A new study recently published in the journal Nature Genetics revealed a molecular portrait of the spatial heterogeneity of localized, multifocal prostate tumors in patients, disclosing a new gene family that drives cancer development. The study is entitled “Spatial genomic heterogeneity within localized, multifocal prostate cancer” and was conducted by an international research team led by researchers at the University of Toronto, the Ontario Institute for Cancer Research and the Princess Margaret Cancer Centre, University Health Network (UHN) in Canada.
Prostate cancer is the second most common cancer in men with almost one million new cases diagnosed every year worldwide. It is a curable cancer that can range from slow-growing tumors to rapidly progressing aggressive tumors, which are more difficult to treat.
In the study, researchers analyzed the molecular profile of 74 prostate cancer patients with a Gleason Score 7, which corresponds to a medium-grade cancer in terms of aggressiveness. Among them, multiple tumors from five patients who had their prostates surgically removed were submitted to whole-genome sequencing (23 tumor samples). The team conducted a careful detailed analysis of each tumor genetics and was able to assign specific “aggression scores”. Researchers found that even small tumors can contain aggressive cells that are able to change a patient’s prognosis.
“Our research shows how prostate cancers can vary from one man to another – despite the same pathology under the microscope – as well as how it can vary within one man who may have multiple tumor types in his prostate,” explained the study’s senior author Dr. Robert Bristow in a news release. And he adds, “these sub-types may be important to determining the response to surgery or radiotherapy between patients.”
In their analysis, the team found that two members of the MYC cancer gene family in particular – C-MYC and L-MYC – were involved in cancer development, with the C-MYC gene being the one that drives an aggressive phenotype. Researchers reported that around half of all prostate cancer patients have either C-MYC or L-MYC mutations, but never both.
“This discovery of a new prostate cancer-causing gene gives researchers a new avenue to explore the biology of the disease and improve treatment,” noted the study’s lead author Dr. Paul Boutros. “By showing that mutations in prostate cancer vary spatially in different regions of a tumor, this study will aid in the development of new diagnostic tests that will improve treatment by allowing it to be further personalized.”
“Our findings suggest we are getting closer to subtyping prostate cancer based on which gene is present to determine a patients’ disease aggression in terms of the risk of spread outside the prostate gland at time of treatment. In developing this research tool into a clinical test within three years, we hope to inform doctors and patients about specialized treatments for each prostate cancer patient.” concluded Dr. Bristow.
The team believes that their findings may be valuable to determine disease aggression phenotype, representing a step further in the road to personalize prostate cancer treatment.
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