[1rarebird]

Lani-- You are correct about the unpublished value of blocking both ends of the Her2 receptor. I probably used an imprecise term when referring to "cross-talk" and am guilty of mixing apples with oranges. The dual blocking I was trying to discuss involves the ER and Her2+ receptors. I was trying to point out that I believe some research has been documented which shows ER+ and Her2+ breast cancers may not respond as well as hoped to either tratuzumab or anti-estrogen therapy, when they are used alone and not concurrently with the other. I came away with this understanding by reading information in web-based references such as:

http://www.medpagetoday.com/MeetingCoverage/IMPAKT/19995
http://her2support.org/vbulletin/showthread.php?t=38998
http://www.medpagetoday.com/MeetingCoverage/AACR/19632
http://clincancerres.aacrjournals.org/content/11/2/865s.abstract?ijkey=a0c53aa508e1b27bedaf4f4a7dfc44 c0acc4c701&keytype2=tf_ipsecsha

What was described in the above references sounded to my untrained ears as something akin to "cross-talk". At any rate, I believe the researchers hypothesize that using an anti-estrogen compound plus an agent to impact Her2+ receptors should yield better response to these double positive cancers. I recall that Tykerb, Herceptin and probably Neratinib could be used as the Her2 + drugs, while the SERMs and A/Is could be used as the anti-estrogen drugs.

I could have this all wrong and I hope I have not confused anyone. It was not intentional on my part. I would note that at my last meeting with my oncologist, when I brought this "cross-talk" issue up, he seemed to know what I was concerned about and promised we would discuss it in more detail when I get nearer to the end of my Herceptin-year.

As you can see from my signature, this is important stuff to me and it becomes quite complicated to me at times. Thanks for asking.--bird