An aggressive, ETS-negative subtype of prostate cancer

A paper just published in Cancer Research suggests that a particular ETS-negative subtype of prostate cancer (ERGMAP3K7delCHD1del) is highly aggressive, and that coordinate loss of the MAP3K7 and CHD1 genes are potentially a unique driver of development of aggressive prostate cancer.

The paper by Rodrigues et al. is complex, and uses development and cell line xenograft models to evaluate the author’s hypothesis, which will need further careful study. However, as explained in a media release issued the University of Colorado Cancer Center:

  • About 10 percent of men with progressive prostate cancer die from their disease.
  • About 10 percent of all prostate cancers harbor combined MAP3K7-CHD1 deletions.
  • About half the prostate cancer patients with combination MAP3K7 and CHD1 deletions will have recurrent prostate cancer, which ultimately leads to death (if the patients do not not die earlier of other causes).

These data suggest that a significant percentage of all prostate cancer deaths may be associated with the ERGMAP3K7delCHD1del prostate cancer subtype, and, if that is the case, efforts to find an effective way to treat this subtype of prostate cancer may have a dramatic impact on prostate cancer-specific mortality rates.

4 Responses

  1. In trying to decipher this report, it appears that 10% of men are found to have this MAP3K7 and CHD1 protein presence, and if this presence is then not retained, the suppression of both causes the aggressiveness of their prostate cancer that will likely lead to early demise. So, please correct me if I am wrong in that what has to be determined is “what causes their suppression” so that medications possibly prescribed prostate cancer patients are not among those being that cause. Also not explained is how is one tested to determine the presence of these MAP3K7 and CHD1 protein?

  2. Dear Chuck:

    I haven’t seen the full text of this paper (and I suspect you haven’t either), but I am not sure you are interpreting the abstract correctly at all.

    The media release and the abstract both state clearly that about 10% of all prostate cancers harbor combined MAP3K7-CHD1 deletions. In other words, this is a normal genetic subtype of prostate cancer that develops even prior to any treatment. Thus, it is not necessarily caused by a specific type of treatment (drug therapy or other) at all.

    I am sure that the full text of the paper explains how to test for these genetic deletions in detail, but the way that I would expect this to be done would be by using fluorescence in situ hybridization (FISH) analysis (a very common method for identification of specific gene deletions) and similar methodologies. These types of analysis are commonplace in the cytogenetic work-up of patients with various types of blood cancer, so I don’t think it would be hard to apply them to a solid tumor like prostate cancer.

  3. Thanks, Sitemaster … So it is the absence at diagnosis of these proteins that are the biomarkers that the patient has an aggressive and deadly form of prostate cancer.

  4. I believe so … but I would need to see the full text of the paper to be 100% clear about this.

    The additional point that the authors seem to be making is that in theory it might be possible to develop specific types of treatment protocol for patients with the combined MAP3K7/CHD1 deletions. However, that might be difficult to accomplish and so I wouldn’t be placing a large bet on that happening in the immediate future.

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