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HEC carcinogenesis results in resistance to 5-fluorouracil-induced apoptosis.

Women's Health Weekly

| July 03, 2003 | COPYRIGHT 2003 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2003 JUL 3 - (NewsRx.com & NewsRx.net) -- HEC carcinogenesis results in resistance to 5-fluorouracil-induced apoptosis.

According to recent research published in the European Journal of Pharmacology, "Apoptosis has received widespread attention for its essential roles in biology, medicine and cancer.

"We previously found that normal, human papillomavirus (HPV) 16-immortalized and their transformed endocervical cells were increasingly resistant to apoptosis induced by a cancer therapeutic drug," wrote B. Mo and colleagues, Memorial University of Newfoundland, Faculty of Medicine.

"Here, analogously, another common anticancer drug, 5-fluorouracil, in an ectocervical cell carcinogenesis model induced apoptosis in primary human ectocervical cells (HEC), whereas HPV18-immortalized HEC (HEC-18) and transformed HEC-18 (HEC-18T) were more resistant," the researchers wrote.

"Growth in serum/low density lipoprotein (LDL)-containing medium reversed resistance to 5-fluorouracil-induced apoptosis, particularly in HEC-18T. Cell viability results confirmed these findings. Using Western blots to compare protein levels with those of HEC not treated with 5-fluorouracil, the fold changes in HEC-18 and HEC-18T in LDL-free medium were 1.6-6.1-fold lower for pro-apoptotic p53, Bak and Bax," the researchers stated.

"Four anti-apoptotic proteins were altered - 2.1 to + 14.6-fold for Bcl-2 and BAG-1 isoform p33 and ...

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