Christopher Barbieri, a fifth year urology resident at Weill Cornell insisted that the motivation to search for genes in this way came about because of the observation that SPOP appeared to be mutated in some cases of prostate cancer.
In addition to SPOP mutations, which occurred in 6 to 15 percent of tumours across multiple independent cohorts, investigators found mutations in the FOXA1 and MED12 genes, each of which are found in about 4 percent of patient tumors.
Further examination revealed the interesting nature of SPOP mutations.
SPOP belongs to a class of proteins named 'ubiquitin ligases', whose role is to mark other proteins in the cell for degradation.
The team discovered that the mutations occur where the SPOP protein binds to the other proteins it should tag.
Because these mutations were also found in premalignant lesions, the researchers suspect SPOP mutations occur early in development of the cancer.
However, they do not yet know if SPOP mutations define a more aggressive type of prostate cancer.
Rubin further revealed that SPOP mutations and TMPRSS2-ERG fusion genes never occur in the same tumour.
As the results suggest, BPOP (columns  and , SPOP
(columns , , and ), LFPR (columns , , and ), and GGDP (columns , , and ) are all positive.
Rubin and colleagues have identified a unique class of prostate cancer patients that have mutations in the gene for SPOP (Speckle-type POZ Protein).
Discovery of SPOP inhibitors will potentially create a new therapy for metastatic prostate cancer and, in time, will support highly personalized treatment for patients.