HER2 Support Group Forums - View Single Post - thought provoking hypothesis--?new way to treat breast cancer

AlaskaAngel · 01-11-2009, 02:13 PM

The question that comes to mind for me is, would the difference in endostatin also happen to contribute to the Down syndrome or similar problems (such as chemobrain due to lack of adequate oxygenation from having less angiogenesis, or fewer blood vessels)? Can you have the beneficial effect without the detrimental effect?

I don't want to confuse the concept of reducing angiogenesis with mental meanderings -- but I have speculated as to the reasons why at 7 years out I am still NED (especially since I have not had trastuzumab). One basis that I've wondered about that may be related to blood vessel development is the fact that since starting treatment in 2002, my blood counts have stayed just below normal. I also refused the use of ESAs during treatment, and those would have brought my counts back to normal (or far above normal) during treatment. The effect of that was that my chemo was delayed all 6 times until my counts increased just enough for another dose. It also meant that the duration of low counts was much longer than it was for other patients. If that contributes enough to the lack of angiogenesis, then perhaps my choice not to use ESAs during treatment and the resulting continued low blood count has helped me out and may be continuing to do so.

01-11-2009, 02:13 PM	#4
AlaskaAngel Senior Member Join Date: Sep 2005 Location: Alaska Posts: 2,018	Don't let this post sidetrack the discussion, please The question that comes to mind for me is, would the difference in endostatin also happen to contribute to the Down syndrome or similar problems (such as chemobrain due to lack of adequate oxygenation from having less angiogenesis, or fewer blood vessels)? Can you have the beneficial effect without the detrimental effect? I don't want to confuse the concept of reducing angiogenesis with mental meanderings -- but I have speculated as to the reasons why at 7 years out I am still NED (especially since I have not had trastuzumab). One basis that I've wondered about that may be related to blood vessel development is the fact that since starting treatment in 2002, my blood counts have stayed just below normal. I also refused the use of ESAs during treatment, and those would have brought my counts back to normal (or far above normal) during treatment. The effect of that was that my chemo was delayed all 6 times until my counts increased just enough for another dose. It also meant that the duration of low counts was much longer than it was for other patients. If that contributes enough to the lack of angiogenesis, then perhaps my choice not to use ESAs during treatment and the resulting continued low blood count has helped me out and may be continuing to do so.