“Why gene tests for cancer don’t offer more answers”

An article with the above title appears to be scheduled for upcoming publication in Scientific American but is already available on line on the Scientific American web site. It may be of interest to a number of our readers.

This article, by Jessica Wapner, offers readers a well-explained overview of just why it is so hard to correlate data about genetic defects in cancer cells with tests and treatments that ought to be able to improve patient outcomes associated with specific forms of cancer. The article does not deal in particular with the genetics of prostate cancer, however, … and it is worth noting that prostate cancer is probably one of those form of cancer in which several “driver” mutations (see the article) may be necessary for a cancer to become aggressive.

4 Responses

  1. First, Sitemaster, thanks for spotting this article and bringing it to our attention. It is very much a “glass half full vs glass half empty” piece — the title suggest a “half empty” spin — and this title has already been watered down from the original; reading the article offers many reasons to consider the glass half full!

    Genome sequencing is only about information … just like the PSA test. We need to be careful not to blame the sequencing for any consequences, as has happened with the PSA test.

    For a minority of patients, gene sequencing may offer a productive solution … many men show “actionable genes”, that is to say genes that may be susceptible to treatment; however, only a small percentage appear to respond and the drugs are very expensive. I encourage all who are interested and want to learn more to listen to yesterday’s 45′ webcast by Dr. Larry Fong of UCSF sponsored by the Cancer Research Institute.

    Anecdotally, I have worked with several men this year who have benefited from drugs developed for other cancers — several used olaparib approved for ovarian cancer, with at least one seeing bone tumors melt away; one used a drug approved for lung cancer and melanoma, where sadly he was identified as a candidate too late in the disease cycle — a problem we are addressing; and one with lung cancer is successfully responding to Herceptin, developed for breast cancer.

    We need to acknowledge this is still very early days for both immunotherapy and other drugs targeted at gene mutations. However, the starting point is the sequencing — otherwise how do we identify that a patient may be treatable? The point is to recognize that genome sequencing does not assure a magic bullet to cure any cancer.

    Onward & upwards.

  2. Rick:

    I think what is important about this article is that it places all of the “mays” in some degree of context. Many people are under the illusion that genetic profiling will inevitably lead to identification of drugs that can “cure” things like cancer in the appropriately identified patients. That type of thinking is delusional. At best genetic profiling (at least over the next 25 years or so) is only going to help relatively small subsets of patients, and many in those small subsets will still only gain small improvements in their disease-specific and overall survival times — potentially at cripplingly high cost.

  3. I thought it was already established that men who had progressed to mCRPC and with a family history of cancer would favorably test for a BRCA1 or BRCA2 gene mutation. The TOPARP clinical trial in London has shown that men with with these mutations respond well to olaparib.

  4. Dear Terje:

    The BRCA1 and BRCA2 genes are just two of a whole spectrum of genes that may be found in men with mCRPC and a family history of cancer. They are by no means the only ones.

    Also, having a BRCA1 or BRCA2 gene mutation does not necessarily lead to a diagnosis of prostate cancer in men unless it is associated with other events that are still being investigated. The presence of these germline mutations does, however, increase a person’s risk for cancer.

    If you have a look at this article you might get a better idea of the various genes that are known to be associated with development of the various DNA repair mutations that people hope will be responsive to PARP inhibitors like olaparib.

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