Do SPOP mutations define a new molecular subtype of prostate cancer?

A Letter to the Editor just published in the journal Nature Genetics has suggested that that so-called SPOP mutations may be responsible for between 6 and 15 percent of the prostate cancers diagnosed in the USA each year.

Barbieri et al. carried out DNA sequencing of the exomes of 112 prostate tumor and normal tissue pairs. They found that SPOP was the most frequently mutated gene. Prostate cancers with mutant SPOP genes appear to be missing ETS gene family gene rearrangements and — according to Barbieri et al. — demonstrated a clear pattern of genomic alterations. They postulate that prostate cancer tumors with SPOP mutations may define a new molecular subtype of prostate cancer.

Regular readers of the cancer literature will have noticed the increasing frequency with which we are starting to be able to identify subtypes of cancer based on specific genetic mutations (as opposed to which organ a cancer grows in). Among the more striking recent findings was the anaplastic lymphoma kinase (ALK)-positive subtype of non-small-cell lung cancer, which can now be treated with a very specific new drug called crizotinib (Xalkori®). Just last week it was announced (in a paper to be presented at the upcoming ASCO annual meeting) that crizotinib also has activity in certain rare pediatric cancers that are also associated with expression of the ALK-positive gene. Carriers of the ALK-positive gene can be identified through the use of a complementary test.

Identification of specific genetic subtypes of prostate cancer may — similarly — allow us to develop therapies that can be targeted to genetic subsets of prostate cancer.

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