Intersite Variation of Estrogen Receptors in Human Breast Cancers and Response to Endocrine Therapy

Oncology ◽  
1992 ◽  
Vol 49 (2) ◽  
pp. 89-92 ◽  
Author(s):  
Yuichi lino ◽  
Noritaka Sugamata ◽  
Michio Maemura ◽  
Takeshi Takeo ◽  
Susumu Owada ◽  
...  
1995 ◽  
Vol 64 (4) ◽  
pp. 269-273 ◽  
Author(s):  
Julia M. W. Gee ◽  
Ian O. Ellis ◽  
John F. R. Robertson ◽  
Peter Willsher ◽  
Richard A. McClelland ◽  
...  

Author(s):  
Nikki Aldi Massardi

Breast cancer is a hormone-dependent disease that relies on the mitogenic effect ofestrogen to increase tumorigenesis and tumor growth. Clinically significant levels ofestrogen-α receptor (ERα) expression are seen in 80% of human breast cancers,whereas progesterone receptor is expressed in 55% of human breast cancers. Thesedata are one of the bases for the development of endocrine therapy. Endocrinetherapy is therapy that targets the pathway and synthesis of estrogen, by blocking itvia receptors, reducing circulating levels of estrogen, or suppressing estrogensynthesis in the tissues of women diagnosed with breast cancer.


1985 ◽  
Vol 35 (5) ◽  
pp. 477-480
Author(s):  
YUICHI IINO ◽  
KENNEI YAMAZAKI ◽  
HIROSHI ISHIKAWA ◽  
MASARU IZUO ◽  
HIROO TAKIKAWA

1989 ◽  
Vol 32 (4) ◽  
pp. 485-492 ◽  
Author(s):  
Casper H. van Aswegen ◽  
Robert H. Purdy ◽  
James L. Wittliff

1994 ◽  
Vol 59 (5) ◽  
pp. 619-628 ◽  
Author(s):  
Julia M. W. Gee ◽  
John F. R. Robertson ◽  
Ian O. Ellis ◽  
Peter Willsher ◽  
Richard A. McClelland ◽  
...  

1973 ◽  
Vol 9 (5) ◽  
pp. 353-357 ◽  
Author(s):  
U. Spaeren ◽  
S. Olsnes ◽  
I. Brennhovd ◽  
J. Efskind ◽  
A. Pihl

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 942
Author(s):  
Mei Qi Kwa ◽  
Rafael Brandao ◽  
Trong H. Phung ◽  
Jianfeng Ge ◽  
Giuseppe Scieri ◽  
...  

MRCKα is a ubiquitously expressed serine/threonine kinase involved in cell contraction and F-actin turnover, which is highly amplified in human breast cancer and part of a gene expression signature for bad prognosis. Nothing is known about the in vivo function of MRCKα. To explore MRCKα function in development and in breast cancer, we generated mice lacking a functional MRCKα gene. Mice were born close to the Mendelian ratio and showed no obvious phenotype including a normal mammary gland formation. Assessing breast cancer development using the transgenic MMTV-PyMT mouse model, loss of MRCKα did not affect tumor onset, tumor growth and metastasis formation. Deleting MRCKα and its related family member MRCKβ in two triple-negative breast cancer cell lines resulted in reduced invasion of MDA-MB-231 cells, but did not affect migration of 4T1 cells. Further genomic analysis of human breast cancers revealed that MRCKα is frequently co-amplified with the oncogenes ARID4B and AKT3 which might contribute to the prognostic value of MRCKα expression. Collectively, these data suggest that MRCKα might be a prognostic marker for breast cancer, but probably of limited functional importance.


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