Altered expression of cell cycle regulators in adult T-cell leukemia/lymphoma patients

سال انتشار: 1396
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 241

فایل این مقاله در 7 صفحه با فرمت PDF قابل دریافت می باشد

استخراج به نرم افزارهای پژوهشی:

لینک ثابت به این مقاله:

شناسه ملی سند علمی:

JR_RBMB-6-1_012

تاریخ نمایه سازی: 10 شهریور 1400

چکیده مقاله:

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.

نویسندگان

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.

مراجع و منابع این مقاله:

لیست زیر مراجع و منابع استفاده شده در این مقاله را نمایش می دهد. این مراجع به صورت کاملا ماشینی و بر اساس هوش مصنوعی استخراج شده اند و لذا ممکن است دارای اشکالاتی باشند که به مرور زمان دقت استخراج این محتوا افزایش می یابد. مراجعی که مقالات مربوط به آنها در سیویلیکا نمایه شده و پیدا شده اند، به خود مقاله لینک شده اند :
  • Kawano N, Yoshida S, Kuriyama T, Tahara Y, Yamashita K, ...
  • Yamashiro T, Kamiya H, Miyara T, Gibo S, Ogawa K, ...
  • Boostani R, Vakili R, Hosseiny SS, Shoeibi A, Fazeli B, ...
  • Rafatpanah H, Hedayati-Moghaddam MR, Fathimoghadam F, Bidkhori HR, Shamsian SK, ...
  • Azarpazhooh MR, Hasanpour K, Ghanbari M, Rezaee SA, Mashkani B, ...
  • Horlad H, Ohnishi K, Ma C, Fujiwara Y, Niino D, ...
  • Kannian P, Green PL. Human T lymphotropic virus type ۱ ...
  • Nakano K, Watanabe T. HTLV-۱ Rex Tunes the Cellular Environment ...
  • Badia R, Pujantell M, Riveira-Munoz E, Puig T, Torres-Torronteras J, ...
  • Beale G, Haagensen EJ, Thomas HD, Wang LZ, Revill CH, ...
  • Giam C-Z, Semmes OJ. HTLV-۱ Infection and Adult T-Cell Leukemia/Lymphoma—A ...
  • Jiao Y, Jiang Z, Wu Y, Chen X, Xiao X, ...
  • Nicot C. HTLV-I Tax-Mediated Inactivation of Cell Cycle Checkpoints and ...
  • Guerra E, Cimadamore A, Simeone P, Vacca G, Lattanzio R, ...
  • Lv H, Liu R, Fu J, Yang Q, Shi J, ...
  • Shimoyama M. Diagnostic criteria and classification of clinical subtypes of ...
  • Matsuoka M, Jeang KT. Human T cell leukemia virus type ...
  • Satou Y, Yasunaga J, Yoshida M and Matsuoka M. (۲۰۰۶). ...
  • Iwanaga M, Watanabe T, Utsunomiya A, Okayama A, Uchimaru K, ...
  • Okayama A, Stuver S, Matsuoka M, Ishizaki J, Tanaka G, ...
  • Akbarin MM, Rahimi H, HassanNia T, Shoja Razavi G, Sabet ...
  • Witzel I, Mueller V. The Role of CDK ۴/۶ Inhibitors ...
  • Bartsch R, Fitzal F, Hubalek M, Knauer M, Untch M. ...
  • Roberts PJ, Bisi JE, Strum JC, Combest AJ, Darr DB, ...
  • Schmitt I, Rosin O, Rohwer P, Gossen M, and Grassmann ...
  • Iwanaga R, Ohtani K, Hayashi T, Nakamura M. Molecular mechanism ...
  • Zhao T. The Role of HBZ in HTLV-۱-Induced Oncogenesis. Viruses. ...
  • Nakayama K, Yamada Y,Koji T, Hayashi T, Tomonaga M, Kamihira ...
  • Ellis M, Stern O, Ashur-Fabian O. The double benefit of ...
  • Li N, Xie C, Lu NH. p۵۳, a potential predictor ...
  • Ariumi Y, Kaida A, Lin JY, Hirota M, Masui O, ...
  • Gatza ML, Watt JC, Marriott SJ. Cellular transformation by the ...
  • Mesnard JM, Devaux C. Multiple control levels of cell proliferation ...
  • Wright DG, Marchal C, Hoang K, Ankney JA, Nguyen ST, ...
  • نمایش کامل مراجع