M J Stampfer

Harvard University, Cambridge, Massachusetts, United States

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Publications (420)4648.45 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Increasing nut consumption has been associated with reduced risk of obesity and type II diabetes, the risk factors for colorectal cancer. However, the association between nut consumption and colorectal cancer risk is unclear. We aimed to examine the association of long-term nut consumption with risk of colorectal cancer. We prospectively followed 75 680 women who were free of cancer at baseline in the Nurses' Health Study, and examined the association between nut consumption and colorectal cancer risk. Nut consumption was assessed at baseline and updated every 2-4 years. Relative risks (RRs) and 95% confidence intervals (95% CIs) were estimated using Cox proportional hazards models. During 2 103 037 person-years of follow-up, we identified 1503 colorectal cancer cases. After adjustment for other known or suspected risk factors, women who consumed nuts 2 or more times per week (that is, ⩾56 g per week) had a 13% lower risk of colorectal cancer compared with those who rarely consumed nuts, but the association was not statistically significant (RR: 0.87; 95% CI: 0.72-1.05; P-trend: 0.06). No association was observed for peanut butter. In this large prospective cohort of women, frequent nut consumption was not significantly associated with colorectal cancer risk after adjusting for other risk factors.European Journal of Clinical Nutrition advance online publication, 6 May 2015; doi:10.1038/ejcn.2015.66.
    European journal of clinical nutrition 05/2015; DOI:10.1038/ejcn.2015.66 · 2.95 Impact Factor
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    ABSTRACT: Few genetic variants have been confirmed as being associated with prostate cancer-specific mortality (PCSM). A recent study identified 22 candidate single-nucleotide polymorphisms (SNPs) associated with PCSM in a Seattle-based patient cohort. Five of these associations were replicated in an independent Swedish cohort. We genotyped these 22 SNPs in Physicians' Health Study (PHS) participants diagnosed with prostate cancer (PCa). Using the same model that was found to be most significant in the Seattle cohort, we examined the association of these SNPs with lethal disease with Cox proportional hazards models. One SNP, rs5993891 in the ARVCF gene on chromosome 22q11, which had also replicated in the Swedish cohort, was also significantly associated with PCSM in the PHS cohort (hazard ratio (HR)=0.32; P=0.01). When we tested this SNP in an additional cohort (Health Professionals Follow-up Study, HPFS), the association was null (HR=0.95, P=0.90); however, a meta-analysis across all studies showed a statistically significant association with a HR of 0.52 (0.29-0.93, P=0.03). The association of rs5993891 with PCSM was further replicated in PHS and remains significant in a meta-analysis, though there was no association in HPFS. This SNP may contribute to a genetic panel of SNPs to determine at diagnosis whether a patient is more likely to exhibit an indolent or aggressive form of PCa. This study also emphasizes the importance of multiple rounds of replication.Prostate Cancer and Prostatic Disease advance online publication, 5 May 2015; doi:10.1038/pcan.2015.18.
    Prostate cancer and prostatic diseases 05/2015; DOI:10.1038/pcan.2015.18 · 2.83 Impact Factor
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    ABSTRACT: Most patients with pancreatic ductal adenocarcinoma (PDAC) are diagnosed with advanced disease and survive less than 12 months. PDAC has been linked with obesity and glucose intolerance, but whether changes in circulating metabolites are associated with early cancer progression is unknown. To better understand metabolic derangements associated with early disease, we profiled metabolites in prediagnostic plasma from individuals with pancreatic cancer (cases) and matched controls from four prospective cohort studies. We find that elevated plasma levels of branched-chain amino acids (BCAAs) are associated with a greater than twofold increased risk of future pancreatic cancer diagnosis. This elevated risk was independent of known predisposing factors, with the strongest association observed among subjects with samples collected 2 to 5 years before diagnosis, when occult disease is probably present. We show that plasma BCAAs are also elevated in mice with early-stage pancreatic cancers driven by mutant Kras expression but not in mice with Kras-driven tumors in other tissues, and that breakdown of tissue protein accounts for the increase in plasma BCAAs that accompanies early-stage disease. Together, these findings suggest that increased whole-body protein breakdown is an early event in development of PDAC.
    Nature Medicine 09/2014; DOI:10.1038/nm.3686 · 28.05 Impact Factor
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    ABSTRACT: Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 x 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and gamma-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition.
    Nature 07/2014; 514(7520):92-7. DOI:10.1038/nature13545 · 42.35 Impact Factor
  • Cancer Prevention Research 01/2014; 5(11_Supplement):B90-B90. DOI:10.1158/1940-6207.PREV-12-B90 · 5.27 Impact Factor
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    ABSTRACT: Background:Increasing nut intake has been associated with reduced risk of diabetes mellitus, which is a risk factor for pancreatic cancer.Methods:We prospectively followed 75 680 women in the Nurses' Health Study, and examined the association between nut consumption and pancreatic cancer risk. Participants with a previous history of cancer were excluded. Nut consumption was assessed at baseline and updated every 2 to 4 years. Relative risks (RRs) and 95% confidence intervals (95% CIs) were estimated using Cox proportional hazards models.Results:We documented 466 incident cases of pancreatic cancer. After adjusting for age, height, smoking, physical activity, and total energy intake, women who consumed a 28-g (1 oz) serving size of nuts 2 times per week experienced a significantly lower risk of pancreatic cancer (RR, 0.65; 95% CI, 0.47-0.92; P for trend=0.007) when compared with those who largely abstained from nuts. The results did not appreciably change after further adjustment for body mass index (BMI) and history of diabetes mellitus (RR, 0.68; 95% CI, 0.48-0.95; P for trend=0.01). The inverse association persisted within strata defined by BMI, physical activity, smoking, and intakes of red meat, fruits, and vegetables.Conclusion:Frequent nut consumption is inversely associated with risk of pancreatic cancer in this large prospective cohort of women, independent of other potential risk factors for pancreatic cancer.British Journal of Cancer advance online publication, 22 October 2013; doi:10.1038/bjc.2013.665 www.bjcancer.com.
    British Journal of Cancer 10/2013; 109(11). DOI:10.1038/bjc.2013.665 · 4.82 Impact Factor
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    ABSTRACT: Background/Objectives:Obesity is associated with increased triglyceride levels. We examined whether overall obesity (body mass index (BMI)) and abdominal obesity (waist circumference (WC)) are independently associated with hypertriglyceridemia among the Korean population.Subjects/Methods:A national sample of 5036 Koreans aged 19-64 was examined with cross-sectional surveys, the Korea National Health and Nutrition Examination Survey, in 2007 and 2008. BMI, WC and other lifestyle information were assessed.Results:We documented 1344 cases (26.7%) of hypertriglyceridemia (fasting triglycerides of >150 mg/dl). Both BMI and WC were each independently associated with hypertriglyceridemia. Multivariate odds ratios (ORs) of increasing categories of BMI (<18.5, 18.5-<23, 23-<25, 25-<28, 28 kg/m(2)), were 0.49, 1.00 (reference), 1.26, 1.63 and 1.84, respectively (P=0.0007) adjusting for WC. There was a positive association between WC and hypertriglyceridemia across increasing quintiles of WC (multivariate-adjusted ORs: 1.00 (reference), 1.54, 2.54, 2.21 and 2.36; P<0.0001), adjusting for BMI. WC was positively related to hypertriglyceridemia in both gender. However, only women's BMI was independently associated with hypertriglyceridemia after adjusting for WC. The joint relation between BMI and WC and hypertriglyceridemia showed that within each BMI category, higher WC predicted a greater prevalence of hypertriglyceridemia and vice versa. The receiver operating characteristic curves indicated that BMI (0.69) and WC (0.72) were similar in predicting hypertriglyceridemia.Conclusions:Both BMI and WC were strongly independently associated with hypertriglyceridemia among the population. Both measurements should be considered for use in assessing health risk at clinical settings and epidemiologic research among Asian population.European Journal of Clinical Nutrition advance online publication, 21 November 2012; doi:10.1038/ejcn.2012.181.
    European journal of clinical nutrition 11/2012; DOI:10.1038/ejcn.2012.181 · 2.95 Impact Factor
  • International Journal of Radiation OncologyBiologyPhysics 11/2012; 84(3):S58. DOI:10.1016/j.ijrobp.2012.07.358 · 4.18 Impact Factor
  • International Journal of Radiation OncologyBiologyPhysics 11/2012; 84(3):S57-S58. DOI:10.1016/j.ijrobp.2012.07.357 · 4.18 Impact Factor
  • Cancer Prevention Research 10/2011; 4(10 Supplement):A60-A60. DOI:10.1158/1940-6207.PREV-11-A60 · 5.27 Impact Factor
  • Fuel and Energy Abstracts 10/2011; 81(2). DOI:10.1016/j.ijrobp.2011.06.881
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    ABSTRACT: Insulin may play a role in prostate cancer tumorigenesis. Postprandial blood glucose and insulin responses of foods depend importantly on the carbohydrate quality and quantity, represented by glycemic index (GI), glycemic load (GL), fiber and whole-grain content, but are also influenced by intake of protein and other characteristics. The recently developed insulin index (II) quantifies the postprandial insulin secretion, also taking into account these additional characteristics. We investigated the association between dietary GI, GL, II, fiber, and whole grains and risk of total prostate cancer (n = 5,112) and subgroups of prostate cancer as defined by stage or grade in 49,934 male participants of the Health Professionals Follow-up Study. Multivariate adjusted hazard ratios (HR) and 95% confidence intervals (95% CI) were estimated using Cox proportional hazards regression. Dietary GI, GL, II, or fiber was not associated with risk of total or subgroups of prostate cancer. We observed a positive association between dietary intake of whole grains and total prostate cancer (HR highest versus lowest quintile 1.13, 95% CI 1.03-1.24), which was attenuated after restriction to PSA-screened participants (HR 1.03, 95% CI 0.91-1.17). These results suggest that long-term exposure to a diet with a high insulin response does not affect prostate cancer incidence.
    Cancer Causes and Control 10/2010; 22(1):51-61. DOI:10.1007/s10552-010-9671-x · 2.96 Impact Factor
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    ABSTRACT: The phosphatidylinositol 3-kinase (PI3K) pathway regulates various cellular processes, including cellular proliferation and intracellular trafficking, and may affect prostate carcinogenesis. Thus, we explored the association between single-nucleotide polymorphisms (SNP) in PI3K genes and prostate cancer. Pooled data from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium were examined for associations between 89 SNPs in PI3K genes (PIK3C2B, PIK3AP1, PIK3C2A, PIK3CD, and PIK3R3) and prostate cancer risk in 8,309 cases and 9,286 controls. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using logistic regression. SNP rs7556371 in PIK3C2B was significantly associated with prostate cancer risk [OR(per allele), 1.08 (95% CI, 1.03-1.14); P(trend) = 0.0017] after adjustment for multiple testing (P(adj) = 0.024). Simultaneous adjustment of rs7556371 for nearby SNPs strengthened the association [OR(per allele), 1.21 (95% CI, 1.09-1.34); P(trend) = 0.0003]. The adjusted association was stronger for men who were diagnosed before the age of 65 years [OR(per allele), 1.47 (95% CI, 1.20-1.79); P(trend) = 0.0001] or had a family history [OR(per allele) = 1.57 (95% CI, 1.11-2.23); P(trend) = 0.0114], and was strongest in those with both characteristics [OR(per allele) = 2.31 (95% CI, 1.07-5.07), P-interaction = 0.005]. Increased risks were observed among men in the top tertile of circulating insulin-like growth factor-I (IGF-I) levels [OR(per allele) = 1.46 (95% CI, 1.04-2.06); P(trend) = 0.075]. No differences were observed with disease aggressiveness (Gleason grade >or=8 or stage T(3)/T(4) or fatal). In conclusion, we observed a significant association between PIK3C2B and prostate cancer risk, especially for familial, early-onset disease, which may be attributable to IGF-dependent PI3K signaling.
    Cancer Research 03/2010; 70(6):2389-96. DOI:10.1158/0008-5472.CAN-09-3575 · 9.28 Impact Factor
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    ABSTRACT: Background: In an earlier study, a 25-hydroxyvitamin D3 (25(OH)D) score calculated from known predictors of vitamin D status significantly predicted plasma levels of 25(OH)D and the risk of colorectal cancer, but the influence of the 25(OH)D score on survival after diagnosis is unknown. Materials and methods: We prospectively examined the influence of post-diagnosis predicted 25(OH)D levels on mortality among 1017 participants in the Nurses' Health Study and Health Professionals Follow-Up Study who were diagnosed with colorectal cancer from 1986 to 2004. Colorectal cancer-specific and overall mortality according to quintiles of predicted 25(OH)D levels were assessed. Cox proportional hazards models were used to calculate hazard ratios (HRs) adjusted for other risk factors of survival. Results: Higher predicted 25(OH)D levels were associated with a significant reduction in colorectal cancer-specific (P trend=0.02) and overall mortality (P trend=0.002). Compared with levels in the lowest quintile, participants with predicted 25(OH)D levels in the highest quintile had an adjusted HR of 0.50 (95% CI, 0.26–0.95) for cancer-specific mortality and 0.62 (95% CI, 0.42–0.93) for overall mortality. Conclusion: Higher predicted 25(OH)D levels after a diagnosis of colorectal cancer may be associated with improved survival. Further study of the vitamin D pathway in colorectal cancer is warranted.
    British Journal of Cancer 03/2010; 102(6):1079. DOI:10.1038/sj.bjc.6605614 · 4.82 Impact Factor
  • Cancer Prevention Research 01/2010; 3(1 Supplement):A122-A122. DOI:10.1158/1940-6207.PREV-09-A122 · 5.27 Impact Factor
  • Cancer Prevention Research 01/2010; 3(1 Supplement):A123-A123. DOI:10.1158/1940-6207.PREV-09-A123 · 5.27 Impact Factor
  • Cancer Prevention Research 01/2010; 3(1 Supplement):A117-A117. DOI:10.1158/1940-6207.PREV-09-A117 · 5.27 Impact Factor
  • Cancer Prevention Research 01/2010; 3(1 Supplement):B101-B101. DOI:10.1158/1940-6207.PREV-09-B101 · 5.27 Impact Factor
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    ABSTRACT: Insulin receptor substrate-1 (IRS-1) acts as a docking protein between the insulin-like growth factor-1 (IGF-1) receptor and intracellular signaling molecules in the IGF-1 signaling pathway. Accumulating data support a role of IGF-1 in prostate carcinogenesis. We assessed the influence of the most common IRS-1 gene polymorphism (Gly972Arg) on prostate cancer risk, alone and in combination with IGF-1 and other components in the IGF-1 signaling pathway. In a nested case-control study within the Physicians' Health Study, the IRS-1 polymorphism was assayed from prospectively collected samples from 564 incident prostate cancer cases and 758 controls matched on age and smoking. We calculated relative risks (RR) and 95% confidence intervals (CI) using conditional logistic regression. Among the controls, 0.8% were homozygous (AA) and 12% were heterozygous (GA) for the polymorphic allele. There was no association between carriage of the A allele and total prostate cancer risk (RR = 1.1 95% CI = 0.8-1.5), advanced disease (stage C or D or lethal prostate cancer, RR = 1.3 95% CI = 0.8-2.3), or plasma IGF-1 levels. We explored possible interactions with body mass index and components in the IGF-1 pathway including IGFBP3, PI3k, and PTEN but none of these factors influenced the relation between IRS-1 genotype and prostate cancer risk. Our data do not support an association between carriage of the variant IRS-1 gene and prostate cancer risk.
    The Prostate 09/2008; 68(13):1416-20. DOI:10.1002/pros.20797 · 3.57 Impact Factor
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    ABSTRACT: The magnitude of the link between cigarette smoking and lung cancer may vary by histological type. We used polytomous logistic regression to evaluate whether aspects of smoking have different effects across four histological types in the Nurses' Health Study. From 1976 to 2002, we identified 1062 cases of lung cancer: squamous cell (n = 201), small cell (n = 236), adenocarcinoma (n = 543) and large cell carcinoma (n = 82), among 65 560 current or former smokers. Risk reduction after quitting ranged from an 8% reduction (relative risk (RR): 0.92, 95% CI 0.91 to 0.94) to a 17% reduction (RR: 0.83, 95% CI 0.80 to 0.86) per year for adenocarcinoma and small cell carcinoma, respectively, with a 9% reduction observed for large cell carcinoma and an 11% reduction observed for squamous cell carcinoma. The association of age at smoking initiation and former cigarette smoking was similar across types, while the association of smoking duration differed. The risk of adenocarcinoma increased by 6% per year of smoking, compared to 7% for large cell, 10% for squamous cell and 12% for small cell. The 6% difference between adenocarcinoma and small cell carcinoma is equivalent to a 3.2 to 9.7-fold increase in risk for 20 years of smoking. The effects of the number of cigarettes smoked per day and years since quitting smoking are different across the major types of lung cancer, which are fully appreciated at long durations of smoking and smoking cessation. Smoking prevention and cessation should continue to be the focus of public health efforts to reduce lung cancer incidence and mortality.
    Tobacco control 07/2008; 17(3):198-204. DOI:10.1136/tc.2007.022582 · 5.15 Impact Factor

Publication Stats

65k Citations
4,648.45 Total Impact Points

Institutions

  • 1989–2013
    • Harvard University
      • • Department of Nutrition
      • • Department of Health Policy and Management
      Cambridge, Massachusetts, United States
    • Erasmus Universiteit Rotterdam
      • Department of Epidemiology
      Rotterdam, South Holland, Netherlands
  • 1987–2012
    • Harvard Medical School
      • • Department of Medicine
      • • Division of Nutrition
      Boston, Massachusetts, United States
  • 1988–2010
    • Brigham and Women's Hospital
      • • Department of Medicine
      • • Division of Preventive Medicine
      Boston, Massachusetts, United States
  • 1992–2008
    • Massachusetts Department of Public Health
      Boston, Massachusetts, United States
  • 2002
    • Icahn School of Medicine at Mount Sinai
      Manhattan, New York, United States
  • 2001
    • University of Wisconsin–Madison
      • Department of Population Health Sciences
      Madison, Wisconsin, United States
    • National Cancer Institute (USA)
      • Division of Cancer Epidemiology and Genetics
      Maryland, United States
    • Fred Hutchinson Cancer Research Center
      • Cancer Prevention Program
      Seattle, Washington, United States
    • Partners HealthCare
      Boston, Massachusetts, United States
  • 2000–2001
    • Dana-Farber Cancer Institute
      • • Lank Center for Genitourinary Oncology
      • • Department of Medical Oncology
      Boston, MA, United States
    • Geisel School of Medicine at Dartmouth
      • Department of Community and Family Medicine
      Hanover, New Hampshire, United States
  • 1999
    • Karolinska Institutet
      • Department of Medical Epidemiology and Biostatistics
      Solna, Stockholm, Sweden
    • University of Massachusetts Amherst
      • Division of Biostatistics and Epidemiology
      Amherst Center, MA, United States
  • 1994–1996
    • Wageningen University
      Wageningen, Gelderland, Netherlands
  • 1993
    • Chicago Center For Family Health
      Chicago, Illinois, United States
  • 1991
    • Providence Hospital
      Mobile, Alabama, United States
  • 1990
    • Northern Inyo Hospital
      BIH, California, United States