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

Lani · 01-13-2011, 09:40 AM

this goes back to studies done on mice by Dr Kent Osborne back about 6or 7 years ago. He blocked egfr, her2 and her3 and the tumors went away and didn't recur for the life of the mouse even when ER was not blocked on those tumors that were er+

I think it will depend on an individual tumor's driving signalling pathways as well as the tumor's response to the drugs--some tumors secrete a large mucin molecule that acts like an oil slick around the cell and keeps the drug from getting to the receptors. Other tumors lack PTEN or other parts of the signalling pathway or have a truncated her2 so herceptin can't get at the extracellular domain to bind to the receptor.

I think we are getting close to having enough drugs to mix and match to keep her2+ bc under control if not cure it. However we are now nowhere near being able to discover for any one particular patient's tumor which combination will be the right one for them. I think we can catch up relatively quickly to be able to find a way to predict that magic tailor-made combination if government funding were to be increased (it is now being decreased), research emphasis were placed on this problem and people let their computers be used for the hours they are down to share the computing power with researchers off-hours. We are closer than we have ever been and we are understanding a subtype of breast cancer (her2+) better than we have understood any other type. I hope the trends in medicine do not prevent individualized treatments, as there seems to be a consensus that this will be necessary.

We need the will to have the way (like the goal in 1960 of going to the moon in the next 5-8 years)

01-13-2011, 09:40 AM	#13
Lani Senior Member Join Date: Mar 2006 Posts: 4,778	Re: Her 2 and Her 3 signalling and Dr M Moasser this goes back to studies done on mice by Dr Kent Osborne back about 6or 7 years ago. He blocked egfr, her2 and her3 and the tumors went away and didn't recur for the life of the mouse even when ER was not blocked on those tumors that were er+ I think it will depend on an individual tumor's driving signalling pathways as well as the tumor's response to the drugs--some tumors secrete a large mucin molecule that acts like an oil slick around the cell and keeps the drug from getting to the receptors. Other tumors lack PTEN or other parts of the signalling pathway or have a truncated her2 so herceptin can't get at the extracellular domain to bind to the receptor. I think we are getting close to having enough drugs to mix and match to keep her2+ bc under control if not cure it. However we are now nowhere near being able to discover for any one particular patient's tumor which combination will be the right one for them. I think we can catch up relatively quickly to be able to find a way to predict that magic tailor-made combination if government funding were to be increased (it is now being decreased), research emphasis were placed on this problem and people let their computers be used for the hours they are down to share the computing power with researchers off-hours. We are closer than we have ever been and we are understanding a subtype of breast cancer (her2+) better than we have understood any other type. I hope the trends in medicine do not prevent individualized treatments, as there seems to be a consensus that this will be necessary. We need the will to have the way (like the goal in 1960 of going to the moon in the next 5-8 years)