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Faith
there is a lot of this which is not known.
It seems sometimes resistance may result from the cancer utilizing another signalling pathway to circumvent the blocking of another (sort of like the puppy sneaking out the back door when you lock the front door) and sometimes perhaps because other precursor cells now can outcompete the previously dominant cancerous cell type (like crabweed now taking over the lawn after you kill off the dandelions). Dr. Stephanie Jeffrey of Stanford has given a talk about phenotyping (identifying the molecular chaacteristics which typify) circulating tumor cells in her2 + breast cancer patients on herceptin.She reports they are extremely heterogeneous (off all sorts of types ie, E+, E-, her2+, her2-) and in fact reported triple negative ( ER-PR-her2-) circulating tumor cells ciculating in the blood of a patient with Stage IV her2+ breast cancer.
Discussions of the stem cell theory of breast cancer try to explain the origins of her2- metastases possible with her2+ breast cancer, but the answer is elusive and much about this remains controversial, it seems
Hope this helped somehow!
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