What Does Proto-Oncogene Cause Cancer?

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1. Introduction
Cancer develops when mechanisms regulating cell division, proliferation and differentiation are lost. Most cells in the body can turn into malignant cells under specific conditions, but as the understanding about the mechanisms causing malignant tumors to develop increases, prospects for prevention, detection and treatment are improving correspondingly (Casey, 2012).
The most common form of cancer in developed countries is non-melanoma skin cancer, while lung cancer causes the most deaths in both developed and developing countries (World Health Organisation, 2011).
Although the knowledge about the molecular mechanisms of cancer progression and advancement has thoroughly improved, the disease still remains a prevalent health
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Cells provide many mechanisms to detect and repair DNA damage but these may be exhausted over prolonged exposure, overwhelmed by massive exposure or directly affected by exposure to a carcinogen. Key damage to DNA that results in a cancer-causing mutation occurs where there is activation of proto-oncogenes to oncogenes, or inactivation of tumor-suppressor genes (TSGs). Proto-oncogenes control cell proliferation, differentiation and apoptosis, an oncogene is a mutated form of this gene which triggers proliferative activity and leads to tumor formation. Tumor suppressor genes monitor and correct malignant change, therefore their loss is a significant step in the development of cancer (Casey, …show more content…
These typical features have been summarized in a paper by Hanahan and Weinberg (Hanahan et al., 2000) as the hallmarks of cancer. The hallmarks of cancer include initially six biological abilities gained during the multistep transformation of normal cells to cancer (malignant or tumor) cells. The hallmarks include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Fundamental to those hallmarks are two additional traits, genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which promotes multiple hallmark functions. Progress in the last years has further added two arising hallmarks to the list - reprogramming of energy metabolism and evading immune destruction. An additional property of tumors in comparison to cancer cells adds further complexity to the scene: tumors contain a variety of recruited, apparently normal cells that provide the acquisition of hallmark traits by forming a “tumor microenvironment” (Hanahan and Weinberg, 2011) (Casey,

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