Abstract

CANCER AS A METABOLIC DISORDER

Pravin Kumar Gupta*

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Abstract

Traditionally, oncogenes and tumor suppressor genes have been thought to be the main genetic causes of cancer. Nonetheless, mounting data points to a key role for dysregulated cellular metabolism in the initiation and spread of cancer. The Warburg effect, which shows that even in the presence of enough oxygen, cancer cells preferentially choose aerobic glycolysis over oxidative phosphorylation, is an example of this paradigm shift. Elevated glutamine metabolism, changed fatty acid synthesis, and enhanced glucose absorption and fermentation to lactate are important metabolic changes in cancer cells. Mutations in tumor suppressors like p53 and oncogenes like c-Myc and KRAS, which converge on signaling pathways like PI3K/Akt and HIF-1α, are frequently the cause of these alterations. The idea that cancer is a metabolic disease has significant ramifications for both diagnosis and treatment. The increased glucose consumption in tumors is used by metabolic imaging methods, such as PET scans using radio labelled glucose analogs, to detect them. Additionally, focusing on metabolic pathways presents innovative treatment approaches. Ketogenic diets, for example, try to stop cancer cells from getting glucose, which may limit the growth of tumors. Clinical evidence for these therapies is still developing, though.

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