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Year : 2019  |  Volume : 32  |  Issue : 4  |  Page : 1485-1489

Tumor suppressor p53 gene codon 72 polymorphism and imatinib cytogenetic response in chronic myeloid leukemia

Department of Clinical Pathology, Faculty of Medicine, Menoufia University, Menoufia, Egypt

Correspondence Address:
Yasmin A. H Sadek Younis
Department of Clinical Pathology, Menoufia University, Shebein El Kom, Menoufia Governorate
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mmj.mmj_88_16

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Objective To study p53 codon 72 polymorphism in relation to cytogenetic response to imatinib treatment in patients with chronic myeloid leukemia (CML). Background P53 polymorphism involves the substitution of an arginine for a proline at codon position 72. Many studies have investigated a genetic link between this variation and response to treatment in cancer. Patients and methods This study was conducted on 54 CML patients presented to the Clinical Oncology Department, Menoufia University during the period from June 2013 to April 2015. They were classified according to their cytogenetic response to imatinib therapy into 40 CML patients, cytogenetic responders to imatinib and 14 CML patients who are cytogenetic nonresponders to imatinib. Patients were genotyped for p53 codon 72 polymorphism using PCR. Follow up of the patients should be done after 3, 6, 9, 12, and 18 months after diagnosis, and was done by complete blood count, conventional cytogenetic, and fluorescence in-situ hybridization. Results Age, sex, hematologic, and cytogenetic response to imatinib in CML patients did not differ significantly among p53 codon 72 genotypes (arg/arg, arg/pro, and pro/pro) (P = 0.44, P = 0.45, and P = 0.11, respectively). P53 codon 72 polymorphism did not significantly alter the risk to imatinib cytogenetic unresponsiveness (P = 0.9221). Conclusion It could be concluded that p53 codon 72 polymorphism is not associated with imatinib unresponsiveness in CML.

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