[Lani]

It implied that if mutation/deletion occurs in both the ECD(extracellular domain--the part of her2 outside the cell membrane) of her2 and in this PTP1B, then the formation of her2+ breast tumors and their metastasizing to the lung were both impeded (whereas just having the mutation of the ECD of her2 had the opposite effect).

These types of experiments are done ie, mutating or deleting gene 1 only vs gene 1 and 2 vs gene 2 only as a way of trying to dissect out what the function of genes are and how the proteins coded for by the genes are related and influence each other.

In this case mutating/deleting either her2ECD or PTP1B alone lead to tumor formation and/or metastasis whereas mutating/deleting both tended to prevent tumor formation and metastasis.

Obviously the full paper gave more of an explanation to their conclusion that the (down) regulation occcurs via inhibition of both the AKT and MAPK pathways that are downstream (occur after in a chronological fashion) of
her2.

This is basic science research trying to find out how all these genes and the proteins they code for interact, feedback on each other (either positively or negatively) in order to understand what drives a tumor and what inhibits it.

The hope is for deleting or inhibiting both ie, combining herceptin or another her2ECD inhibitor/complexing compound or antibody with another targetted treatment (antibody or small molecule) that targets PTP1B

Sounds very far from the lab bench into the clinic--but each little bit of understanding helps us understand the complex forces that drive tumors to divide and spread.

Hope this helps