Hallmarks of Cancer Cell

Abstract

The fascinating complexity of a cancer cell is derived collectively from six basic alterations of cell physiology that result in sustained malignant proliferation (Hanahan and Weinberg 2000). However in in vitro cancer cells, four of the variations are easily detectable in yielding a phenotype of persistent proliferation and aversion from apoptosis. Cell migration/metastasis and angiogenesis are the other two which may be only observed in vivo. Genetic mutations in proto-oncogenes, onco-suppressors, and environmental conditions like hypoxia or inflammation contribute to malignant growth. The loss of tumor suppressor genes (TSG) by mutation may contribute to uncontrolled cell growth leading to cancer. Similarly proto-oncogenes are active in the signaling pathway for cell growth, and on mutation they transform into oncogenes triggering nonstop cell divisions leading to hyper-proliferation. Data implies that tumor cells are different from normal cells in at least six ways relating to growth control: sustaining proliferative signaling, evading growth suppressors, resisting cell death, inducing angiogenesis, invading replicative immortality, and activating invasion and metastasis (Hanahan and Weinberg 2011) (Fig. 2.1).