Janet L. Stanford
Ph.D., Johns Hopkins University, Epidemiology, 1986.
M.P.H., Emory University, 1982.
B.S., Georgia State University, Nursing, 1980.
The role of environmental, lifestyle and genetic risk factors in relation to cancer etiology, progression and mortality
My main research interests focus on hormonal, environmental, lifestyle and genetic factors that may alter cancer risk, cancer progression, and disease outcomes such as cancer-specific mortality. The role of underlying genetic susceptibility based on rare, and high penetrance mutations as well as more common genetic variants of lower penetrance is a major focus of my research. As a cancer epidemiologist, I have been involved in the development, implementation, and analyses of research studies of the etiology and progression of several different types of cancer, however, my current concentration is on prostate cancer.
The completion of two large population-based case-control studies of risk factors for prostate cancer has allowed us to examine environmental/lifestyle exposures and genetic polymorphisms in candidate genes in relation to prostate cancer etiology and outcomes. Selected results from these studies have shown that: 1) vasectomy is not associated with risk of prostate cancer; 2) higher consumption of cruciferous vegetables, moderate intake of red wine, and regular aspirin use are each associated with reduced risks of prostate cancer; 3) high intensity cigarette smoking increases the risk of prostate cancer; 4) there is an increased risk of prostate cancer among men with a first-degree family history of prostate cancer who carry a specific genetic variant in the CYP17 gene, which is involved in testosterone production; 5) men who are null for the glutathione S-transferase (GST) M1 gene have an increased risk of prostate cancer, particularly among heavy smokers; 6) men who are carriers of BRCA2 mutations have an increased risk of prostate cancer; and 7) genetic variants on chromosome 8q24 are associated with elevated risks of prostate cancer.
We are currently following a large cohort of prostate cancer patients long-term to evaluate how environmental/lifestyle factors and genetic polymorphisms in candidate genes within pathways of interest for prostate cancer as well as single nucleotide polymorphisms (SNPs) identified from genome-wide scans may affect disease progression/recurrence and prostate cancer-specific mortality. Results from these studies indicate that: 1) obesity at the time of prostate cancer diagnosis is associated with over a 2-fold excess risk of adverse outcomes (i.e., progression to metastatic cancer, death from prostate cancer); 2) smoking at the time of prostate cancer diagnosis is associated with adverse patient outcomes; and 3) patients who are treated with androgen deprivation therapy have different outcomes based on genetic variation in the megalin gene, which is involved in androgen transport. Our ongoing studies aim to identify individual SNPs and combinations of genetic variants that may be useful, in addition to standard clinical factors, for better prediction of individual patient outcomes. In addition, we are evaluating how the diagnosis and treatment of prostate cancer affect long-term urinary, sexual and bowel function and general health-related quality of life.
I am principal investigator for the data collection component of the Prostate Cancer Genetic Research Study (PROGRESS), a large family-based study of hereditary prostate cancer. We have enrolled over 300 families with multiple members who have been diagnosed with prostate cancer, some at particularly early ages. Blood samples, baseline and follow-up questionnaires, and medical records are collected on participants. Two genome-wide scans using microsatellite and SNP markers have been completed. Linkage analyses highlighted several regions of interest (e.g., chromosomes 15q, 22q) that we are following up with further studies. We are currently completing a next-generation sequencing project to identify genetic mutation(s) in the 15q linkage region. We are also initiating a whole-exome sequencing project on selected high-risk families with aggressive and/or early onset prostate cancer. The long-term goal of PROGRESS is to identify loci that may contain genes with mutations responsible for hereditary prostate cancer.
Confirmation of genetic variants associated with lethal prostate cancer in a cohort of men from hereditary prostate cancer families.. International journal of cancer. Journal international du cancer. 136(9):2166-71.. 2015.
Obesity and Prostate Cancer Risk According to Tumor TMPRSS2:ERG Gene Fusion Status.. American journal of epidemiology. 181(9):706-13.. 2015.
Self-Reported Health Status Predicts Other-Cause Mortality in Men with Localized Prostate Cancer: Results from the Prostate Cancer Outcomes Study.. Journal of general internal medicine.. 2015.
Risk Analysis of Prostate Cancer in PRACTICAL, a Multinational Consortium, Using 25 Known Prostate Cancer Susceptibility Loci.. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology.. 2015.
Influence of age on incident diabetes and cardiovascular disease in prostate cancer survivors receiving androgen deprivation therapy.. The Journal of urology. 193(4):1226-31.. 2015.
A Large-Scale Analysis of Genetic Variants within Putative miRNA Binding Sites in Prostate Cancer.. Cancer discovery. 5(4):368-79.. 2015.
Two susceptibility loci identified for prostate cancer aggressiveness.. Nature communications. 6:6889.. 2015.
Generalizability of established prostate cancer risk variants in men of African ancestry.. International journal of cancer. Journal international du cancer.. 2014.
Genetic predisposition to prostate cancer: Update and future perspectives.. Urologic oncology.. 2014.
Diet and lifestyle factors and risk of subtypes of esophageal and gastric cancers: classification tree analysis.. Annals of epidemiology. 24(1):50-7.. 2014.
Is digoxin use for cardiovascular disease associated with risk of prostate cancer? The Prostate. 74(1):97-102.. 2014.
Leveraging population admixture to characterize the heritability of complex traits.. Nature genetics. 46(12):1356-62.. 2014.
Validation study of genes with hypermethylated promoter regions associated with prostate cancer recurrence.. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology.. 2014.
Germline Missense Variants in the BTNL2 Gene Are Associated with Prostate Cancer Susceptibility.. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 22(9):1520-8.. 2013.
Circulating levels of 25-hydroxyvitamin D and prostate cancer prognosis.. Cancer epidemiology. 37(5):666-70.. 2013.
Effect of age, tumor risk, and comorbidity on competing risks for survival in a U.S. population-based cohort of men with prostate cancer.. Annals of internal medicine. 158(10):709-17.. 2013.
Mortality after radical prostatectomy or external beam radiotherapy for localized prostate cancer.. Journal of the National Cancer Institute. 105(10):711-8.. 2013.
Long-term functional outcomes after treatment for localized prostate cancer.. The New England journal of medicine. 368(5):436-45.. 2013.
Consumption of deep-fried foods and risk of prostate cancer.. The Prostate.. 2013.
A meta-analysis of genome-wide association studies to identify prostate cancer susceptibility loci associated with aggressive and non-aggressive disease.. Human molecular genetics. 22(2):408-15.. 2013.