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Angel
you are right that if you might also be Her1+ or Her3+ there would be cross talk between the estrogen receptor and a Her1 or3 receptor and that could render tamoxifen resistance even though the Her2 receptor is blocked by Herceptin. However, EVERYTHING loves the Her2 receptor (to cross talk with - what an attractive fellow Her2 is). So, if you have blocked Her2 with Herceptin and then blocked ER with tamoxifen, there is alot of interference on the surface of the cell to deal with - alot of molecules getting in the way for Her1 to have to cross talk to itself (and from what I have read, Her1 likes to cross talk with others and not itself). Also, I went to a presentation at ASCO on ER+ but PR negative. I went because that is what I am and it is pretty unique. If you are PR+ it is better yet since if you are PR- you also tend to be Her2+ (like me) but if you are also Her2 negative, you are probably Her1+ (because only Her2 likes to also cross talk with itself but everything else likes to cross talk with something different) so if ER+ but PR neg - something else is there and if it isn't Her2 then it is Her1 (but some Her2+ are also Her1+ but if they are ER+ as well, they probably are not Her1+ (or only mildly so)). So, this paper said if you are only ER+, tamoxifen does not seem to work (had lots of results) and this is because these women's tumor blocks tested positive for Her2 and/or Her1. These women tended to be younger or African American.
Lastly, some women do not respond to Herceptin because of several factors:
1. they are actually also Her 1 or Her 3 as well so that continues to drive the cancer
2. if they were hormone negative, they may have changed to positive
3. they may have the truncated version of Her2 (no receptor on the outside for Herceptin to bind so the receptor is always on the "on" position - Tykerb could work here as it works inside the cell and not outside the cell).
Becky
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