پنجشنبه 5 تیر 1404
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دوره ۱۹، شماره ۷۴ - ( ۱-۱۳۹۰ )
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Hamta A, SHariatzadeh S M A, Soleimani M, Seifi F. Introduction and Bioinformatic's Evaluation of Candidate Genes in Breast Cancer Using Cytogenetic Studies of Cancer Induction. J Adv Med Biomed Res 2011; 19 (74) :63-77
URL: http://journal.zums.ac.ir/article-1-1418-fa.html
URL: http://journal.zums.ac.ir/article-1-1418-fa.html
همتا احمد، شریعت زاده سید محمد علی، سلیمانی مهرنجانی ملک، سیفی فاطمه. معرفی و بررسی بیوانفورماتیکی ژن‌های کاندید در بروز سرطان پستان به روش مطالعه‌ی سیتوژنتیکی سرطان القایی. Journal of Advances in Medical and Biomedical Research. ۱۳۹۰; ۱۹ (۷۴) :۶۳-۷۷
۱- دکترای تخصصی ژنتیک مولکولی و سیتوژنتیک، استادیار دانشگاه اراک ، a-hamta@araku.ac.ir
۲- دکترای تخصصی جنین‌شناسی و بافت‌شناسی، استاد دانشگاه اراک
۳- دکترای تخصصی جنین‌شناسی و بافت‌شناسی، دانشیار دانشگاه اراک
۴- کارشناس ارشد سلولی تکوینی، دانشگاه اراک
۲- دکترای تخصصی جنین‌شناسی و بافت‌شناسی، استاد دانشگاه اراک
۳- دکترای تخصصی جنین‌شناسی و بافت‌شناسی، دانشیار دانشگاه اراک
۴- کارشناس ارشد سلولی تکوینی، دانشگاه اراک
چکیده: (۱۷۶۰۷۴ مشاهده)
Background and Objective: Discovery of genetic changes which contribute to cellular neoplastic and malignant tumor transformation is one of the major aims in oncology researches. The aim of this study was to investigate the DMBA-induced breast cancer in SD rat strains using bioinformatical methods and also to find their homologous regions in human chromosomes. Materials and Methods: In this research, we used SD rat strains as a suitable model for DMBA-induced breast cancer. We gavaged the rats twice with 10 mg DMBA solved in 0.5 ml sesame oil. After tumors appeared in DMBA-treated rats, they were subjected to histopathology and immunohistochemistery studies, cell culture, metaphase chromosomal preparation, and finally G-banding stain. According to databases, we collected genes in the affected area and prepared a gene list by comparing genome of the rats and human in changed chromosomal segments. Results: Our data showed numerical and frequent structural changes in different number of chromosomes. For example, we found recurrent gain in chromosomes 3, 4, 8, 12, 17, loss in chromosomes 3, 9, 12 and 15, also deletion in chromosomes 2, 3, 4, 6, 7, 20 and addition in chromosomes 11, 15 and 19. Conclusion: According to these chromosomal changes and based on bioinformatics studies we predict that the genesTGFBR3, HACE1, UBR5, CALB2, HPR, LCP1, RRM2B, ABO, ZFHX3, TNFSF11, ABL1, EPSTI1, PRDM1, REG3A, FOXA1 and PRKD1, probably may contribute to the development of breast cancer.
نوع مطالعه: مقاله پژوهشی |
دریافت: 1389/12/17 | پذیرش: 1393/4/2 | انتشار: 1393/4/2
دریافت: 1389/12/17 | پذیرش: 1393/4/2 | انتشار: 1393/4/2
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