Just to follow up Becky's point (and underscore my own about involving an endo) research is showing that hormone resistance is a relative state, i.e., once you become resistant to hormone therapy, there is a possibility that the sensitivity can be restored by changing the treatment. I don't know if the same holds true for antibiotics; we are talking about mutated bacteria in the latter, while in the former (hormone sensitive bc) we are looking at an extensive array of complex signaling that seems capable of being sucessfully maniupulated if we only had the key. We need more study in this arena, less in the "blast it to heck" cytotoxic field. Incremental benefits are seen to accure from large random tests in the latter where dosage, timing and combinations may be slightly modified for marginal gains. The measurable improvements in bc tx have come from entirely different approaches and agents, most notably, Herceptin. Since something like 70% of all bc is ER+, it is appalling to me so little is done to explore areas other than SERMS and AI's for tx, which are relatively simple approaches to controlling the disease, as research continues to reveal more and more layers of complexity in signaling and greater opportunity for intervention. The fact that ER+ bc has a longer and more persistent relapse rate over time than ER- bc is all the more reason to put the pressure on researchers to focus their efforts on what can be done to maintain ER+ bc patients NED for 20, 30 or more years after initial dx and tx.
Thanks for letting me get on my soapbox
Hopeful
Antiestrogen conclusion (SERMs and AIs)
</O
Keeping one step ahead of cancer
Linear Mode
