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The only pathways that matter are those that keep the miscreants alive and thriving. Or as Dr. Weinberg told me, tumor stem cells may explain why you can have tumor shrinkage but not life
extension. If current chemotherapies don't target tumor stem cells, the cells keep making more tumor." '
Hi All -
The above struck a nerve with me, as I have been wondering (and been often asked the question by others) how my liver mets could have come so fast and furiously after having 12 weeks of adriamycin and 4 taxotere and then the 36 rad sessions. (Tumor was small at 1.5cm and 8 of 18 pos nodes.)Only 3 months (!) after completing radiation my liver was over HALF overtaken with tumors.
A real shocker, not only to me and my family, but to my doc and all the people at the cancer center who treated me the first time around. Sure, I was high risk, but this was beyond HIGH!
Now I am wondering how the combination of taxol, navelbine and herceptin that got me out of that situation worked together against ALL the cells, including the nasty little stem cells that must have been working WAY overtime to do what they did.
I know how the drugs work on cells that are dividing as anti-mitotics, etc and how the herceptin latches onto the her-2/neu cells, but what about the stem cells???
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