Meet the Investigator: Dr. Janet Stanford

In addition to genetics, social and environmental dynamics can also play a role in determining an individual’s risk for prostate cancer. As the principal investigator of large population-based case-control studies, cancer epidemiologist Dr. Janet Stanford focuses on evaluating how these environmental and lifestyle factors may affect disease risk, progression/recurrence and prostate cancer-specific mortality.

Close family ties led Janet Stanford, PhD, to become a prostate cancer researcher. After learning her father had been diagnosed with the disease in 1984, she questioned what variable risk factors might have caused his prostate cancer diagnosis. She quickly realized that there was little research to address this issue.

“There was very little support for prostate cancer research during the 1970’s and 80’s – few investigators were doing it,” says Dr. Stanford, co-Head of Program in Prostate Cancer Research at the Fred Hutchinson Cancer Research Center in Seattle. “Back then the assumption was that almost 100% of men would develop prostate cancer in their lifetime, but they wouldn’t develop it until they were quite elderly and would die from some other cause.”

Recognizing the lack of research findings on the causes of prostate cancer and the emerging evidence that a family history of the disease conveyed an increased risk, Dr. Stanford and colleagues Drs. Elaine Ostrander and Lee Hood decided to tackle the problem by initiating a family-based study called the Prostate Cancer Genetic Research Study (or PROGRESS).

The study, which received its initial four years of funding in 1994 from CaP CURE (now the Prostate Cancer Foundation), currently tracks members of 307 high-risk prostate cancer families - analyzing the correlation between prostate cancer and genetic markers across the genome in order to find the location of genes with mutations that lead to development of the disease.

Mike Milken Makes TV Appeal
In 1995, PROGRESS gained considerable momentum after PCF-founder and Chairman Mike Milken made a public appeal to viewers on the Larry King Live Show. With a 1-800 number scrolled at the bottom of television screens during the interview, Milken urged those who had a family history of prostate cancer to call and be a part of the study.

According to Dr. Stanford, Milken’s appearance resulted in thousands of phone calls throughout the night of the broadcast. She and her staff had to forward calls to voicemail after inquiries about the study continued to pour in up until the wee hours of 2 a.m.

“The Larry King Live Show was the best recruitment plan ever,” said Dr. Stanford. “The 1-800 number made it easy for people to contact us directly, and it didn’t require them to get a physician’s referral.”

Since that Larry King Show airing, PROGRESS has surveyed more than 2,200 members of families throughout North America who fit the criteria of having at least three first-degree relatives who have had prostate cancer--three generations of relatives with prostate cancer, or at least two first-degree relatives who have had prostate cancer diagnosed at an early age. 

To date, the compilation of the family records has given Dr. Stanford and other scientists a much needed resource for advancing prostate cancer.

“The families make me want to keep going to do something that will be meaningful for all the time, effort, and commitment they’ve given to this study,” said Dr. Stanford

PROGRESS has been made
Due to the ongoing data collection and analyses of PROGRESS families, Dr. Stanford and colleagues recently published findings from a genome-wide SNP (single nucleotide polymorphism) linkage scan in the Human Molecular Genetics journal – highlighting linkage between specific chromosomes and susceptibility to hereditary prostate cancer.

Findings from this and earlier studies of PROGRESS data have drawn attention to three chromosomes in particular - chromosomes 1p36, 22q and 15q – that were found in the study, and confirmed by independent researchers, to play a role in families with early onset or more aggressive forms of prostate cancer. Previous analyses by Dr. Stanford also showed chromosome 1p36 was important factor for a subset of families with hereditary prostate cancer that also had relatives with primary brain cancer. 

“The PCF’s funding was critical, absolutely critical for starting this research,” said Dr. Stanford. “PROGRESS would have never happened if it weren’t for that initial funding. That support went towards the first critical stages of collecting the families’ information, collecting the blood samples and getting them processed, and making the DNA available to researchers for genotyping.”

Dr. Stanford’s long-term goal is to continue to identify chromosome locations that may contain genes with mutations responsible for prostate cancer and to work with colleagues to characterize those genes and genetic mutations.  Follow-up studies will look to determine the role of such genetic mutations in mediating risk in men with hereditary prostate cancer as well as in men with sporadic prostate cancer (i.e., those without a family history of the disease).

Meet the other prostate cancer investigators PCF has profiled.