HER2 Support Group Forums - View Single Post - Her 2 and Her 3 signalling and Dr M Moasser

Lani · 01-13-2011, 08:36 AM

at SABCS they reported on combining herceptin and lapatinib as well as herceptin and pertuzumab, the latter also blocking her3. 2009 SABCS also reported on neratinib.

There are several trials on now I believe with mTor inhibitors, of which rapamycin was the template drug--there are other mTor inhibitor like everolimus which are already FDA approved (for keeping vascular stents open)

For about five years not, researcher have realized that the trick will probably be getting the right combination of targeted therapies for the patient's individual tumor characteristics (which oncogenes and signalling pathways are particularly driving its growth and spread)

Finding the best test to determine which pathways are the critical ones and then giving the right drugs seems to be the way of the future, but a way which clinical trials as currently designed are ill-designed for.

Better ways to test for minimal residual disease (or more bone marrow testing to see if treatments were effective, or better ctc testing) may help.

01-13-2011, 08:36 AM	#10
Lani Senior Member Join Date: Mar 2006 Posts: 4,778	Re: Her 2 and Her 3 signalling and Dr M Moasser at SABCS they reported on combining herceptin and lapatinib as well as herceptin and pertuzumab, the latter also blocking her3. 2009 SABCS also reported on neratinib. There are several trials on now I believe with mTor inhibitors, of which rapamycin was the template drug--there are other mTor inhibitor like everolimus which are already FDA approved (for keeping vascular stents open) For about five years not, researcher have realized that the trick will probably be getting the right combination of targeted therapies for the patient's individual tumor characteristics (which oncogenes and signalling pathways are particularly driving its growth and spread) Finding the best test to determine which pathways are the critical ones and then giving the right drugs seems to be the way of the future, but a way which clinical trials as currently designed are ill-designed for. Better ways to test for minimal residual disease (or more bone marrow testing to see if treatments were effective, or better ctc testing) may help.