Reza Torshizi - Department of Modern Sciences and Technologies, Molecular Medicine Department, Faculty of Medicine, Mashhad University of Medical sciences, Mashhad, Iran.
Ehsan Ghayour Karimani - Molecular Diagnostic Unit, Research and Education Department, Razavi Hospital, Mashhad, Iran.
Kobra Etminani - Department of Medical Informatics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran, Iran.
Mohammad Mehdi Akbarin - Inflammation and Inflammatory Diseases Research Centre, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Khadijeh Jamialahmadi - 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 - Hematology Department, Ghaem Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Hossein Rahimi - Hematology Department, Ghaem Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Abolghasem Allahyari - Hematology Department, Imam Reza Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Amin Golabpour - Department of Medical Informatics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran, Iran
Houshang Rafatpanah - Inflammation and Inflammatory Diseases Research Centre, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Background: Adult T-cell leukemia/lymphoma (ATLL) is caused by human T-cell lymphotropic virus type-۱ (HTLV-۱). HTLV-۱ 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-۱ proviral load and the gene expression levels of cyclin-dependent kinase-۲ (CDK۲), CDK۴, p۵۳, and retinoblastoma (Rb) in ATLL and carriers groups. Methods: A total of twenty-five ATLL patients (۱۲ females and ۱۳ males) and ۲۱ asymptomatic carriers (۱۰ females and ۱۱ 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 CDK۲, CDK۴, p۵۳, and Rb. Statistical analysis was used to compare proviral load and gene expression levels between two groups, using SPSS version ۱۸. Results: The mean scores of the HTLV-۱ proviral load in the ATLL patients and healthy carriers were ۱۳۰۶۷.۲۰±۶۴۰۰.۴۱ and ۳۴۵.۷۹±۷۸.۸۰ copies/۱۰۴ cells, respectively (P=۰.۰۰۰). There was a significant correlation between the gene expression levels of CDK۲ and CDK۴ (P=۰.۰۱) 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 p۵۳ and CDK۴; accordingly, proviral load and expression levels of these genes may be useful in the assessment of disease progression and prediction of HTLV-۱ infection outcomes.

Adult T-cell leukemia/lymphoma, CDKs, HTLV-۱, p۵۳, Retinoblastoma