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Journal: Prostate Cancer and Prostatic Diseases
In the constant search for better approaches to treat and ultimately prevent prostate cancer, it is essential that we better understand the underlying etiology of prostate cancer. In times like this, I am often discouraged by the common mantra that the only known risk factors for prostate cancer are “age, race, and family history”. Surely, there must be other risk factors. Over time, certain risk factors have revealed themselves – obesity (aggressive prostate cancer), diet (likely, but exact details still evolving), and smoking (aggressive prostate cancer) to mention a few. One common factor, but certainly not the only factor, linking obesity, diet, and smoking is they all increase inflammation. If true that increased inflammation drives more prostate cancer, then it begs the question of whether other conditions that are clearly inflammatory-related are linked with prostate cancer. With this background in mind, Ge and colleagues tested the association between inflammatory bowel disease (IBD) and prostate cancer risk.
Stephen J. Freedland, MD
Stephen J. Freedland, MD, is director of the Center for Integrated Research in Cancer and Lifestyle and co-director of the Cancer Genetics and Prevention Program and Associate Director for Faculty Development at the Cedars-Sinai Samuel Oschin Comprehensive Cancer Institute. He is also a faculty physician in the Division of Urology within the Department of Surgery at Cedars-Sinai. He has served on numerous American Urological Association guideline panels for prostate cancer and co-chaired a prostate cancer guideline panel for the American Society of Clinical Oncology.
Dr. Freedland's clinical area of expertise focuses on urological diseases, particularly benign prostatic hyperplasia and prostate cancer. His approach toward cancer prevention and awareness focuses on treating the whole patient, not just the disease, by combining traditional Western medicine with complementary holistic interventions. His research interests include investigations on urological diseases and the role of diet, lifestyle and obesity in prostate cancer development and progression, as well as prostate cancer among racial groups and risk stratification for men with prostate cancer.
PCAN: June 2019
Prevalence of DNA Repair Gene Mutations in Localized Prostate Cancer According to Clinical and Pathologic Features: Association of Gleason Score and Tumor Stage - Full Text Article
Background - DNA repair gene mutations are present in 8–10% of localized prostate cancers. It is unknown whether this is influenced by clinicopathologic factors.
Methods - We interrogated localized prostate adenocarcinomas with tumor DNA sequencing information from the TCGA validated (n = 333) and Nature Genetics (n = 377) datasets. Homologous recombination repair genes included in our
PCAN: May 2019
Efficacy and Safety of Enucleation vs. Resection of Prostate for Treatment of Benign Prostatic Hyperplasia: A Meta-analysis of Randomized Controlled Trials - Full Text ArticleThe purpose of this study is to compare the efficacy and safety of transurethral enucleation and resection of the prostate for treatment of benign prostatic hyperplasia (BPH).
This meta-analysis was conducted through a systematic search before 1 September 2018. All included publications were randomized controlled trials (RCTs). Efficacy was evaluated based on International Prostate Symptom Score (IPSS), maximum urinary flow rate (Qmax), and quality of life (QoL).
PCAN: April 2019
Statin Use and Time to Progression in Men on Active Surveillance for Prostate Cancer - Full Text ArticleRecent evidence suggests that statins may improve prostate cancer outcomes; however, their role in active surveillance (AS) is poorly characterized. We aimed to evaluate the association between statin use at diagnosis and time to progression on AS.
Data were obtained from a prospectively maintained cohort of men undergoing AS between 1995 and 2016 at our institution. All men satisfied the low-risk criteria: Gleason score <7, <4 positive cores, <50% involvement of any core, and prostate-specific antigen level <10.0 ng/dL. Kaplan–Meier curves and