FSH receptor and imaging of extracapsular prostate cancer

An article by a French and American research team in today’s issue of the New England Journal of Medicine suggests that it may be possible to target follicle stimulating hormone (FSH) receptor in the early detection of prostate cancer that is not organ-confined.

The report by Radu et al. explains how they were able to use FSH-receptor-specific monoclonal antibodies to bind to tumor samples from patients with many different types of cancer, specifically including prostate cancer. What is not yet entirely clear is the sensitivity of this method to detect the very earliest extraprostatic tumors.

The implication is that by attaching imaging agents to FSH-receptor-specific monoclonal antibodies, it would be possible to use techniques like magnetic resonance imaging (MRI) and positron emission tomography (PET) scanning to selectively identify tumors growing outside the prostate.  However, FSH is expressed primarily in endothelial cells, and so a tumor would have to have developed a sufficient number of endothelial cells to express sufficient FSH receptor for the monoclonal antibodies to bind in actual patients.

This paper is interesting from a scientific point of view, but a lot of work will be needed before we know whether it can lead to a clinically practical mechanism to improve early imaging of extracapsular prostate cancer. The research is also discussed in articles in the Milwaukee Journal Sentinel, on MedPage Today, and on HealthDay.

4 Responses

  1. A fine point. The article says, “If it can be shown that intravenously administered antibodies can detect tumor endothelial cells, the presence of FSH receptor on the surface of these cells in a wide range of tumors makes it a potential target for both tumor imaging and therapy.” PET is not mentioned and is not the most likely method for imaging with antibodies when radionuclides are used, although I found a link about possible development of PET for that purpose. Radioimmunoimaging has generally been with single-photon radionuclides like indium-111, as in ProstaScint. A related matter is therapy with antibodies, which may or may not entail an attached radionuclide, in which case they have been beta-emitting radionuclides, for example, yttrium-90 in Zevalin for certain lymphomas.

  2. Having had my curiosity piqued, I googled to see if there were any MRI-based antibody imaging methods and found this, which includes mention of MRI with a “Herceptin antibody to target Her2/neu expressing breast cancer tumours.” This isn’t state of the art at this time, to the best of my knowledge. I’m getting a bit far afield. My point simply was that, if we stay within conventional methods, imaging FSH receptors with monoclonal antibodies would likely entail single-photon emitting radionuclides and nuclear medicine imaging by planar (2D) and SPECT (3D) techniques rather than PET or MRI. Still, all kinds of wonderful things may happen in the future.

  3. As I understand, FSH (follicle-stimulating hormone) signaling is believed to contribute to the progression of androgen-independent prostate cancer (AIPC) and the GnRH antagonist degarelix suppresses FSH more effectively than LHRH agonists. Supposedly, degarelix is a re-engineering of a drug known as abarelix (Plenaxis). Abarelix was known to directly suppress luteinizing hormone (LH) and follicle stimulating hormone (FSH) secretion. Abarelix was discontinued back in 2005 by Praecis Pharmaceuticals for sale to new patients in the United States “for economic reasons” because of restrictions the FDA had placed on the use of the drug. So, my question is whether the action of degarelix on FSH is sufficient to provide the service described in this paper, or am I completely misunderstanding what is to be accomplished by targeting FSH?

  4. Dear Chuck:

    This paper is referring to a very different effect. It has nothing to do with suppression of FSH. To the contrary, the effect described here would not be possible if FSH was suppressed since it is dependent (in patients with prostate cancer) on significant expression of FSH receptor in extraprostatic tumor cells. You should also note that the effect described is not limited to prostate cancer.

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