Abstract
Loss of genomic stability in the cell due to defects in the checkpoint of DNA
damage, mitotic checkpoint, and telomere maintenance led to increased incidences of
base pair alterations. Therefore, that genomic instability plays a critical role in tumor
initiation and progression. Tumor progression requires a dynamic tumor/normal
exchange in their microenvironment to support tumor growth. The histological
alteration seen in the tumor at early stages confirms that the surface between the
epithelium and the stroma undergoes progressive disturbance. Tumor progression is
also affected by the immune system in which chronic inflammations promote the
growth of tumor. Tumor cells experience altered metabolic profiling to support their
growth. Cancer cells are characterized by uncontrolled cell division. For that, they
utilize glucose as a source of energy to help them grow faster than normal cells. Hence,
Glycolysis is a key metabolomics pathway consumed at a high rate during
carcinogenesis.