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Tamoxifen, Genes and Efficacy Rates

Posted Nov 19 2009 10:02pm

I am thrilled to see discussion in today’s NY Times about the promise of genetic testing for drug metabolism. In particular, I’m excited to see mainstream media discussion of tamoxifen efficacy and genotype.

Much has been made of research published in the past few months regarding aromatase inhibitors — to what degree they prevent breast cancer recurrence, long-term survival, overall survival, and to what degree they’re better than tamoxifen (current studies indicate ~2-3%). That’s very exciting.

What you’re not hearing about, and which could take treatment decision-making to a higher level, is research into gene variants that may indicate who is likely to respond to tamoxifen and who isn’t. This could alter what we’ve previously thought of as tamoxifen efficacy rates. Gina Kolata explains and quotes Dr. David Flockhart, a leading researcher in this area:

As many as 7 percent of white women and a significant proportion of black women have two copies of a variant gene and are unable to activate tamoxifen. Others, with one copy of the variant gene, have a greatly reduced ability to activate it.

“These are huge effects — 100-fold differences in activity,” Dr. Flockhart said.

He wonders, he said, if tamoxifen is restricted to responders whether it may actually be more effective than the newer drugs called aromatase inhibitors.

The ability to determine who cannot process tamoxifen means that researchers can study the efficacy rates in women who can process tamoxifen. If such research were to show an overall increase in the efficacy rates of tamoxifen for this population, the question then becomes, would tamoxifen be more effective for these people than AIs?

So why aren’t we hearing about this? Naturally, people are excited about the new kid on the block (aromatase inhibitors). But AIs are still under patent, which means they’re significantly more expensive than tamoxifen. It also means that the pharma companies have a vested interest in cashing in on the patented drug. Who’s got the money to pay for comprehensive studies about genes, drug metabolism, AIs and tamoxifen? Who wants to move us one step closer to personalized medicine? What happens to all the women on tamoxifen and considering tamoxifen in the meantime?

Full disclosure: In the near future, my company will be offering genetic testing for CYP2D6 status. Personally, I think this test provides one more data point that can help postmenopausal women make sense of the increasingly complex options for breast cancer treatment/prevention.

Update: DNA Direct now offers 2D6 testing for tamoxifen as well as other genes involved in the metabolism of other drugs and medications, including the common blood-thinner, warfarin (Coumadin).

Technorati Tags: tamoxifen, breast cancer, prevention, treatment, genes, genetic testing, drug metabolism, drug response, aromatase inhibitors, David Flockhart

This entry was posted on Tuesday, July 11th, 2006 at 11:54 am and is filed under Breast Cancer, Drug Response, Genetic Testing. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.

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