scholarly journals High level expression of differentially localized BAG-1 isoforms in some oestrogen receptor-positive human breast cancers

1999 ◽  
Vol 81 (6) ◽  
pp. 1042-1051 ◽  
Author(s):  
M Brimmell ◽  
J S Burns ◽  
P Munson ◽  
L McDonald ◽  
M J O’Hare ◽  
...  
1981 ◽  
Vol 67 (6) ◽  
pp. 549-552 ◽  
Author(s):  
Maria Laura Codegone ◽  
Raffaele Di Carlo ◽  
Giampiero Muccioli ◽  
Gianni Bussolati

Histology and cytometrics were evaluated in 50 cases of human breast infiltrating carcinomas (44 ductal, 6 lobular) assayed for the presence of prolactin receptors (PR). The tumors were considered PR positive when the level of specific binding reached or exceeded 0.5 %. Twenty-six ductal infiltrating carcinomas and 4 lobular ones were PR positive. No strict correlation was found between PR and degree of histologic differentiation (expressed in grades) or menopausal status. Better differentiated (grade I) ductal carcinomas were, however, mostly PR negative. Evaluation of the mean nuclear diameter (MND) and of the maximal epithelial cellularity (MEC) revealed that in ductal carcinomas a high level of PR (> 3 % specific binding) was significantly correlated with a high MND. It is concluded that, contrary to that observed in estrogen receptor-positive tumors, PR-positive human ductal carcinomas are more likely to have large nuclei, i.e., cytologically anaplastic, whereas better differentiated (grade I) carcinomas are generally PR negative.


2011 ◽  
Vol 22 (3) ◽  
pp. 551-558 ◽  
Author(s):  
Gabriella Baio ◽  
Marina Fabbi ◽  
Laura Emionite ◽  
Michele Cilli ◽  
Sandra Salvi ◽  
...  

2017 ◽  
Vol 2 (1) ◽  
Author(s):  
Roswita Hamunyela ◽  
Mogammad Hamid ◽  
Antonio Serafin ◽  
John Akudugu

Patients with triple-negative breast cancers (TNBC) constitute about one-fifth of all breast cancer patients. TNBC is an aggressive and heterogeneous disease entity in comparison with other types of breast cancer and, therefore, tends to be  resistant to existing treatment regimens, such as, targeted and hormone therapies. There is evidence to suggest that proliferative and survival pathways of triple-negative tumours are still poorly understood, which could be the reason for the  observed treatment resistance. Novel treatment approaches are, therefore, needed to overcome the challenges in the treatment of triple-negative breast cancers. Three human breast cell lines (MDAMB- 231, MCF-7 and MCF-12A) were pre-treated  ith inhibitors of phosphoinositide 3-kinase (PI3K), mammalian target of rapamycin (mTOR), and the pro-survival gene (Bcl-2), and their radiosensitivities were evaluated using the clonogenic cell survival assay. Inhibition of PI3K, mTOR,  and Bcl-2 with a cocktail of small molecule inhibitors NVP-BEZ235 and ABT-263 resulted in a 4- to 14-fold radiosensitisation of human breast cell lines with features similar to those of triple-negative cancers. These findings suggest that inhibition of  I3K, mTOR, and Bcl-2 can significantly enhance the sensitivity of breast cells devoid of progesterone and oestrogen receptor expression. This approach may have therapeutic potential for breast cancer management.


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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