Personalized medicine actually has two meanings. The first, and probably the one most familiar to us in San Francisco, is the trend to have "concierge" style medicine - usually an internist, family practitioner, or Ob/Gyn who takes a panel of patients for a set fee per patient, rather than taking insurance. This is a prominent phenomena in many cities, for a variety of reasons. We may touch on this in another column.
What I want to touch on is the idea of personalized medicine for cancer patients. This is the vision we all see as treating physicians of being able to use tailor made, or personalized, treatments for cancer patients.
Breast cancer was one of the earliest cancers to have this personalized touch through the works of pioneers in cell biology, researchers (such as the eminent Sir Craig V Jordan, formerly at Northwestern and now at Fox Chase) and most importantly patients.
Every breast cancer patient has her cancer tested for estrogen receptor, progesterone receptor, and Her2 status - Her2 being the latest addition to the personalized medicine armamentarium and arising in just the past ten years.
We know that medicines such as tamoxifen and the aromatase inhibitors work only in women with estrogen positive breast cancers, and that Herceptin only works in Her2+ breast cancers. We have personalized breast cancer treatment in terms of offering therapy for each woman that will give her the greatest chance of cure - or in the metastatic setting the greatest chance of response and durable remission.
Personalized medicine is about to get more interesting. If one looks at choices of therapy in colon cancer, for example, we now know that one drug will work only in patients who have a "wild type K-ras" meaning that a protein involved in the cell cycle division process (dividing into two new cancer cells) must be preserved in structure for the drug to work. This is the biologic equivalent of stealth bombing.
These targets will arise in breast cancer as well since all cancer cells have similar biologic molecules involved in their unfettered cell division. A recent paper alluded to the higher probability of response with Bevacizumab based treatment, a targeted therapy against a molecule called vascular endothelial growth factor, in patients who have certain receptors for this molecule. Whereas now treatment is often empiric, we are moving towards the more specific.
Gene chip microarray technology - looking at genes expressed - will be utilized more in the future, as will its cousin proteonomics - assaying which proteins are expressed. What will this mean for the patients? It will hopefully mean better targeted therapies, with higher chances of working, and with less toxicity. Science marches on!