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en Altered expression of cell cycle regulators in adult T-cell leukemia/lymphoma patients زیست شناسی ملکولی Molecular Biology مقالات اصلی Original Article <div style="text-align: justify;">Background: Adult T-cell leukemia/lymphoma (ATLL) is caused by human T-cell lymphotropic virus type-1 (HTLV-1). HTLV-1 oncogenes can induce malignancy through controlled gene expression of cell cycle checkpoints in the host cell. HTLV-I genes play a pivotal role in overriding cell cycle checkpoints and deregulate cellular division. In this study, we aimed to determine and compare the HTLV-1 proviral load and the gene expression levels of cyclin-dependent kinase-2 (CDK2), CDK4, p53, and retinoblastoma (Rb) in ATLL and carriers groups. Methods: A total of twenty-five ATLL patients (12 females and 13 males) and 21 asymptomatic carriers (10 females and 11 males) were included in this study. TaqMan real-time polymerase chain reaction assay was used for evaluation of proviral load and gene expression levels of CDK2, CDK4, p53, and Rb. Statistical analysis was used to compare proviral load and gene expression levels between two groups, using SPSS version 18. Results: The mean scores of the HTLV-1 proviral load in the ATLL patients and healthy carriers were 13067.20±6400.41 and 345.79±78.80 copies/104 cells, respectively (P=0.000). There was a significant correlation between the gene expression levels of CDK2 and CDK4 (P=0.01) in the ATLL group. Conclusions: Our findings demonstrated a significant difference between the ATLL patients and healthy carriers regarding the rate of proviral load and the gene expression levels of p53 and CDK4; accordingly, proviral load and expression levels of these genes may be useful in the assessment of disease progression and prediction of HTLV-1 infection outcomes.</div> Adult T-cell leukemia/lymphoma, CDKs, HTLV-1, p53, Retinoblastoma 88 94 http://rbmb.net/browse.php?a_code=A-10-64-1&slc_lang=en&sid=1 Reza Torshizi 10031947532846006247 10031947532846006247 No Department of Modern Sciences and Technologies, Molecular Medicine Department, Faculty of Medicine, Mashhad University of Medical sciences, Mashhad, Iran. Ehsan Ghayour Karimani 10031947532846006248 10031947532846006248 No Molecular Diagnostic Unit, Research and Education Department, Razavi Hospital, Mashhad, Iran. Kobra Etminani 10031947532846006249 10031947532846006249 No Department of Medical Informatics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran, Iran. Mohammad Mehdi Akbarin 10031947532846006250 10031947532846006250 No Inflammation and Inflammatory Diseases Research Centre, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Khadijeh Jamialahmadi 10031947532846006251 10031947532846006251 No Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran - Department of Medical Biotechnology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Abbas Shirdel 10031947532846006252 10031947532846006252 No Hematology Department, Ghaem Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Hossein Rahimi 10031947532846006253 10031947532846006253 No Hematology Department, Ghaem Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Abolghasem Allahyari 10031947532846006254 10031947532846006254 No Hematology Department, Imam Reza Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Amin Golabpour 10031947532846006255 10031947532846006255 Yes Department of Medical Informatics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran, Iran Houshang Rafatpanah 10031947532846006256 10031947532846006256 No Inflammation and Inflammatory Diseases Research Centre, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.