Retinoic acid inhibits growth of breast cancer cells in the short-term but not the long-term

1996 ◽  
Vol 24 (3) ◽  
pp. 365S-365S ◽  
Author(s):  
RUTH STEPHEN ◽  
DAVID CORCORAN ◽  
PHILIPPA D. DARBRE
2017 ◽  
Author(s):  
I. A. Zamulaeva ◽  
O. N. Matchuk ◽  
K. A. Churyukina ◽  
V. A. Kudryavtzev ◽  
N. G. Yabbarov ◽  
...  

1995 ◽  
Vol 109 (1) ◽  
pp. 77-86 ◽  
Author(s):  
Bas-jan M. van der Leede ◽  
Gert E. Folkers ◽  
Christina E. van den Brink ◽  
Paul T. van der Saag ◽  
Bart van der Burg

Author(s):  
Igor N. Sergeev

AbstractModulation of apoptosis is emerging as a promising strategy for prevention and treatment of breast cancer and obesity because removal of mammary cancer cells and mature adipocytes through this process will result in decreasing tumor size and produce long-term reduction in adipose tissue mass. The hormone 1,25-dihydroxyvitamin D


Author(s):  
Valerio Ciccone ◽  
Erika Terzuoli ◽  
Sandra Donnini ◽  
Antonio Giachetti ◽  
Lucia Morbidelli ◽  
...  

1995 ◽  
Vol 14 (3) ◽  
pp. 391-394 ◽  
Author(s):  
S Y James ◽  
A G Mackay ◽  
K W Colston

ABSTRACT The effects of the novel vitamin D analogue, EB1089 alone, or in combination with the retinoid, 9-cis retinoic acid (9-cis RA) on indices of apoptosis in MCF-7 breast cancer cells have been examined. EB1089 was capable of reducing bcl-2 protein, a suppressor of apoptosis, and increasing p53 protein levels in MCF-7 cell cultures following 96h treatment. In the presence of 9-cis RA, EB1089 acted to further enhance the down-regulation and up-regulation of bcl-2 and p53 respectively. Furthermore, EB1089 induces DNA fragmentation in MCF-7 cells, a key feature of apoptosis, alone and in combination with 9-cis RA in situ. The observation that EB1089 and 9-cis RA act in a cooperative manner to enhance induction of apoptosis in these cells may have therapeutic implications.


Sign in / Sign up

Export Citation Format

Share Document