scholarly journals Polysomy of chromosome 17 in breast cancer tumors showing an overexpression of ERBB2: a study of 175 cases using fluorescence in situhybridization and immunohistochemistry

2005 ◽  
Vol 7 (2) ◽  
Author(s):  
Marta Salido ◽  
Ignasi Tusquets ◽  
Josep M Corominas ◽  
Marta Suarez ◽  
Blanca Espinet ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Chromosome 17 ◽  
In Situhybridization ◽  
Fluorescence In Situhybridization

scholarly journals Chromosome 17 Centromere Duplication and Responsiveness to Anthracycline-Based Neoadjuvant Chemotherapy in Breast Cancer

Neoplasia ◽  
2014 ◽  
Vol 16 (10) ◽  
pp. 861-867 ◽  
Author(s):  
Ariadna Tibau ◽  
Laura López-Vilaró ◽  
Maitane Pérez-Olabarria ◽  
Tania Vázquez ◽  
Cristina Pons ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Neoadjuvant Chemotherapy ◽  
Chromosome 17

scholarly journals Clinical array-based karyotyping of breast cancer with equivocal HER2 status resolves gene copy number and reveals chromosome 17 complexity

BMC Cancer ◽  
2010 ◽  
Vol 10 (1) ◽  
Author(s):  
Shelly Gunn ◽  
I-Tien Yeh ◽  
Irina Lytvak ◽  
Budi Tirtorahardjo ◽  
Natasha Dzidic ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Copy Number ◽  
Gene Copy Number ◽  
Chromosome 17 ◽  
Gene Copy ◽  
Her2 Status

scholarly journals Unraveling the chromosome 17 patterns of FISH in interphase nuclei: an in-depth analysis of the HER2amplicon and chromosome 17 centromere by karyotyping, FISH and M-FISH in breast cancer cells

BMC Cancer ◽  
2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Milena Rondón-Lagos ◽  
Ludovica Verdun Di Cantogno ◽  
Nelson Rangel ◽  
Teresa Mele ◽  
Sandra R Ramírez-Clavijo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Chromosome 17 ◽  
Interphase Nuclei ◽  
Depth Analysis

scholarly journals ‘BRCA1’ RESPONSIVENESS TOWARDS BREAST CANCER-A POPULATION-WISE PHARMACOGENOMIC ANALYSIS

2016 ◽  
Vol 8 (9) ◽  
pp. 267 ◽  
Author(s):  
Preethi M. Iyer ◽  
Sanjay Kumar P. ◽  
Karthikeyan S. ◽  
P. K Krishnan Namboori
Keyword(s):  
Breast Cancer ◽  
Risk Factors ◽  
New Zealand ◽  
Environmental Factors ◽  
Chromosome 17 ◽  
Base Pairs ◽  
Single Nucleotide ◽  
Factors Associated ◽  
Variation Database ◽  
Different Populations

<p><strong>Objective: </strong>In the present pharmacogenomic work, the genetic, epigenetic and environmental factors associated with BRCA1 induced breast cancer, cancer proneness and its variants across different populations like Indian, Netherland, Belgium, Denmark, Austrian, New Zealand, Sweden, Malaysian and Norwegian and the ‘mutation and methylation-prone’ region of BRCA1 have been computed.</p><p><strong>Methods: </strong>The global variations associated with the disease have been identified from the ‘Leiden open variation database (LOVD 3.0)’ and ‘Indian genome variation database (IGVDB)’. The variants, ‘single nucleotide polymorphisms (SNPs)’ are then characterized. The epigenetic factors associated with breast cancer have been identified from the clinical reports and further scrutinized using EpiGRAPH tool. The various contributing environmental factors responsible for the variations have been considered.</p><p><strong>Results: </strong>All the variants across different populations such as Indian, Netherland, Belgium, Denmark, Austrian, New Zealand, Sweden, Malaysian and Norwegian are found to be in a specific transcript of BRCA1 that ranges within 41,196,312-41,277,500 (81,189 base pairs) of the chromosome 17. Two ‘single nucleotide variations (SNVs)’ (5266dupC: rs397507246 and 68_69delAG: rs386833395) have been identified as risk factors in hereditary breast and ovarian cancer syndrome in the global population and 39 SNPs have been identified as pathogenic and deleterious. ‘Evolutionary history’ seems to be the most significant attribute in the predictability of methylation of BRCA1. Unhealthy dietary habits, obesity, use of unsafe cosmetics, estrogen exposure, ‘hormone replacement therapy (HRT)’, use of oral contraceptives and smoking are the major environmental risk factors associated with breast cancer incidence.</p><p><strong>Conclusion: </strong>This chromosome location (41,196,312-41,277,500 (81,189 base pairs)) can be considered as the population-specific sensitive region corresponding to BRCA1 mutation. This supports the fact that stabilization within the region can be a promising technique to control the epigenetic variants associated with the global position. The global variation in the proneness of the disease may be due to a cumulative effect of genetic, epigenetic and environmental factors subject to further experimentations with identical variations and populations. </p>

Predisposing Genes in Breast and Ovarian Cancer: An Overview

1993 ◽  
Vol 79 (5) ◽  
pp. 291-296 ◽  
Author(s):  
Simon A. Smith ◽  
Bruce A.J. Ponder
Keyword(s):  
Breast Cancer ◽  
Ovarian Cancer ◽  
At Risk ◽  
Chromosome 17 ◽  
Cancer Syndrome ◽  
Breast And Ovarian Cancer ◽  
Li Fraumeni Syndrome ◽  
Predisposing Genes ◽  
Li Fraumeni ◽  
Cancer Syndromes

The isolation of genes that predispose to familial disease is an important goal in cancer research. The identification of such genes « opens up » the possibility of genetic diagnosis in families so that individuals who are at risk of cancer through inheriting a predisposing mutation can be Identified. Genes that are involved in familial cancer syndromes may also be important in the pathogenesis of sporadic forms of the disease, which are often more common. In the search for genes that predispose to familial breast and ovarian cancer much recent progress has been made. A locus on the long arm of chromosome 17, in the interval 17q12-21, has been identified by genetic linkage, and appears to be responsible for disease in approximately 40 % of breast cancer families and most families that contain breast and ovarian cancer. The region containing this locus, which has been called BRCA1, has been narrowed to a 3-4 cM interval defined by THRA1, the thyroid hormone receptor locus alpha, and D17S183, an anonymous microsatellite polymorphism. Loci other than BRCA1 that have been identified appear not only to predispose to breast and/or ovarian tumors, but to tumors at other sites too. A new locus has been identified on chromosome 2 which is linked to hereditary non-polyposis colorectal cancer (HNPCC). Families with HNPCC are also at risk of endometrial cancer and tumors of the ovary, amongst other cancer sites. Finally, mutations in the p53 gene are inherited in families with Li-Fraumeni syndrome, a rare cancer syndrome predisposing to breast tumors, sarcomas, leukemia and other cancers. Li-Fraumeni syndrome is also the only inherited cancer syndrome that predisposes at least in part to breast cancer where the actual predisposing gene is known. For the other cancer syndromes, the cloning of the predisposing genes is eagerly awaited.

scholarly journals Amplification of the neu (c-erbB-2) oncogene in human mammmary tumors is relatively frequent and is often accompanied by amplification of the linked c-erbA oncogene.

1987 ◽  
Vol 7 (5) ◽  
pp. 2019-2023 ◽  
Author(s):  
M van de Vijver ◽  
R van de Bersselaar ◽  
P Devilee ◽  
C Cornelisse ◽  
J Peterse ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Chromosome ◽  
High Frequency ◽  
Human Breast Cancer ◽  
Functional Role ◽  
Chromosome 17 ◽  
Human Breast ◽  
Copy Numbers ◽  
Neu Oncogene ◽  
Human Chromosome 17

We investigated alterations in the structure and expression of oncogenes in mammary tumors and mammary tumor-derived cell lines. In 16 of 95 samples, we detected amplification of the human neu oncogene, also known as c-erB-2, accompanied by overexpression in the tumors from which intact RNA could be isolated. In 10 of these DNAs, the linked oncogene c-erbA was also amplified, whereas another gene on human chromosome 17, p53, was present in normal copy numbers. Overexpression of c-erbA could not be detected in the tumors analyzed. The relatively high frequency of neu amplification points to a functional role in human breast cancer. Coamplification of the c-erbA oncogene could contribute to this disease as well but is most likely fortuitous.

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