Women with breast cancer are now categorized into three different subtypes.
One is strongly ER (estrogen receptor) and PR (progesterone receptor) positive and tends to do well with hormonal therapy.
Another group finds negative for ER and PR in testing tends to do better with platinum-based chemotherapy.
The final group carries the human epidermal growth factor receptor #2 (HER-2) and responds to agents that specifically target HER-2.
When HER-2 was first described by Dennis Slamon at UCLA he recognized that these cancers responded well to treatment with drugs that selectively target the HER2 protein. He then developed trastuzumab (Herceptin).
As medical understanding evolves new treatment methods do as well. Subsequent iterations of treatment for HER-2 led to the combination of carboplatin with docetaxel and Herceptin (TCH) and later (due to the CLEOPATRA clinical trial) the combination of a Trastuzumab with a second antibody Pertuzumab (Perjeta) with docetaxel is now used.
In recent years, physicians have begun adding carboplatin to this multi-drug multi-antibody regimen offering patients a sort of “kitchen–sink” approach to their HER-2 (+) disease.
More Isn’t Always Better
The problem is that no treatment, however aggressive or complex, is right for every patient. Adding more and more drugs indiscriminately, however well-intentioned, may be absolutely wrong for some patients.
Testing and developing recommendations specific to each patient is what leads to the best outcome for that patient.
This became abundantly clear when we examined a number of HER2 (+) patients for drug response. What we found was that these patients were not sensitive to the standard-of-care regimens currently in use.
Cancer Success Stories
One patient arrived from St. Louis riddled with disease. Our extensive testing identified
extremely high activity for a treatment combination that did not include the standard docetaxel-based regimen. When her physicians refused to apply our recommended, but well-established and published alternative regimen the patient had us assume her clinical care. After 2 cycles of our chosen treatment, she went into complete remission.
Another patient traveled from Florida to California to undergo biopsy and was also found sensitive to a non-docetaxel regimen. Her physician applied our recommendations, and she went on to achieve a remission that remains durable a year later.
Most recently I was contacted by a patient in Santa Cruz, California with HER2 (+) disease who showed a similar pattern of sensitivity to a non-docetaxel-based regimen. She achieved a complete remission and recently wrote a note to thank us and to say how well she was doing and that “My hair thanks you.”
Each of these patients represents a success that might not have occurred with the standard treatment. While I am perfectly prepared to use docetaxel-based therapy when we find it active and have used this combination in many patients, those patients who reveal other patterns of sensitivity must get the right treatment the first time.
These select HER-2 (+) patients not only do better but also suffer less toxicity when they get the right therapy upfront. Despite advances in breast cancer management, we must all recognize that every patient is unique and that their treatments should be too.