heblaj01
12-16-2006, 11:04 PM
Could someone in the group attending the SBCS find out from the experts if there is an answer to these questions:
some patients initially treated for HER-2+ breast cancer with Herceptin develop resistance &/or revert to ER+ cancer.
It seems (from readings) there are two different outcomes: some cases are said to be the result of crosstalk whereby ER are stimulated by HER-2 independantly of circulating estrogen.
Other cases are reported to be responsive to estrogen inhibition treatments
such as aromatase inhibitors.
Is this distinction accurate?
If so, what diagnostic tools are available to determine to which of the two cases a patient belong?
Among the oncs at SABCS who might have a clue & be interested is Dr RJ PIETRAS who had an unrelated presentation saturday. He is otherwise involved in the Phase 2 clinical trial of Fulvestrant+ Herceptin which aims at proving that suppression of estrogen receptors with Fulvestrant prevents HER-2 stimulation of ER independantly of circulating estrogen.
Thanks!
some patients initially treated for HER-2+ breast cancer with Herceptin develop resistance &/or revert to ER+ cancer.
It seems (from readings) there are two different outcomes: some cases are said to be the result of crosstalk whereby ER are stimulated by HER-2 independantly of circulating estrogen.
Other cases are reported to be responsive to estrogen inhibition treatments
such as aromatase inhibitors.
Is this distinction accurate?
If so, what diagnostic tools are available to determine to which of the two cases a patient belong?
Among the oncs at SABCS who might have a clue & be interested is Dr RJ PIETRAS who had an unrelated presentation saturday. He is otherwise involved in the Phase 2 clinical trial of Fulvestrant+ Herceptin which aims at proving that suppression of estrogen receptors with Fulvestrant prevents HER-2 stimulation of ER independantly of circulating estrogen.
Thanks!