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8 results on '"Peisch, Sam"'

1. Expression of IGF/insulin receptor in prostate cancer tissue and progression to lethal disease.

Author

Ahearn TU, Peisch S, Pettersson A, Ebot EM, Zhou CK, Graff RE, Sinnott JA, Fazli L, Judson GL, Bismar TA, Rider JR, Gerke T, Chan JM, Fiorentino M, Flavin R, Sesso HD, Finn S, Giovannucci EL, Gleave M, Loda M, Li Z, Pollak M, and Mucci LA

Subjects
Aged, Apoptosis genetics, Biomarkers, Tumor genetics, Cell Proliferation genetics, Disease Progression, Gene Expression Regulation, Neoplastic genetics, Humans, Insulin genetics, Male, Oncogene Proteins, Fusion genetics, Receptor, IGF Type 1, Signal Transduction genetics, Transcriptional Regulator ERG genetics, Insulin-Like Growth Factor I genetics, Prostatic Neoplasms genetics, Prostatic Neoplasms pathology, Receptor, Insulin genetics, Receptors, Somatomedin genetics
Abstract

Circulating insulin-like growth factor-1 (IGF-1) is consistently associated with prostate cancer risk. IGF-1 binds to IGF-1 receptor (IGF1R) and insulin receptor (IR), activating cancer hallmark pathways. Experimental evidence suggests that TMPRSS2:ERG may interact with IGF/insulin signaling to influence progression. We investigated IGF1R and IR expression and its association with lethal prostate cancer among 769 men. Protein expression of IGF1R, IR and ERG (i.e. a surrogate of ERG fusion genes) were assayed by immunohistochemistry. Cox models estimated hazard ratios (HR) and 95% confidence intervals (CI) adjusted for clinical characteristics. Among patients, 29% had strong tumor IGF1R expression and 10% had strong IR expression. During a mean follow-up of 13.2 years through 2012, 80 men (11%) developed lethal disease. Tumors with strong IGF1R or IR expression showed increased cell proliferation, decreased apoptosis and a higher prevalence of ERG. In multivariable models, strong IGF1R was associated with a borderline increased risk of lethal prostate cancer (HR 1.7; 95% CI 0.9-3.1). The association appeared greater in ERG-positive tumors (HR 2.8; 95% CI 0.9-8.4) than in ERG-negative tumors (HR 1.3; 95% CI 0.6-3.0, p-heterogeneity 0.08). There was no association between IR and lethal prostate cancer (HR 0.8; 95% CI 0.4-1.9). These results suggest that tumor IGF1R expression may play a role in prostate cancer progression to a lethal phenotype and that ERG-positive tumors may be more sensitive to IGF signaling. These data may improve our understanding of IGF signaling in prostate cancer and suggest therapeutic options for disease subtypes.

Published
2018
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3. Prostate cancer progression and mortality: a review of diet and lifestyle factors.

Author

Peisch SF, Van Blarigan EL, Chan JM, Stampfer MJ, and Kenfield SA

Subjects
Adult, Aged, Attitude to Health, Humans, Incidence, Male, Middle Aged, Overweight epidemiology, Risk Assessment, Risk Factors, Smoking adverse effects, Survival Analysis, Diet, Healthy, Disease Progression, Exercise physiology, Life Style, Prostatic Neoplasms epidemiology, Prostatic Neoplasms physiopathology
Abstract

Purpose: To review and summarize evidence on the role of diet and lifestyle factors and prostate cancer progression, with a specific focus on habits after diagnosis and the risk of subsequent disease recurrence, progression, or death., Methods: Given the well-documented heterogeneity of prostate cancer and the long survivorship of the majority of diagnoses, our goal was to summarize and describe modifiable risk factors for clinically relevant prostate cancer. We focused where possible on epidemiologic studies of post-diagnostic habits and prostate cancer progression, defined as recurrence (e.g., PSA risk, secondary treatment), metastasis, or death. Where data were limited, we also describe evidence on risk factors and indicators of prostate cancer aggressiveness at diagnosis., Results: A variety of dietary and lifestyle factors appear to affect prostate cancer progression. Several generally widely recommended lifestyle factors such as not smoking, maintaining a healthy body weight, and regular vigorous physical exercise also appear to affect prostate cancer progression. Several dietary factors, such as tomato sauce/lycopene, cruciferous vegetables, healthy sources of vegetable fats, and coffee, may also have a role in reducing risk of prostate cancer progression., Conclusion: Diet and lifestyle factors, in particular exercise and smoking cessation, may reduce the risk of prostate cancer progression and death. These promising findings warrant further investigation, as their overall impact might be large.

Published
2017
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4. Selenium- or Vitamin E-Related Gene Variants, Interaction with Supplementation, and Risk of High-Grade Prostate Cancer in SELECT.

Author

Chan JM, Darke AK, Penney KL, Tangen CM, Goodman PJ, Lee GM, Sun T, Peisch S, Tinianow AM, Rae JM, Klein EA, Thompson IM Jr, Kantoff PW, and Mucci LA

Subjects
Aged, Biological Transport genetics, Cohort Studies, Humans, Male, Middle Aged, Neoplasm Grading, Pharmacogenomic Variants, Polymorphism, Single Nucleotide, Proportional Hazards Models, Prostatic Neoplasms blood, Prostatic Neoplasms pathology, Risk Factors, Vitamin E genetics, Biomarkers, Tumor blood, Genetic Variation, Prostatic Neoplasms genetics, Selenium metabolism, Vitamin E metabolism
Abstract

Background: Epidemiologic studies and secondary analyses of randomized trials supported the hypothesis that selenium and vitamin E lower prostate cancer risk. However, the Selenium and Vitamin E Cancer Prevention Trial (SELECT) showed no benefit of either supplement. Genetic variants involved in selenium or vitamin E metabolism or transport may underlie the complex associations of selenium and vitamin E., Methods: We undertook a case-cohort study of SELECT participants randomized to placebo, selenium, or vitamin E. The subcohort included 1,434 men; our primary outcome was high-grade prostate cancer (N = 278 cases, Gleason 7 or higher cancer). We used weighted Cox regression to examine the association between SNPs and high-grade prostate cancer risk. To assess effect modification, we created interaction terms between randomization arm and genotype and calculated log likelihood statistics., Results: We noted statistically significant (P < 0.05) interactions between selenium assignment, SNPs in CAT, SOD2, PRDX6, SOD3, and TXNRD2, and high-grade prostate cancer risk. Statistically significant SNPs that modified the association of vitamin E assignment and high-grade prostate cancer included SEC14L2, SOD1, and TTPA In the placebo arm, several SNPs, hypothesized to interact with supplement assignment and risk of high-grade prostate cancer, were also directly associated with outcome., Conclusion: Variants in selenium and vitamin E metabolism/transport genes may influence risk of overall and high-grade prostate cancer, and may modify an individual man's response to vitamin E or selenium supplementation with regards to these risks., Impact: The effect of selenium or vitamin E supplementation on high-grade prostate cancer risk may vary by genotype. Cancer Epidemiol Biomarkers Prev; 25(7); 1050-8. ©2016 AACR., (©2016 American Association for Cancer Research.)

Published
2016
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5. Expression of IGF/insulin receptor in prostate cancer tissue and progression to lethal disease

Author

Ahearn, Thomas U, Peisch, Sam, Pettersson, Andreas, Ebot, Ericka M, Zhou, Cindy Ke, Graff, Rebecca E, Sinnott, Jennifer A, Fazli, Ladan, Judson, Gregory L, Bismar, Tarek A, Rider, Jennifer R, Gerke, Travis, Chan, June M, Fiorentino, Michelangelo, Flavin, Richard, Sesso, Howard D, Finn, Stephen, Giovannucci, Edward L, Gleave, Martin, Loda, Massimo, Li, Zhe, Pollak, Michael, Mucci, Lorelei A, and Transdisciplinary Prostate Cancer Partnership (ToPCaP)

Subjects
Male, Urologic Diseases, Aging, Oncology and Carcinogenesis, Somatomedin, Apoptosis, Transcriptional Regulator ERG, Clinical Research, Receptors, Humans, Insulin, 2.1 Biological and endogenous factors, IGF Type 1, Oncology & Carcinogenesis, Insulin-Like Growth Factor I, Aetiology, Fusion, Cell Proliferation, Aged, Cancer, Oncogene Proteins, Neoplastic, Tumor, Prostate Cancer, Diabetes, Prostatic Neoplasms, Gene Expression Regulation, Disease Progression, Transdisciplinary Prostate Cancer Partnership, Biomarkers, Receptor, Signal Transduction
Abstract

Circulating insulin-like growth factor-1 (IGF-1) is consistently associated with prostate cancer risk. IGF-1 binds to IGF-1 receptor (IGF1R) and insulin receptor (IR), activating cancer hallmark pathways. Experimental evidence suggests that TMPRSS2:ERG may interact with IGF/insulin signaling to influence progression. We investigated IGF1R and IR expression and its association with lethal prostate cancer among 769 men. Protein expression of IGF1R, IR and ERG (i.e. a surrogate of ERG fusion genes) were assayed by immunohistochemistry. Cox models estimated hazard ratios (HR) and 95% confidence intervals (CI) adjusted for clinical characteristics. Among patients, 29% had strong tumor IGF1R expression and 10% had strong IR expression. During a mean follow-up of 13.2 years through 2012, 80 men (11%) developed lethal disease. Tumors with strong IGF1R or IR expression showed increased cell proliferation, decreased apoptosis and a higher prevalence of ERG. In multivariable models, strong IGF1R was associated with a borderline increased risk of lethal prostate cancer (HR 1.7; 95% CI 0.9-3.1). The association appeared greater in ERG-positive tumors (HR 2.8; 95% CI 0.9-8.4) than in ERG-negative tumors (HR 1.3; 95% CI 0.6-3.0, p-heterogeneity 0.08). There was no association between IR and lethal prostate cancer (HR 0.8; 95% CI 0.4-1.9). These results suggest that tumor IGF1R expression may play a role in prostate cancer progression to a lethal phenotype and that ERG-positive tumors may be more sensitive to IGF signaling. These data may improve our understanding of IGF signaling in prostate cancer and suggest therapeutic options for disease subtypes.

Published
2018

6. Prostate cancer progression and mortality: a review of diet and lifestyle factors

Author

Peisch, Sam F, Van Blarigan, Erin L, Chan, June M, Stampfer, Meir J, and Kenfield, Stacey A

Subjects
Adult, Male, Urologic Diseases, Aging, Clinical Sciences, Risk Assessment, Risk Factors, Tobacco, Complementary and Integrative Health, Humans, 2.1 Biological and endogenous factors, Obesity, Aetiology, Exercise, Life Style, Aged, Nutrition, Cancer, Healthy, Tobacco Smoke and Health, Prostate cancer progression, Incidence, Prostate Cancer, Prevention, Smoking, Prostatic Neoplasms, Middle Aged, Overweight, Urology & Nephrology, Lifestyle, Survival Analysis, Diet, Lethal prostate cancer, Disease Progression, Attitude to Health
Abstract

PurposeTo review and summarize evidence on the role of diet and lifestyle factors and prostate cancer progression, with a specific focus on habits after diagnosis and the risk of subsequent disease recurrence, progression, or death.MethodsGiven the well-documented heterogeneity of prostate cancer and the long survivorship of the majority of diagnoses, our goal was to summarize and describe modifiable risk factors for clinically relevant prostate cancer. We focused where possible on epidemiologic studies of post-diagnostic habits and prostate cancer progression, defined as recurrence (e.g., PSA risk, secondary treatment), metastasis, or death. Where data were limited, we also describe evidence on risk factors and indicators of prostate cancer aggressiveness at diagnosis.ResultsA variety of dietary and lifestyle factors appear to affect prostate cancer progression. Several generally widely recommended lifestyle factors such as not smoking, maintaining a healthy body weight, and regular vigorous physical exercise also appear to affect prostate cancer progression. Several dietary factors, such as tomato sauce/lycopene, cruciferous vegetables, healthy sources of vegetable fats, and coffee, may also have a role in reducing risk of prostate cancer progression.ConclusionDiet and lifestyle factors, in particular exercise and smoking cessation, may reduce the risk of prostate cancer progression and death. These promising findings warrant further investigation, as their overall impact might be large.

Published
2017

7. Selenium- or Vitamin E-Related Gene Variants, Interaction with Supplementation, and Risk of High-Grade Prostate Cancer in SELECT

Author

Chan, June M, Darke, Amy K, Penney, Kathryn L, Tangen, Catherine M, Goodman, Phyllis J, Lee, Gwo-Shu Mary, Sun, Tong, Peisch, Sam, Tinianow, Alex M, Rae, James M, Klein, Eric A, Thompson, Ian M, Kantoff, Philip W, and Mucci, Lorelei A

Subjects
Male, Urologic Diseases, Aging, and promotion of well-being, Pharmacogenomic Variants, Epidemiology, Clinical Trials and Supportive Activities, Medical and Health Sciences, Cohort Studies, Selenium, Risk Factors, Clinical Research, Complementary and Integrative Health, Genetics, Humans, Vitamin E, 2.1 Biological and endogenous factors, Polymorphism, Aetiology, 3.3 Nutrition and chemoprevention, Proportional Hazards Models, Aged, Nutrition, Cancer, Tumor, Prevention, Prostate Cancer, Prostatic Neoplasms, Genetic Variation, Biological Transport, Single Nucleotide, Middle Aged, Prevention of disease and conditions, Good Health and Well Being, Patient Safety, Neoplasm Grading, Biomarkers
Abstract

BackgroundEpidemiologic studies and secondary analyses of randomized trials supported the hypothesis that selenium and vitamin E lower prostate cancer risk. However, the Selenium and Vitamin E Cancer Prevention Trial (SELECT) showed no benefit of either supplement. Genetic variants involved in selenium or vitamin E metabolism or transport may underlie the complex associations of selenium and vitamin E.MethodsWe undertook a case-cohort study of SELECT participants randomized to placebo, selenium, or vitamin E. The subcohort included 1,434 men; our primary outcome was high-grade prostate cancer (N = 278 cases, Gleason 7 or higher cancer). We used weighted Cox regression to examine the association between SNPs and high-grade prostate cancer risk. To assess effect modification, we created interaction terms between randomization arm and genotype and calculated log likelihood statistics.ResultsWe noted statistically significant (P < 0.05) interactions between selenium assignment, SNPs in CAT, SOD2, PRDX6, SOD3, and TXNRD2, and high-grade prostate cancer risk. Statistically significant SNPs that modified the association of vitamin E assignment and high-grade prostate cancer included SEC14L2, SOD1, and TTPA In the placebo arm, several SNPs, hypothesized to interact with supplement assignment and risk of high-grade prostate cancer, were also directly associated with outcome.ConclusionVariants in selenium and vitamin E metabolism/transport genes may influence risk of overall and high-grade prostate cancer, and may modify an individual man's response to vitamin E or selenium supplementation with regards to these risks.ImpactThe effect of selenium or vitamin E supplementation on high-grade prostate cancer risk may vary by genotype. Cancer Epidemiol Biomarkers Prev; 25(7); 1050-8. ©2016 AACR.

Published
2016

8. Expression of IGF/insulin receptor in prostate cancer tissue and progression to lethal disease

Author

Thomas U. Ahearn, Andreas Pettersson, Ericka M. Ebot, Michelangelo Fiorentino, Stephen P. Finn, Lorelei A. Mucci, Howard D. Sesso, Jennifer A. Sinnott, Sam Peisch, Edward Giovannucci, Massimo Loda, Zhe Li, Jennifer R. Rider, Richard Flavin, Cindy Ke Zhou, June M. Chan, Travis Gerke, Ladan Fazli, Michael Pollak, Rebecca E. Graff, Tarek A. Bismar, Gregory L Judson, Martin E. Gleave, Ahearn, Thomas U, Peisch, Sam, Pettersson, Andrea, Ebot, Ericka M, Zhou, Ke, Graff, Rebecca E, Sinnott, Jennifer A, Fazli, Ladan, Judson, Gregory L, Bismar, Tarek A, Rider, Jennifer R, Gerke, Travi, Chan, June M, Fiorentino, Michelangelo, Flavin, Richard, Sesso, Howard D, Finn, Stephen, Giovannucci, Edward L, Gleave, Martin, Loda, Massimo, Li, Zhe, Pollak, Michael, and Mucci, Lorelei A

Subjects
0301 basic medicine, Male, Cancer Research, Oncogene Proteins, Fusion, Apoptosis, TMPRSS2, Receptor, IGF Type 1, Fusion gene, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Transcriptional Regulator ERG, medicine, Biomarkers, Tumor, Humans, Insulin, Insulin-Like Growth Factor I, Cancer Biomarkers and Molecular Epidemiology, Insulin-like growth factor 1 receptor, Aged, Cell Proliferation, biology, business.industry, Cancer, Prostatic Neoplasms, Receptors, Somatomedin, General Medicine, medicine.disease, Receptor, Insulin, Gene Expression Regulation, Neoplastic, Insulin receptor, 030104 developmental biology, 030220 oncology & carcinogenesis, immunohistochemistry, biology.protein, Cancer research, IGF-1, Disease Progression, Immunohistochemistry, business, Erg, Signal Transduction
Abstract

Circulating insulin-like growth factor-1 (IGF-1) is consistently associated with prostate cancer risk. IGF-1 binds to IGF-1 receptor (IGF1R) and insulin receptor (IR), activating cancer hallmark pathways. Experimental evidence suggests that TMPRSS2:ERG may interact with IGF/insulin signaling to influence progression. We investigated IGF1R and IR expression and its association with lethal prostate cancer among 769 men. Protein expression of IGF1R, IR and ERG (i.e. a surrogate of ERG fusion genes) were assayed by immunohistochemistry. Cox models estimated hazard ratios (HR) and 95% confidence intervals (CI) adjusted for clinical characteristics. Among patients, 29% had strong tumor IGF1R expression and 10% had strong IR expression. During a mean follow-up of 13.2 years through 2012, 80 men (11%) developed lethal disease. Tumors with strong IGF1R or IR expression showed increased cell proliferation, decreased apoptosis and a higher prevalence of ERG. In multivariable models, strong IGF1R was associated with a borderline increased risk of lethal prostate cancer (HR 1.7; 95% CI 0.9-3.1). The association appeared greater in ERG-positive tumors (HR 2.8; 95% CI 0.9-8.4) than in ERG-negative tumors (HR 1.3; 95% CI 0.6-3.0, p-heterogeneity 0.08). There was no association between IR and lethal prostate cancer (HR 0.8; 95% CI 0.4-1.9). These results suggest that tumor IGF1R expression may play a role in prostate cancer progression to a lethal phenotype and that ERG-positive tumors may be more sensitive to IGF signaling. These data may improve our understanding of IGF signaling in prostate cancer and suggest therapeutic options for disease subtypes.

Published
2018

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