| چکیده انگلیسی مقاله |
Breast carcinoma is the most common cause of cancer mortality among women globally. Primary and secondary prevention through avoiding known risk factors, screening for early detection of tumors with different methods as well as timely treatment, can be effective in reduction of the burden of this devastating disease. This can in turn prevent death and also increase survival in patients with breast cancer. Both environmental and genetic factors are involved in the pathogenesis of breast cancer. Multiple genetic factors can influence the risk and development of breast cancer. Identification of genetic variants including single nucleotide polymorphisms (SNPs), which are associated with the risk of breast cancer development, are mostly done through genetic association studies. It is demonstrated that SNP allele frequencies vary amongst different populations. It has been shown that genetic risk factors like variations in TOX high mobility group box family member 3 (TOX3), which affect the liability for neoplasm, play an important role in the development of breast cancer. Although TOX3 is expressed mainly in the brain, its expression in other tissues especially breast has also been reported. TOX3 maps to chromosome 16q12 and encodes the nuclear high-mobility group (HMG)-box. It has calcium (Ca2+)-dependent transcriptional activities and is a co-factor of cAMP response element (CRE)-binding protein (CREB) and CREB-binding protein (CBP). TOX3, activated with Ca2+, is related with activation of the promoter of some other genes including BCL2 and C3 complement and also CITED1 gene expression. It also induces activation of the c-fos promoter and therefore its expression. Genome-wide association studies (GWAS) in different populations including European, Asian and African-American have demonstrated that a SNP near its 5ʹ end and the promoter of TOX3 gene appears to be significantly associated with breast cancer susceptibility. Furthermore, breast cancer–associated SNPs lead to enhanced FOXA1 bindings and in turn, a reduction in TOX3 gene expression. This review has highlighted the importance of TOX3 function, SNPs and its association with breast cancer risk and also its potential effects on breast cancer treatment; TOX3 plays dual and somehow conflicting roles in cancer initiation and progression which remains to be further investigated. |
| نویسندگان مقاله |
امیر تاج بخش | amir tajbakhsh
department of modern sciences amp;amp; technologies, faculty of medicine, mashhad university of medical sciences, mashhad, iran. student research committee, department of modern sciences amp;amp; technologies, faculty of medicine, mashhad university of medical sciences, mashhad, iran.
گروه علوم و فنون نوین، دانشکده پزشکی، دانشگاه علوم پزشکی مشهد، مشهد، ایران. کمیته تحقیقات دانشجویی، گروه علوم و فنون نوین، دانشکده پزشکی، دانشگاه علوم پزشکی مشهد، مشهد، ایران.
سازمان اصلی تایید شده: دانشگاه علوم پزشکی مشهد (Mashhad university of medical sciences)
فهیمه افضل جوان | fahimeh afzal javan
department of modern sciences amp;amp; technologies, faculty of medicine, mashhad university of medical sciences, mashhad, iran. student research committee, department of modern sciences amp;amp; technologies, faculty of medicine, mashhad university of medical sciences, mashhad, iran.
گروه علوم و فنون نوین، دانشکده پزشکی، دانشگاه علوم پزشکی مشهد، مشهد، ایران. کمیته تحقیقات دانشجویی، گروه علوم و فنون نوین، دانشکده پزشکی، دانشگاه علوم پزشکی مشهد، مشهد، ایران.
سازمان اصلی تایید شده: دانشگاه علوم پزشکی مشهد (Mashhad university of medical sciences)
مصطفی فاضلی | mostafa fazeli
department of modern sciences amp;amp; technologies, faculty of medicine, mashhad university of medical sciences, mashhad, iran. student research committee, department of modern sciences amp;amp; technologies, faculty of medicine, mashhad university of medical sciences, mashhad, iran.
گروه علوم و فنون نوین، دانشکده پزشکی، دانشگاه علوم پزشکی مشهد، مشهد، ایران. کمیته تحقیقات دانشجویی، گروه علوم و فنون نوین، دانشکده پزشکی، دانشگاه علوم پزشکی مشهد، مشهد، ایران.
سازمان اصلی تایید شده: دانشگاه علوم پزشکی مشهد (Mashhad university of medical sciences)
مهدی ریوندی | mahdi rivandi
department of modern sciences amp;amp; technologies, faculty of medicine, mashhad university of medical sciences, mashhad, iran. student research committee, department of modern sciences amp;amp; technologies, faculty of medicine, mashhad university of medical sciences, mashhad, iran.
گروه علوم و فنون نوین، دانشکده پزشکی، دانشگاه علوم پزشکی مشهد، مشهد، ایران. کمیته تحقیقات دانشجویی، گروه علوم و فنون نوین، دانشکده پزشکی، دانشگاه علوم پزشکی مشهد، مشهد، ایران.
سازمان اصلی تایید شده: دانشگاه علوم پزشکی مشهد (Mashhad university of medical sciences)
محمد مهدی کوشیار | mohammad mahdi kushyar
department of hematology-oncology, emam reza hospital, mashhad university of medical sciences, mashhad, iran.
گروه هماتولوژی-انکولوژی، بیمارستان امام رضا ع ، دانشگاه علوم پزشکی مشهد، مشهد، ایران.
سازمان اصلی تایید شده: دانشگاه علوم پزشکی مشهد (Mashhad university of medical sciences)
محمدرضا نصیری | mohammadreza nassiri
biotechnology institute, ferdowsi university of mashhad, mashhad, iran.
پژوهشکده فناوری زیستی، دانشگاه فردوسی مشهد، مشهد، ایران.
سازمان اصلی تایید شده: دانشگاه فردوسی (Ferdowsi university)
علیرضا پاسدار | alireza pasdar
medical genetics research center, faculty of medicine, mashhad university of medical sciences, university campus, azadi sq., mashhad, iran. p.o.box 9177948564 tel 98- 51- 38002287
مشهد، میدان آزادی، پردیس دانشگاه، دانشگاه علوم پزشکی مشهد، دانشکده پزشکی، مرکز تحقیقات ژنتیک پزشکی. صندوق پستی 9177948564 تلفن 38002287 -051
سازمان اصلی تایید شده: دانشگاه علوم پزشکی مشهد (Mashhad university of medical sciences)
|