Abstract 1813: FOXM1 target genes associated with cell cycle regulation predict breast cancer metastatic outcome.

Author(s):  
Christina Yau ◽  
Laurence Meyer ◽  
Stephen Benz ◽  
Charles Vaske ◽  
Gary Scott ◽  
...  
Author(s):  
Yaniv Shpilberg ◽  
Michael K. Connor ◽  
Michael C. Riddell

AbstractBreast cancer is the second leading cause of cancer-related mortality in women. Glucocorticoids (GCs) have the potential to directly affect breast cancer or indirectly via changes to the tumor growth microenvironment a breast cancer is exposed to. The role of GCs in breast cancer progression by direct and indirect means are not fully understood.To study the direct and indirect effects of GCs on breast cancer cell cycle regulation.MCF7 breast cancer cells were incubated with increasing concentrations of corticosterone (CORT) to investigate the direct effects. In addition, MCF7 cells were cultured in conditioned media (CM) from primary adipose tissue excised from CORT-supplemented lean and obese male rats.CORT alone resulted in dose-dependent increases in p27 and hypophosphorylated retinoblastoma protein (Rb) which was accompanied by a reduction in the number of cells in S-phase. CM prepared from adipose tissue overrode these direct CORT effects, suggesting that the tumor growth microenvironment created in the CM dominates MCF7 cell cycle regulation.The direct inhibitory effects of CORT on cancer cell cycle progression are largely limited by the hormone’s effects on adipose tissue biology.


2001 ◽  
Vol 12 (7) ◽  
pp. 320-327 ◽  
Author(s):  
James S. Foster ◽  
Donald C. Henley ◽  
Shamila Ahamed ◽  
Jay Wimalasena

2022 ◽  
Vol 8 (1) ◽  
Author(s):  
Luca Gianni ◽  
Marco Colleoni ◽  
Giancarlo Bisagni ◽  
Mauro Mansutti ◽  
Claudio Zamagni ◽  
...  

AbstractThe crosstalk between estrogen and HER2 receptors and cell-cycle regulation sustains resistance to endocrine therapy of HER2- and hormone receptor-positive breast cancer. We earlier reported that women with HER2 and ER-positive breast cancer receiving neoadjuvant dual HER2-block and palbociclib in the NA-PHER2 trial had Ki67 decrease and 27% pathological complete responses (pCR). We extended NA-PHER2 to Cohort B using dual HER2-block and palbociclib without fulvestrant and report here Ki67 drops at week-2 (mean change −25.7), at surgery (after 16 weeks, mean change −9.5), high objective response (88.5%) and pCR (19.2%). In Cohort C [Ki67 > 20% and HER2low (IHC 1+/2+ without gene amplification)], women also received fulvestrant, had dramatic Ki67 drop at week 2 (−29.5) persisting at surgery (−19.3), and objective responses in 78.3%. In view of the favorable tolerability and of the efficacy-predictive value of Ki67 drop at week-2, the chemotherapy-free approach of NA-PHER2 deserves further investigation in HER2 and ER-positive breast cancer. The trial is registered with ClinicalTrials.gov, number NCT02530424.


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