Investigation of P16INK4A and P14RF Genes Expression in Different Phase of Chronic Myeloid Leukemia (CML)

• Main Authors: SA Mousavi, M Iravani, A Ghavamzadeh, K Alimoghadam, N Shayan, H Dargahi, Y Mortazavi, SH Mousavi, SH Ghaffari
• Format: Article
• Language: fas
• Published: Tehran University of Medical Sciences 2008-08-01
• Series: پیاورد سلامت
• Subjects: Chronic Myeloid Leukemia; P16INK4A; P14ARF; RT-PCR
• Online Access: http://journals.tums.ac.ir/PdfMed.aspx?pdf_med=/upload_files/pdf/13546.pdf&manuscript_id=13546

Background & Aim : Chronic myeloid leukemia (CML) is a disorder of pluripotential hematopoietic stem cell that is as a myeloproliferative disease and occurs in about 15 percent of all leukemia. Two cell cycle regulatory proteins that function as tumor suppressor are P16INK4A and P14ARF. The origin of these two proteins is a human INK4A-ARF gene locus that located on chromosome 9p21. P16INK4A control retinoblastoma (Rb) and P14ARF control with p53 thought negative feedback. The purposes of this study, this was that whether these genes are preferable use as a factor in prognosis and progression of disease.Materials and Methods: This research was a Cross sectional study. The expression of p16INK4A and p14ARF mRNA in about 73 peripheral bloods (PB) Samples were collected from 45 CML patients at different phases of disease were assayed by reverse transcriptase polymerase chain reaction (RT-PCR). 26 samples were from patients at chronic phase before any treatment, 26 samples 3 month after treatment with imatinib, 9 samples in accelerated phase and 12 samples in Blastic phase.Results. From 45 patients with CML, 33 patients (73%) were men and 12 patients (27%) were women. About 26 samples (35%) were p16INK4A positive and 55 samples (75%) were p14ARF RT-PCR positive. This expression of the two genes at different phases of disease were not statistically significant (p>0.05).Conclusion: High percentage of the CML patients expressed P14ARF and P16INK4A genes. The expression of these gene at different phases of disease (diagnosis, accelerate, and Blastic phases) was not statistically significant; even though, the expression of these genes was higher after the treatment. The increased expression of these genes was probably because of the Imatinib treatment.