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Biotech / Medical : Celgene-CELG -- Ignore unavailable to you. Want to Upgrade?

To: scaram(o)uche who wrote (231)	1/6/1999 12:11:00 AM
From: Miljenko Zuanic	Read Replies (1) \| Respond to of 804

Again TGF-b! From article: <<"There are other ways of inactivating TGF-b, there are other ways of blocking TGF-b," said lead author Dr. Carlos Arteaga, of Vanderbilt University in Nashville, Tennessee, in an interview with Reuters Health. "Unfortunately those are not quite developed, but we'll get there soon. So antibodies are not the only way of doing this." >> Of course there are new drugs! And they will get there, better sooner than later! Miljenko PS: For those who don't know, T is also in PII trial (in combination with Taxol, I think) for advance metastatic breast cancer. Reversing resistance to tamoxifen NEW YORK, Jan 05 (Reuters Health) -- Blocking a particular growth factor appears to increase tamoxifen's ability to fight breast cancer cells that have become resistant to the drug, suggests a study in mice. However, it is not yet clear if such a strategy will work in women with breast cancer that has become resistant to tamoxifen treatment. Breast cancer cells that have estrogen receptors on their surface -- between 40% to 60% of breast cancers -- usually can be treated with tamoxifen, a drug that blocks the growth-promoting effects of estrogen. However, some cells produce high levels of transforming growth factor-beta (TGF-b), a naturally occurring cell growth regulator, and tend to be resistant to tamoxifen. In a new study, one breed of mice did not grow tumors if researchers treated them with tamoxifen in combination with injections of an antibody that blocked TGF-b. Such mice normally develop tumors when injected with breast cancer cells that overproduce TGF-b and are resistant to tamoxifen treatment, according to a report in the January 6th issue of the Journal of the National Cancer Institute. Such mouse antibodies could not be used for a treatment in humans because they would quickly be recognized as foreign and destroyed by the immune system. "There are other ways of inactivating TGF-b, there are other ways of blocking TGF-b," said lead author Dr. Carlos Arteaga, of Vanderbilt University in Nashville, Tennessee, in an interview with Reuters Health. "Unfortunately those are not quite developed, but we'll get there soon. So antibodies are not the only way of doing this." The cause of the tumor inhibition still needs to be determined. Tamoxifen-resistant cells grown in culture dishes did not regain their sensitivity to the drug in the presence of the TGF-b blocking antibody. And a second type of mouse developed tumors despite the added TGF-b blocking antibody injections. This type of mouse, known as a beige mouse, lacks natural killer (NK) cells, a specific type of immune system cell. Therefore, the authors speculate that NK cells play an important role in the killing of breast cancer cells by tamoxifen. TGF-b is known to suppress the activity of NK cells, so that blocking TGF-b may increase activity of the cells. "There are several pieces of information that indicate that tamoxifen stimulates natural killer activity in people," Arteaga said. "And some people, not many, have proposed that this could be part of the antitumor effect of tamoxifen." "The most important finding is that by blocking something produced by the tumor cells -- that can be measured in some of these tumor tissues and that can be interfered with by strategies in preclinical development -- we can enhance tamoxifen action, which is again, a relatively nontoxic, widely available agent with a proven track record against breast cancer," he concluded. SOURCE: Journal of the National Cancer Institute 1999;91:46-53.