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Tumor cell metabolic and proliferative pathways represent a broad set of interconnected biological processes that enable cancer cells to sustain rapid growth, survival, and adaptation to the microenvironment. Unlike normal quiescent cells, tumor cells undergo significant metabolic reprogramming, most notably the Warburg effect, where they prioritize aerobic glycolysis and glutaminolysis to generate the building blocks required for biomass synthesis (Hanahan & Weinberg, 2011, Cell). These pathways are regulated by key signaling nodes such as the PI3K/AKT/mTOR axis and the MYC oncogene, which coordinate nutrient uptake with cell cycle progression (Vander Heiden et al., 2009, Science). Because this term encompasses a wide array of enzymes, transporters, and signaling proteins rather than a single molecular entity, it is considered a therapeutic category rather than a specific drug target. Therapeutic strategies in this area involve the use of small molecules or antibodies to inhibit specific rate-limiting enzymes or receptors within these cascades (Pavlova & Thompson, 2016, Cell Metabolism). However, the high degree of overlap between tumor and normal cell metabolism often presents a significant challenge for achieving a wide therapeutic window (DeBerardinis & Chandel, 2016, Science).
Inhibition of specific enzymes (e.g., DHFR, Thymidylate synthase) and signaling proteins (e.g., mTOR, AKT) that regulate nutrient acquisition, nucleotide synthesis, and mitotic progression.
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