Pinchas Cohen
· Distinguished Professor of Gerontology, Medicine and Biological Sciences Dean, USC Leonard Davis School of Gerontology William and Sylvia Kugel Dean’s Chair in GerontologyVerifiedUniversity of Southern California · Geroscience
Active 1962–2026
About
Pinchas Cohen, MD, is a Professor of Gerontology, Medicine, and Biological Sciences, and serves as the Dean of the USC Leonard Davis School of Gerontology. He holds the William and Sylvia Kugel Dean’s Chair in Gerontology and is the Executive Director of the Ethel Percy Andrus Gerontology Center as well as the Director of the Ney Center for Healthspan Science Education. Dr. Cohen earned his MD from the Faculty of Medicine at Technion, Haifa, Israel in 1986 and completed his postdoctoral training at Stanford University from 1986 to 1992. He began his faculty career at the University of Pennsylvania from 1992 to 1999, and until 2012, he was a professor and Vice Chair for Research at the Mattel Children’s Hospital at UCLA, where he also co-directed the UCSD/UCLA Diabetes Research Center. Dr. Cohen has received numerous prestigious awards for his research, including the National Institute of Aging “EUREKA” Award, the NIH-Director-Transformative RO1 Grant, and the Glenn Award for Research in Biological Mechanisms of Aging. He holds several patents for novel peptides and is the co-founder of CohBar, a biotechnology company focused on developing mitochondrial peptides for diseases of aging. His research has been published in over 300 papers in leading scientific journals, with a focus on aging, diabetes, Alzheimer’s disease, cancer, growth hormone/IGF biology, and the emerging science of mitochondrial-derived peptides, a field he pioneered.
Research topics
- Genetics
- Biology
- Cell biology
- Internal medicine
- Molecular biology
- Neuroscience
- Endocrinology
- Medicine
- Cancer research
Selected publications
bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-14
articleOpen accessSenior authorCorrespondingAbstract Context The environmental or other genetic factors might influence the effect of Klotho ( KL) on glucose metabolism. Objective We investigated mitochondrial genetic variants that interact with KL single nucleotide polymorphisms (SNPs) to modulate diabetes risk. Methods We used the data from 7,047 non-Hispanic white participants of the Health and Retirement Study, a prospective observational study including adults aged 50 years and older from the United States. First, we performed single gene-wide association scans to identify KL SNPs associated with diabetes. Next, we performed a nuclear-by-mitochondrial interaction test (NuMIT) in which we use an identified KL SNP from the gene-wide scan to evaluate potential interactions with 85 mitochondrial SNPs in relation to diabetes. Results We failed to identify a significant association between diabetes and the KL SNP in our single gene-wide association test. However, we identified a novel variant ( KL rs9563121) which showed a trend of increasing klotho mRNA levels with each additional minor allele. A NuMIT analysis identified mitochondrial SNPs, which showed significant interactions with rs9563121 in relation to diabetes risk. MitoG15929A showed significant interactions with rs9563121 in both men and women. MitoG15929A diminished the potential beneficial effect of KL rs9563121 on diabetes risk in women. Among men with the MitoG15929A variant, KL rs9563121 was associated with higher prevalence of diabetes. Conclusion The NuMIT approach revealed significant interactions between mitochondrial and nuclear DNA variants of KL . Furthermore, MitoG15929A may have a role in the interaction between diabetes and KL in a sex-dependent manner.
Mitochondrial-derived microproteins: from discovery to function
Trends in Genetics · 2025-03-05 · 4 citations
erratumOpen accessSenior author2025-09-02
articleOpen accessSenior author<p>Supplemental Figure S2 shows the comparison of control Mitochondrial DNA copy number levels in White and Black Individuals</p>
2025-09-02
articleOpen accessSenior author<p>Supplemental Table S2 shows demographic and clinical characteristics at the time of biopsy stratified by prostate cancer grade for all individuals and by race.</p>
Journal of the American Society of Nephrology · 2025-10-01
article2025-09-02
articleOpen accessSenior author<p>Supplemental Figure S3 shows receiver operating characteristic (ROC) curves between univariable models adjusted for PSA (log-transformed) only, Plasma mtDNA only, and WBC mtDNA only, stratified by Black and White individuals.</p>
Journal of Clinical Oncology · 2025-02-10 · 1 citations
article312 Background: Men on active surveillance for prostate cancer are extremely interested in dietary changes or supplements to prevent progression of their disease. There are presently no prospective trials supporting such changes. We sought to determine if a high omega-3, low omega-6 fatty acid diet with fish oil capsules (D+FO) decreases proliferation (Ki-67) in prostate biopsies in men with prostate cancer on active surveillance over a 1-year time period. Methods: In this Phase II, prospective randomized trial, men (N=100) with grade group 1 or 2 prostate cancer that elected active surveillance were randomized to the D+FO or a control group. Same site prostate biopsies were obtained at baseline and 1-year tracked using an image-fusion device. The primary endpoint was the change in Ki-67 index from baseline to 1-year from same site biopsies compared between the groups. Ki-67 index was determined using multiplex immunofluorescence analysis. Secondary outcomes included compliance, grade group, maximum tumor length, the Decipher 22 gene score, serum PSA, lipid levels, and adverse events. Results: The Ki-67 index decreased in the D+FO group by approximately 15% from baseline to 1-year (1.34% at baseline, 1.14% at 1-year) and increased in the control group by approximately 24% from baseline to 1-year (1.23% at baseline, 1.52% at 1-year) resulting in a statistically significant difference in the change of Ki-67 index between the groups (95% CI 2%, 52%, p=0.043). There was no significant difference in the secondary outcomes grade group, tumor length, decipher genomic score or PSA between the two groups. There was a significant decrease in serum triglyceride (p=0.016) and serum colony stimulating factor-1 (p=0.017) in the D+FO group compared to control. Four patients in the D+FO group were withdrawn from the trial due to adverse events related to the FO. Conclusions: A high omega-3, low omega-6 diet with FO for 1-year resulted in a significant reduction in Ki-67 index (compared to the control group), a biomarker for prostate cancer progression, metastasis and death. These findings support future Phase III trials incorporating this intervention in men on active surveillance. Clinical trial information: NCT02176902 .
Journal of Clinical Oncology · 2025-01-27 · 1 citations
article223 Background: CRC is the third leading cause of cancer related deaths worldwide with age and diet among the strongest risk factors. Emerging evidence suggests gut microbiome plays important role in CRC and is highly impacted by the exposome primarily the food intake. Since diet and age plays an important role in gut microbiome diversity, the present study aimed to investigate the alterations in the gut microbiome in young versus old mice harboring CRC allografts and fed with different diets. Methods: Two cohorts of C57BL/6 including young (n = 9, age = 6 weeks) and old (n = 9, age = 20-24 months) mice were implanted with 1x10 6 MSI (microsatellite instable) CRC MC38 tumor cells. Mice in both cohorts were randomized into three different diet groups: normal diet (ND; standard chow), high-fat (HF) and calorie-restricted (CR: 30% reduction in total calories). Mice were housed individually under standard laboratory conditions. Mice fecal samples were collected and subjected to DNA isolation (ZymoBIOMICS-96 MagBead DNA Kit), followed by metagenomic shotgun and whole genome sequencing (ZymoBIOMICSe and Illumina NovaSeq, respectively). P ≤ 0.05 were considered as statistically significant. Results: Fecal microbiome analysis showed that old microbiome has higher alpha diversity compared to the young mice. No statistically significant differences in were found in microbiome diversities between the diet groups. Pairwise permanova results showed statistically significant differences between microbiomes of old vs. young groups ( P : 0.001), CR vs. HF groups ( P : 0.012) and HF vs. ND groups ( P : 0.021). ANCOM-BC analysis determined the differentiating features and microbial functional pathways in the young mice compared to the old mice group and in different diet groups with relative abundance differences of larger than log 10 2. Bacteroides thetaiotaomicron ( P : 1.43E-39) and Parabacteroides goldsteinii ( P : 2.20E-23) were enriched in young and old groups, respectively. Akkermansia muciniphila ( P : 0.008) was significantly enriched in ND compared to CR group. Lactococcus lactis ( P : 9.94E-160) and Lachnospiraceae bacterium A4 ( P : 4.95E-10) were significantly enriched in HF compared to ND diet groups and vice-versa, respectively. Among the functional pathways, CMP-legionaminate biosynthesis I ( P : 2.38E-13) and L-arginine biosynthesis IV (archaebacteria) ( P : 4.77E-11) were the most significantly enriched in young and old groups, respectively. Conclusions: Our findings highlight the differential diversity and microbial features of gut microbiome in age- and diet-induced CRC progression. Collectively, alteration in diet and age of the host lead to changes in gut microbiota which has a direct impact on activation of specific signaling pathways, metabolism and local and systemic immune responses, which may in turn affect chemosensitivity and outcome in CRC
Cancer Prevention Research · 2025-05-13 · 1 citations
articleOpen accessSenior authorBlack individuals are disproportionately burdened by prostate cancer compared with White individuals. The mitochondrion is an untapped source for prostate cancer biomarkers, and previous work has shown that altered mitochondrial DNA (mtDNA) copy number is linked to mitochondrial dysfunction and tumorigenesis. We assess whether mtDNA copy number is altered in patients with and without prostate cancer in a racially specific manner. Circulating cell-free mtDNA copy number from plasma and mtDNA copy number from white blood cells (WBC) were measured in 199 patients undergoing biopsy (50:50 White cases/controls and 50:49 Black cases/controls). mtDNA copy number was determined via Droplet Digital PCR. Logistic regressions tested associations between mtDNA and prostate cancer by race. The AUC was compared between covariate-only models and models with mtDNA. In both plasma and WBCs, mtDNA copy number was significantly increased in cases compared with controls in White patients, but not in Black patients. Interestingly, Black controls had higher mtDNA copy number levels than White controls. Multivariable analysis revealed significant associations of plasma mtDNA and WBC mtDNA with prostate cancer for White patients only. Elevated mtDNA copy number was more accurate in predicting prostate cancer in White patients than in Black patients. Higher mtDNA copy number levels were associated with prostate cancer in both Black and White patients. Plasma mtDNA may be more accurate than WBC mtDNA in predicting prostate cancer incidence in Black men. Overall, Black controls had higher mtDNA copy number levels than White controls, suggesting mtDNA copy number may be implicated in prostate cancer health disparities. PREVENTION RELEVANCE: Our study shows that mtDNA copy number is a significant predictor of prostate cancer in White individuals, suggesting its potential use in early detection and prevention strategies. The absence of this association in Black individuals highlights the need for race-specific biomarkers in prostate cancer prevention efforts.
Pituitary · 2025-05-07 · 6 citations
reviewOpen access
Recent grants
NIH · $1.1M · 2004
NIH · $369k · 2013
NIH · $1.2M · 2014
NIH · $3.3M · 2023
Role of GPR120 and Macrophages in Dietary Omega-3 Fatty Acid Inhibition of Prostate Cancer
NIH · $1.7M · 2018–2023
Frequent coauthors
- 113 shared
Junxiang Wan
University of Southern California
- 102 shared
William J. Aronson
University of California, Los Angeles
- 93 shared
Jonathan W. Said
University of California, Los Angeles
- 85 shared
David Elashoff
University of California, Los Angeles
- 79 shared
Ron G. Rosenfeld
Stanford University
- 74 shared
Susanne M. Henning
- 73 shared
David Hwang
- 71 shared
Hemal H. Mehta
University of Sydney
Labs
Education
- 1986
MD
Technion Israel Institute of Technology Ruth and Bruce Rappaport Faculty of Medicine
Awards & honors
- National Institute of Aging “EUREKA” Award
- National Institutes of Health Director Transformative RO1 Gr…
- Gerontological Society of America Robert W. Kleemeier Award
- American Federation of Aging Research Irving S. Wright Award…
- Glenn Award for Research in Biological Mechanisms of Aging
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