|  Help  |  About  |  Contact Us

Publication : α-Tocopheryloxyacetic acid is superior to α-tocopheryl succinate in suppressing HER2-high breast carcinomas due to its higher stability.

First Author  Dong LF Year  2012
Journal  Int J Cancer Volume  131
Issue  5 Pages  1052-8
PubMed ID  22038845 Mgi Jnum  J:186122
Mgi Id  MGI:5431052 Doi  10.1002/ijc.26489
Citation  Dong LF, et al. (2012) alpha-Tocopheryloxyacetic acid is superior to alpha-tocopheryl succinate in suppressing HER2-high breast carcinomas due to its higher stability. Int J Cancer 131(5):1052-8
abstractText  Breast cancer is the number one neoplastic disease of women, with the HER2-high carcinomas presenting a considerable challenge for efficient treatment. Therefore, a search for novel agents active against this type of cancer is warranted. We tested two vitamin E (VE) analogs, the esterase-hydrolyzable alpha-tocopheryl succinate (alpha-TOS) and the non-hydrolyzable ether alpha-tocopheryloxyacetic acid (alpha-TEA) for their effects on HER2-positive breast carcinomas using a breast tumor mouse model and breast cancer cell lines. Ultrasound imaging documented that alpha-TEA suppressed breast carcinomas in the transgenic animals more efficiently than found for its ester counterpart. However, both agents exerted a comparable apoptotic effect on the NeuTL breast cancer cells derived from the FVB/N c-neu mice as well as in the human MBA-MD-453 and MCF7(HER) (2-) (18) cells with high level of HER2. The superior anti-tumor effect of alpha-TEA over alpha-TOS in vivo can be explained by longer persistence of the former in mice, possibly due to the enhanced plasma and hepatic processing of alpha-TOS in comparison to the esterase-non-cleavable alpha-TEA. Indeed, the stability of alpha-TOS in plasma was inferior to that of alpha-TEA. We propose that alpha-TEA is a promising drug efficient against breast cancer, as documented by its effect on experimental HER2-positive breast carcinomas that present a considerable problem in cancer management.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

3 Bio Entities

Trail: Publication

0 Expression