Genetic alterations on chromosome 17 in human breast cancer: relationships to clinical features and DNA ploidy

1993 ◽  
Vol 28 (3) ◽  
pp. 231-239 ◽  
Author(s):  
Masahiro Watatani ◽  
Koichi Nagayama ◽  
Yukio Imanishi ◽  
Kazuyoshi Kurooka ◽  
Tomio Wada ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Clinical Features ◽  
Human Breast Cancer ◽  
Dna Ploidy ◽  
Genetic Alterations ◽  
Chromosome 17 ◽  
Human Breast

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.

scholarly journals Dissecting genetic requirements of human breast tumorigenesis in a tissue transgenic model of human breast cancer in mice

2009 ◽  
Vol 106 (17) ◽  
pp. 7022-7027 ◽  
Author(s):  
Min Wu ◽  
Lina Jung ◽  
Adrian B. Cooper ◽  
Christina Fleet ◽  
Lihao Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapies ◽  
Human Breast Cancer ◽  
Cancer Biology ◽  
Genetic Alterations ◽  
Genetically Engineered ◽  
Human Breast ◽  
Breast Tumorigenesis ◽  
Preneoplastic Lesions

Breast cancer development is a complex pathobiological process involving sequential genetic alterations in normal epithelial cells that results in uncontrolled growth in a permissive microenvironment. Accordingly, physiologically relevant models of human breast cancer that recapitulate these events are needed to study cancer biology and evaluate therapeutic agents. Here, we report the generation and utilization of the human breast cancer in mouse (HIM) model, which is composed of genetically engineered primary human breast epithelial organoids and activated human breast stromal cells. By using this approach, we have defined key genetic events required to drive the development of human preneoplastic lesions as well as invasive adenocarcinomas that are histologically similar to those in patients. Tumor development in the HIM model proceeds through defined histological stages of hyperplasia, DCIS to invasive carcinoma. Moreover, HIM tumors display characteristic responses to targeted therapies, such as HER2 inhibitors, further validating the utility of these models in preclinical compound testing. The HIM model is an experimentally tractable human in vivo system that holds great potential for advancing our basic understanding of cancer biology and for the discovery and testing of targeted therapies.

scholarly journals Bcl-2 with loss of apoptosis allows accumulation of genetic alterations: A pathway to metastatic progression in human breast cancer

2000 ◽  
Vol 89 (2) ◽  
pp. 142-147 ◽  
Author(s):  
Angels Sierra ◽  
Xavier Castellsagué ◽  
Agustín Escobedo ◽  
Belen Lloveras ◽  
Marta García-Ramirez ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Genetic Alterations ◽  
Metastatic Progression ◽  
Human Breast

scholarly journals A genomic view of estrogen actions in human breast cancer cells by expression profiling of the hormone-responsive transcriptome

2004 ◽  
Vol 32 (3) ◽  
pp. 719-775 ◽  
Author(s):  
L Cicatiello ◽  
C Scafoglio ◽  
L Altucci ◽  
M Cancemi ◽  
G Natoli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Gene Activation ◽  
Chromosome 17 ◽  
Human Breast ◽  
Cellular Functions ◽  
Extracellular Milieu ◽  
Similar Expression Profile ◽  
A Site ◽  
Turn Over

Estrogen controls key cellular functions of responsive cells including the ability to survive, replicate, communicate and adapt to the extracellular milieu. Changes in the expression of 8400 genes were monitored here by cDNA microarray analysis during the first 32 h of human breast cancer (BC) ZR-75.1 cell stimulation with a mitogenic dose of 17beta-estradiol, a timing which corresponds to completion of a full mitotic cycle in hormone-stimulated cells. Hierarchical clustering of 344 genes whose expression either increases or decreases significantly in response to estrogen reveals that the gene expression program activated by the hormone in these cells shows 8 main patterns of gene activation/inhibition. This newly identified estrogen-responsive transcriptome represents more than a simple cell cycle response, as only a few affected genes belong to the transcriptional program of the cell division cycle of eukaryotes, or showed a similar expression profile in other mitogen-stimulated human cells. Indeed, based on the functions assigned to the products of the genes they control, estrogen appears to affect several key features of BC cells, including their metabolic status, proliferation, survival, differentiation and resistance to stress and chemotherapy, as well as RNA and protein synthesis, maturation and turn-over rates. Interestingly, the estrogen-responsive transcriptome does not appear randomly interspersed in the genome. In chromosome 17, for example, a site particularly rich in genes activated by the hormone, physical association of co-regulated genes in clusters is evident in several instances, suggesting the likely existence of estrogen-responsive domains in the human genome.

Genomic Alterations in Human Breast Cancer: A Review

1989 ◽  
Vol 75 (4) ◽  
pp. 311-320 ◽  
Author(s):  
Renato Mariani-Costantinl ◽  
Giorgio Merlo ◽  
Luigi Frati
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Molecular Level ◽  
Genetic Material ◽  
Point Mutations ◽  
Genetic Alterations ◽  
Breast Carcinomas ◽  
Human Breast ◽  
Human Breast Carcinomas ◽  
Chromosome 11P

We review and discuss data on the genetic alterations documented in human breast carcinomas at the molecular level. These alterations may result in: 1) deletion of genetic material (chromosome 11p, 13q, 3p, 1q, 17p); 2) amplification of genes or entire chromosomal segments (c-myc, c-erb-B2, locus DF3/PUM, loci on 11q13); 3) rearrangements (c-myc); 4) point mutations (c-ras). Presently available informations do not allow the development of cohesive pathogenetic models but indicate that the molecular basis of human breast cancer is heterogeneous.

Relevance of DNA ploidy as a measure of genetic deviation: A comparison of flow cytometry and cytogenetics in 25 cases of human breast cancer

Cytometry ◽  
1988 ◽  
Vol 9 (6) ◽  
pp. 612-618 ◽  
Author(s):  
Y. Remvikos ◽  
M. Gerbault-Seurreau ◽  
P. Vielh ◽  
B. Zafrani ◽  
H. Magdelénat ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Flow Cytometry ◽  
Human Breast Cancer ◽  
Dna Ploidy ◽  
Human Breast
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