AU - Khalifa, Khaled
AU - Essa, Enas
AU - Shehata Radwan, Wafaa
AU - Elkholy, Enas
AU - Sadek Younis, Yasmin
TI - Tumor suppressor p53 gene codon 72 polymorphism and imatinib cytogenetic response in chronic myeloid leukemia
PT - ORIG
DP - 2019 Oct 1
TA - Menoufia Medical Journal
PG - 1485-1489
VI - 32
IP - 4
4099- http://www.mmj.eg.net/article.asp?issn=1110-2098;year=2019;volume=32;issue=4;spage=1485;epage=1489;aulast=Khalifa;type=0
4100- http://www.mmj.eg.net/article.asp?issn=1110-2098;year=2019;volume=32;issue=4;spage=1485;epage=1489;aulast=Khalifa
AB -
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.