks and epigenetic landscapes to disrupt coordinated oncogenic gene expression patterns and revert malignant phenotypes.
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