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Biological and clinical implications of codon 72 p53 genotypes in Indian chronic myeloid leukemia patients

Pragya Saini , Pragya Saini

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New Indian Journal of Surgery 2(4):p 348-348, October-December 2011. | DOI:

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Abstract

 Chronic myeloid leukaemia (CML) is characterized by the increased and unregulated growth of myeloid cells in the bone marrow and the accumulation of these cells in the blood. In 95% of cases it is caused by the product of the BCR-ABL oncogene, located on the Philadelphia (Ph) chromosome, which is generated as a result of a reciprocal t(9;22) chromosomal translocation. P53 is a tumor suppressor gene involved in DNA repair, induction of growth arrest and apoptosis. The p53 gene is the most commonly mutated tumor suppressor gene in human cancers. In addition to the loss of tumor suppression activity, gain of function mutations in p53 can promote tumorigenesis and drug resistance in various types of human cancers. A common p53 polymorphism occurs at codon 72 of exon 4, with two alleles encoding either arginine(CGC) or proline(CCC). This polymorphism is associated with leukemia susceptibility

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