[Lani]

GRB7 is on the same amplicon (segment of DNA) close by her2, but they are not always amplified together. It is similar to TOP2A (which if I recall is quite a bit further away down the amplicon from her2 than GRB7 is) Some her2 amplified patients also have TOP2A amplified, some do not and it influences whether/how effective and necessary anthracyclines are for these patients (Dr. Slamon has had lots to say about this)

There has been talk from time to time that GRB7 is the culprit and not her2, but that her2 amplification was what was noticed in the breast cancers with worse prognosis. Perhaps by making a monoclonal antibody to her2 we have merely found a target which tend to occur together with GRB7 (the possible culprit)--but not always--and that it is the ADCC immune reaction that the herceptin brings about that improves the prognosis of the breast cancer patients rather than the inactivation of her2, her3 etc.

Glad they keep looking at things with open eyes, rather than assuming what has been "considered dogma" in the past is ultimate truth. It may or may not turn out that GRB7 is the culprit and her2 the standerby, but every bit of research brings us a bit closer to the truth and a cure.