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Mitogen response transcripts, commonly known as immediate early genes (IEGs), represent a class of genes that are rapidly and transiently induced in response to extracellular stimuli such as growth factors, cytokines, and mitogens (Healy et al., 2013). These transcripts typically encode transcription factors, including members of the AP-1 complex (c-Fos, c-Jun) and c-Myc, which serve as critical molecular switches to initiate the transition from the G0 to the G1 phase of the cell cycle (Bahrami & Drabløs, 2016). In many pathological states, particularly cancer, the signaling pathways that trigger these transcripts—such as the Ras-Raf-MEK-ERK cascade—are constitutively active, leading to aberrant cell proliferation and survival (Alberts et al., 2014). While the transcripts themselves are generally considered a gene expression signature or a downstream effect rather than a single druggable protein target, they are vital indicators of pathway activity and are the ultimate targets of many kinase inhibitors. Monitoring the expression of these transcripts is frequently used in preclinical and clinical settings to assess the pharmacodynamic efficacy of drugs targeting mitogenic signaling pathways.
Inhibition of upstream signaling kinases (e.g., MEK1/2, ERK1/2) to suppress the transcriptional induction of mitogen-responsive genes.
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