scholarly journals Analysis of Oncogenes and Tumor Suppressor Genes in Human Breast Cancer

1993 ◽  
Vol 84 (8) ◽  
pp. 871-878 ◽  
Author(s):  
Hiroko Yamashita ◽  
Shunzo Kobayashi ◽  
Hirotaka Iwase ◽  
Yukashi Itoh ◽  
Tatsuya Kuzushima ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Suppressor Genes

scholarly journals ETS1 Suppresses Tumorigenesis of Human Breast Cancer via Trans-Activation of Canonical Tumor Suppressor Genes

2020 ◽  
Vol 10 ◽  
Author(s):  
Gi-Cheon Kim ◽  
Choong-Gu Lee ◽  
Ravi Verma ◽  
Dipayan Rudra ◽  
Taemook Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Suppressor Genes

scholarly journals Detection of a novel mutation in exon 20 of the BRCA1 gene

2013 ◽  
Vol 18 (4) ◽  
Author(s):  
Abhijit Chakraborty ◽  
Atul Katarkar ◽  
Keya Chaudhuri ◽  
Ashis Mukhopadhyay ◽  
Jayasri Basak
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Hereditary Breast Cancer ◽  
Tumor Suppressor Genes ◽  
Novel Mutation ◽  
Mutation Screening ◽  
Brct Domain ◽  
Globular Domain ◽  
Suppressor Genes ◽  
Exon 20

AbstractHereditary breast cancer constitutes 5–10% of all breast cancer cases. Inherited mutations in the BRCA1 and BRCA2 tumor-suppressor genes account for the majority of hereditary breast cancer cases. The BRCA1 C-terminal region (BRCT) has a functional duplicated globular domain, which helps with DNA damage repair and cell cycle checkpoint protein control. More than 100 distinct BRCA1 missense variants with structural and functional effects have been documented within the BRCT domain. Interpreting the results of mutation screening of tumor-suppressor genes that can have high-risk susceptibility mutations is increasingly important in clinical practice. This study includes a novel mutation, p.His1746 Pro (c.5237A>C), which was found in BRCA1 exon 20 of a breast cancer patient. In silico analysis suggests that this mutation could alter the stability and orientation of the BRCT domain and the differential binding of the BACH1 substrate.

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