The focal therapy discussion continues


An article in this week’s New England Journal of Medicine has argued that an earlier report, postulating the monoclonal origin of lethal metastatic prostate cancer, increases the justification for focal therapy for early stage prostate cancer.

Earlier this year, Liu et al. presented data from autopsy studies of men who died from metastatic prostate cancer suggesting that their cancer could be traced back to a single malignant clone of cells in their prostate. We commented on this study in a report on April 18.

Now, Ahmed has published an opinion piece in which he ties the research by Liu et al. to the potential of focal therapy for prostate cancer. He writes that focal therapy “is based on the idea that management of localized prostate cancer can follow the organ preservation approach taken in the treatment of almost all other solid tumors,” and that, “In other words, ablation of only the malignant areas within the prostate, along with a margin of normal tissue, and preservation of normal prostate and surrounding structures will help reduce side effects.” 

The full text of Ahmed’s article is not available on line, but a detailed commentary has already appeared on Medscape. Reaction to Ahmed’s article seems to vary from the relatively sensible to the inevitably outraged.

In the view of The “New” Prostate Cancer InfoLink, focal therapy is a potentially promising technique for the treatment of early stage prostate cancer in appropriately and carefully selected patients. However, a great deal more work is going to be needed before it becomes routine, and one of the critical factors is going to be deciding whether man who may be the easiest to treat with focal therapy (men with low risk disease clearly confined to part of one lobe of the prostate) actually need treatment at all. He may do just as well on active surveillance.

While the point originally made by Liu et al. was that you could (in their opinion) trace metastatic prostate cancer back to a single clone of cells in the prostate, and while that observation would certainly justify the theoretical applicability of focal therapy, this research does not mean that it is easy to find and identify the specific clone of cells that might lead to metastatic disease before it happens. We still have a long way to go before we can accurately find an identify such groups of cells and “zap them” — with radiation or cryotherapy or high-intensity focused ultrasound (HIFU) or any other form of treatment — with any degree of confidence that we would actually be able to cure the patient of his risk for progressive disease. On the other hand … it does seem as though we are moving slowly but surely toward such a possibility in the future.

3 Responses

  1. Access to this article, and upwards of 350 others on prostate cancer in the NEJM can be accessed for 21 days by clicking on this link.

  2. What I fail to understand is how you get from “a single clone of cells in the prostate” to multi-focal disease.

  3. First, let us differentiate between multi-focal disease and the transition from localized disease to metastatic disease.

    I do not believe that Bova and his colleagues ever stated that the single clone of cells that led to death from metastatic disease in the patients they studied was the only clone of cells that initially occurred in the prostates of those patients. What they said was that the metastatic disease that killed them could be traced back to a single, specific clone of cells in the patients’ prostates.

    So … multi-focal disease within the prostate can have two possible causes: (a) It may occur because more than one event occurs in the prostate, leading to more than one initial clone of prostate cancer cells (of potentially differing aggressiveness). (b) It may occur because one initial clone of cells metastasizes within the prostate, but demonstrates differing aggression in different environments even within the prostate.

    Remember that as we age and change we all produce potentially cancerous cells all of the time (and probably some of us more commonly than others). For people with highly effective and efficient immune systems, this may be an irrelevant issue because their immune systems simply eliminate the cancer cells as “non-self” nearly as fast as they are produced. For others, with less effective or efficient immune systems, the initial growth of small tumors may be an inevitability, and the question becomes potentially clinically significant. However, we still know remarkably little about the natural history of cancer cell production and demise or development in normal — as opposed to specific, laboratory — animals (let alone in man).

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