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MOLECULAR BIOLOGY OF DPYD (DIHYDRO PYRIMIDINE DEHYDROGENASE) AND OVERVIEW OF MUTATIONS AND POLYMORPHISM IN VARIOUS CANCERS

Mutations of the DPD gene results in severe DPD deficiency, DPD deficient patients have shown splice-site polymorphism, DPD * 2A,IVS14+G>A (i.e., a G to A alteration in the nucleotide at the exon14 acceptor splice site), c.1905+1G>A, IVS14+17A>G, c.1796T>C, 2846A>T, 96A>G, 1845G>T. These mutations interfere with the breakdown of uracil and thymine and result in excess quantities of these molecules in the blood, urine, and the fluid that surrounds the brain and spinal cord (cerebrospinal fluid). It is unclear how the excess uracil and thymine are related to the specific neurological problems that affect some people with dihydropyrimidine dehydrogenase deficiency. Mutations in the DPYD gene also interfere with the breakdown of drugs with structures similar to the pyrimidines, such as the cancer drugs 5-fluorouracil and capecitabine. As a result, these drugs accumulate in the body and cause the severe reactions that can occur in people with dihydropyrimidine dehydrogenase deficiency. Symptoms included severe neutropenia, thrombocytopenia, mucositis and diarrhoea. Here we conducted the literature survey which have been published from 2000 to 2012 on such polymorphism and there risk of developing toxicities in various populations.