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Cancer at the molecular level - Essay Example

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Cancer at Molecular Level Introduction Cancer, also known as malignant neoplasm, the hallmark characteristic involves uncontrolled proliferation of cells. Under normal conditions cell grow, divide and die, but in cancer cells the defect takes place at the gene level leading to the formation of an abnormal DNA…
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Cancer at the molecular level
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Download file to see previous pages (Normal cell cycle) (Genetic mutation- causes alteration in genes) (Alberts, 2007) Cancer is a genetic phenomenon that onsets as a result of trigger in the signal transduction of normal cell cycle, causing alteration in the cellular pathway for uncontrolled proliferation figuring malignant tumors. Cancer cells are not confined to one location and they turn invasive, spread to the nearby tissues initially and gradually their seedlings are carried to different parts/ organs of the body via lymph or blood causing invasion of the cancer to other tissues and organs. This stage is called metastasis. On the contrary, some cancer cells do not display uncontrolled growth, they are non-invasive and do not spread, such stage of cancer only forms benign tumors (Alberts, 2007). Cancer Proliferation Cancer is initiated in the cell, the basic unit of any living entity. Under normal conditions the cell follow the regular cell cycle but any chemical, physical or biological agent may trigger the conversion of proto-oncogene to oncogene, the active form of cancer causing gene which is responsible for the altered metabolism of the cell. The genetic basis of cancer has been revealed through numerous animal models. The human Genome Project aids in improving preclusion, analysis and management of cancer with better efficacy (Luo, 2008). Luo et al (2008) have identified essential genes in 12 cancer cell lines, they were exploited to find the presumed and established oncogenes such as KRAS, EGFR, MYC, MYB, BCR-ABL, CDK4 and CRKL that are vital for cancer cell proliferation and are found to be altered in the human cancers. Their findings postulate that tumoricidal agents trigger the expression of four genes PTPN1, NF1, SMARCB1, and SMARCE1. Moreover, five regulators are also activated in response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1. The information is beneficial for pursuing future cancer studies as well as for therapeutics. A comparative study between normal stem cells and cancer stem cells states that signal transduction namely Bmi1 and Wnt are shared by the normal as well as cancer stem cells for cellular proliferation. Perception and thorough understanding for cancer stem cells will certainly aid in recognition of the drug targets and cancer therapeutics (Lobo, 2007). Basis of cancer Any mutation may result in abnormal proliferation. However, mutations are generally insignificant and mutant cells are eradicated but accretion of mutation may occur in dividing cells resulting in cancer. Cancer causing mutation directly influence the cellular machinery including the genetic damage as well as signaling pathways and hence the entire cell division process is affected. As stem cells are pluripotent, long-lived as compared to their short lived descendant cells, they are vulnerable to the genotoxic elements causing oncogenic mutations (Pardal et al, 2003). Observations reveals that cancer tends to relapse after treatment. The genetic basis that has been postulated encompass the involvement of cancer stem cells. Research disclose that cancer stem cells play a pivotal role in cancer relapse as stem cells are not targeted by the conventional drugs and as these cancer stem cells are pluripotent they have potential to divide thereby generating tumor again. Much understanding of the cancer could be procured ...Download file to see next pagesRead More
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