scholarly journals The functional loss of the retinoblastoma tumour suppressor is a common event in basal-like and luminal B breast carcinomas

2008 ◽  
Vol 10 (5) ◽  
Author(s):  
Jason I Herschkowitz ◽  
Xiaping He ◽  
Cheng Fan ◽  
Charles M Perou
Keyword(s):  
Tumour Suppressor ◽  
Breast Carcinomas ◽  
Luminal B ◽  
Functional Loss ◽  
Common Event ◽  
Retinoblastoma Tumour Suppressor

Structure of the retinoblastoma tumour-suppressor pocket domain bound to a peptide from HPV E7

Nature ◽  
10.1038/36038 ◽  
1998 ◽  
Vol 391 (6670) ◽  
pp. 859-865 ◽  
Author(s):  
Jie-Oh Lee ◽  
Alicia A. Russo ◽  
Nikola P. Pavletich
Keyword(s):  
Tumour Suppressor ◽  
Hpv E7 ◽  
Retinoblastoma Tumour Suppressor ◽  
Pocket Domain

scholarly journals Analysis of the Gene Expression Profile of Stromal Pro-Tumor Factors in Cancer-Associated Fibroblasts from Luminal Breast Carcinomas

Diagnostics ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 865 ◽  
Author(s):  
Noemi Eiro ◽  
Sandra Cid ◽  
María Fraile ◽  
Jorge Ruben Cabrera ◽  
Luis O. Gonzalez ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Cancer Associated Fibroblasts ◽  
Breast Carcinomas ◽  
Luminal A ◽  
Luminal B

Luminal tumors are the most frequent type of breast carcinomas showing less tumor aggressiveness, although heterogeneity exists in their clinical outcomes. Cancer-associated fibroblasts (CAFs) are a key component of the tumor stroma which contribute to tumor progression. We investigated by real-time PCR the gene expression of 19 factors implicated in tumor progression. Those factors included the calcium-binding protein S100A4, several growth factors (FGF2, FGF7, HGF, PDGFA, PDGFB, TGFβ, VEGFA, and IGF2), and we also studied inflammatory cytokines (IL6 and IL8), chemokines (CCL2, CXCL12), important proteases (uPA, MMP2, MMP9 and MMP11), the nuclear factor NFκB, and the metalloprotease inhibitor TIMP1, from luminal A and luminal B breast carcinoma CAFs. We performed a similar analysis after co-culturing CAFs with MCF-7 and MDA-MB-231 breast cancer cell lines. MMP-9 and CCL2 gene expressions were higher in CAFs from luminal B tumors. We also found different patterns in the induction of pro-tumoral factors from different CAFs populations co-cultured with different cancer cell lines. Globally, CAFs from luminal B tumors showed a higher expression of pro-tumor factors compared to CAFs from luminal A tumors when co-cultured with breast cancer cell lines. Moreover, we found that CAFs from metastatic tumors had higher IGF-2 gene expression, and we detected the same after co-culture with cell lines. Our results show the variability in the capacities of CAFs from luminal breast carcinomas, which may contribute to a better biological and clinical characterization of these cancer subtypes.

The retinoblastoma tumour suppressor in development and cancer

2002 ◽  
Vol 2 (12) ◽  
pp. 910-917 ◽  
Author(s):  
Marie Classon ◽  
Ed Harlow
Keyword(s):  
Tumour Suppressor ◽  
Retinoblastoma Tumour Suppressor

Choosing between growth arrest and apoptosis through the retinoblastoma tumour suppressor protein, Abl and p73

2001 ◽  
Vol 29 (6) ◽  
pp. 666-673 ◽  
Author(s):  
J. Y. J. Wang ◽  
S. W. Ki
Keyword(s):  
Growth Arrest ◽  
Genotoxic Stress ◽  
Current Data ◽  
Cell Cycle Checkpoint ◽  
Tumour Suppressor ◽  
Apoptosis Pathway ◽  
Abl Tyrosine Kinase ◽  
Tumour Suppressor Protein ◽  
G1 Cells ◽  
Retinoblastoma Tumour Suppressor

The choice between growth arrest and apoptosis is made during differentiation, leading to survival with permanent arrest (e.g. neurons), or to death (e.g. epithelium). Genotoxic stress can also cause growth arrest or apoptosis, in addition to the activation of cell cycle checkpoint pathways. The p53 tumour suppressor can simulate growth arrest and apoptosis in response to DNA damage. Thus, p53 alone is not sufficient to specify these two mutually exclusive fates in damaged cells. The retinoblastoma tumour suppressor protein (RB) is a necessary downstream effector in p53-mediated growth arrest. RB inhibits E2F and the nuclear c-Abl tyrosine kinase. Interestingly, E2F activates the transcription of p73 mRNA and c-Abl stabilizes the p73 protein and activates its pro-apoptotic function. Because of RB, the c-Abl/p73 apoptosis pathway is activated in S/G2 cells but not in G1 cells. Taken together, the current data suggests RB to be an important player in directing the choice between permanent arrest and apoptosis. The antagonism between RB and c-Abl/p73 may modulate the function of p53 to direct the choice between growth arrest and apoptosis in DNA damaged cells.

The Retinoblastoma Tumour Suppressor in Model Organisms-New Insights from Flies and Worms

2006 ◽  
Vol 6 (7) ◽  
pp. 705-711
Author(s):  
Michael Korenjak ◽  
Alexander Brehm
Keyword(s):  
Tumour Suppressor ◽  
Model Organisms ◽  
Retinoblastoma Tumour Suppressor

scholarly journals Structure studies on the retinoblastoma tumour suppressor protein and its role in the cell cycle

2002 ◽  
Vol 58 (s1) ◽  
pp. c223-c223
Author(s):  
B. Xiao ◽  
J. Spencer ◽  
A. Clements ◽  
N. Ali-Khan ◽  
S. Mittnacht ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumour Suppressor ◽  
Tumour Suppressor Protein ◽  
Retinoblastoma Tumour Suppressor

The Retinoblastoma Tumour Suppressor in Model Organisms-New Insights from Flies and Worms

2006 ◽  
Vol 6 (7) ◽  
pp. 705-711
Author(s):  
Michael Korenjak ◽  
Alexander Brehm
Keyword(s):  
Tumour Suppressor ◽  
Model Organisms ◽  
Retinoblastoma Tumour Suppressor
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