[Lani]

Mandamoo--there are many things that can make a cancer resistant to her2 directed antibodies (you did not say if Lapatinib has worked for you)

Among others:

your her2 is a shortened version which does not have the right area for the antiher2 antibody to grab onto (lapatinib, neratinib and other TKIs might then work for you)

your her2 does not have the right configuration in that area for herceptin to grab onto (pertuzumab may work for you)

Your tumor is also being driven by her3 (pertuzumab may work for you and perhaps other TKIs like neratinib), your tumor is also being driven my IGFR1
or other pathways that crosstalk--in which case you need the right combination to block two or three of these pathways or a pathway downstream (PI3K inhibitors, AKT inhibitors, mTor inhibitors) or something which keeps proteins from being folded/chaperone'ing like a HSP 90 inhibitor.

Your tumor may make a lot of mucin which coats the cells and keeps the antibodies from getting close enough to block the receptors (an antiMuc antibody might be helpful)

But helping the immune system get around some of cancer's tricks to keep it from recognizing and working may be easier than characterizing all the paths your tumor uses to escape herceptin and blocking them all.

That is why this finding, Dr. Ronald Levy's latest work and the adoptive T cell therapy of Dr Rosenberg give so much hope.

Hope this explanation helped

For more discussion of how her2+ cancers get around herceptin, read the works of Dr Carlos Arteaga among others (just google ENTREZ PUBMED and enter Arteaga C)