Genetic Markers Associated with Early Cancer-Specific Mortality

A team of scientists at Wake Forest School of Medicine (Winston-Salem, NC, USA) used a method that can detect these genetic changes in cells from prostate tumors from 125 patients who underwent radical prostatectomy between 1988 and 2004. A second cohort included 103 prostatectomy patients who were treated between 2002 and 2008 with a median follow-up of approximately five years most of whom had a less aggressive form of PCa.

CNAs in tumor DNA samples from 125 patients in the discovery cohort who underwent prostatectomy were assayed with high-resolution Affymetrix 6.0 single-nucleotide polymorphism microarrays (Santa Clara, CA, USA) and then were analyzed using the Genomic Identification of Significant Targets in Cancer (GISTIC) algorithm.

The investigators found that changes in 20 gene regions were likely contribute to prostate cancer development and changes in seven of the 20 regions were linked with early death from prostate cancer. Patients whose cancer cells had a loss of the gene that encodes for phosphatase and tensin homolog protein (PTEN) and an amplification of the gene that encodes for myelocytomatosis viral oncogene homolog (MYC) were more than 50 times as likely to die from prostate cancer than other patients who had similarly staged tumors and prostate-specific antigen levels at the time of diagnosis. Analyses of 333 tumors from additional patients confirmed the link between PTEN and MYC and prostate cancer lethality.


The genetic changes involved in the development and progression of prostate cancer may help guide doctors as they weigh different treatment options for patients with the disease. Jianfeng Xu, MD, DrPh, the senior author said, “Prostate cancer patients who have DNA copy number alterations at PTEN and MYC may not be appropriate candidates for active surveillance and should be treated intensively.” The study was published on April 22, 2013, in the journal Cancer.

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Wake Forest School of Medicine
Affymetrix