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 ◽  
...  

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.

1987 ◽  
Vol 7 (5) ◽  
pp. 2019-2023
Author(s):  
M van de Vijver ◽  
R van de Bersselaar ◽  
P Devilee ◽  
C Cornelisse ◽  
J Peterse ◽  
...  

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.


Science ◽  
1987 ◽  
Vol 235 (4785) ◽  
pp. 177-182 ◽  
Author(s):  
D. Slamon ◽  
G. Clark ◽  
S. Wong ◽  
W. Levin ◽  
A Ullrich ◽  
...  

2004 ◽  
Vol 32 (3) ◽  
pp. 719-775 ◽  
Author(s):  
L Cicatiello ◽  
C Scafoglio ◽  
L Altucci ◽  
M Cancemi ◽  
G Natoli ◽  
...  

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.


1995 ◽  
Vol 64 (2) ◽  
pp. 112-116 ◽  
Author(s):  
Sigurlaug Skirnisdottir ◽  
Gudny Eiriksdottir ◽  
Trausti Baldursson ◽  
Rosa B. Barkardottir ◽  
Valgardur Egilsson ◽  
...  

1993 ◽  
Vol 28 (3) ◽  
pp. 231-239 ◽  
Author(s):  
Masahiro Watatani ◽  
Koichi Nagayama ◽  
Yukio Imanishi ◽  
Kazuyoshi Kurooka ◽  
Tomio Wada ◽  
...  

Author(s):  
G. Kasnic ◽  
S. E. Stewart ◽  
C. Urbanski

We have reported the maturation of an intracisternal A-type particle in murine plasma cell tumor cultures and three human tumor cell cultures (rhabdomyosarcoma, lung adenocarcinoma, and osteogenic sarcoma) after IUDR-DMSO activation. In all of these studies the A-type particle seems to develop into a form with an electron dense nucleoid, presumably mature, which is also intracisternal. A similar intracisternal A-type particle has been described in leukemic guinea pigs. Although no biological activity has yet been demonstrated for these particles, on morphologic grounds, and by the manner in which they develop within the cell, they may represent members of the same family of viruses.


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