SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Stampfer Meir J) "

Sökning: WFRF:(Stampfer Meir J)

  • Resultat 51-60 av 67
  • Föregående 12345[6]7Nästa
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
51.
  • Downer, Mary K, et al. (författare)
  • Dairy intake in relation to prostate cancer survival.
  • 2017
  • Ingår i: International Journal of Cancer. - 0020-7136 .- 1097-0215. ; 140:9, s. 2060-2069
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Dairy intake has been associated with increased risk of advanced prostate cancer. Two US cohort studies reported increased prostate cancer-specific mortality with increased high-fat milk intake. We examined whether dairy and related nutrient intake were associated with prostate cancer progression in a Swedish patient population with high dairy consumption. We prospectively followed 525 men with newly diagnosed prostate cancer (diagnosed 1989-1994). We identified and confirmed deaths through February 2011 (n = 222 prostate cancer-specific, n = 268 from other causes). Cox proportional hazards regression was used to calculate hazard ratios (HR) and 95% confidence intervals (CI) for the associations between food or nutrient intake and prostate cancer-specific death. On average, patients consumed 5.0 servings/day of total dairy products at diagnosis. In the whole population, high-fat milk intake was not associated with prostate cancer-specific death (95% CI: 0.78, 2.10; p-trend = 0.32; multivariate-adjusted model). However, among patients diagnosed with localized prostate cancer, compared to men who consumed &lt;1 servings/day of high-fat milk, those who drank ≥3 servings/day had an increased hazard of prostate cancer mortality (HR = 6.10; 95% CI: 2.14, 17.37; p-trend = 0.004; multivariate-adjusted model). Low-fat milk intake was associated with a borderline reduction in prostate cancer death among patients with localized prostate cancer. These associations were not observed among patients diagnosed with advanced stage prostate cancer. Our data suggest a positive association between high-fat milk intake and prostate cancer progression among patients diagnosed with localized prostate cancer. Further studies are warranted to investigate this association and elucidate the mechanisms by which high-fat milk intake may promote prostate cancer progression.</p>
  •  
52.
  • Epstein, Mara M, et al. (författare)
  • Seasonal variation in expression of markers in the vitamin D pathway in prostate tissue
  • 2012
  • Ingår i: Cancer Causes and Control. - Springer. - 0957-5243 .- 1573-7225. ; 23:8, s. 1359-1366
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>PURPOSE:</strong> Recent studies suggest variation in genes along the vitamin D pathway, as well as vitamin D receptor (VDR) protein levels, may be associated with prostate cancer. As serum vitamin D levels vary by season, we sought to determine whether the expression of genes on the vitamin D pathway, assessed in prostate tumor tissue, do the same.</p><p><strong>METHODS:</strong> Our study incorporates mRNA expression data from 362 men in the Swedish Watchful Waiting cohort, diagnosed between 1977 and 1999, and 106 men enrolled in the US Physicians' Health Study (PHS) diagnosed between 1983 and 2004. We also assayed for VDR protein expression among 832 men in the PHS and Health Professionals Follow-up Study cohorts. Season was characterized by date of initial tissue specimen collection categorically and by average monthly ultraviolet radiation levels. One-way analysis of variance was used to examine variation in the expression levels of six genes on the vitamin D pathway-VDR, GC, CYP27A1, CYP27B1, RXRα, CYP24A1-and VDR protein by season, adjusted for age at diagnosis and Gleason grade. Variation was also examined separately among lethal and nonlethal cases.</p><p><strong>RESULTS:</strong> Tumor expression levels of the six genes did not vary significantly by season of tissue collection. No consistent patterns emerged from subgroup analyses by lethal versus nonlethal cases.</p><p><strong>CONCLUSIONS:</strong> Unlike circulating levels of 25(OH) vitamin D, expression levels of genes on the vitamin D pathway and VDR protein did not vary overall by season of tissue collection. Epidemiological analyses of vitamin D gene expression may not be biased by seasonality.</p>
  •  
53.
  • Fang, Fang, et al. (författare)
  • Immediate risk of suicide and cardiovascular death after a prostate cancer diagnosis : cohort study in the United States
  • 2010
  • Ingår i: Journal of the National Cancer Institute. - New York, USA : Elsevier. - 0027-8874 .- 1460-2105. ; 102:5, s. 307-14
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background: Receiving a cancer diagnosis is a stressful event that may increase risks of suicide and cardiovascular death, especially soon after diagnosis.</p><p>Methods: We conducted a cohort study of 342,497 patients diagnosed with prostate cancer from January 1, 1979, through December 31, 2004, in the Surveillance, Epidemiology, and End Results Program. Follow-up started from the date of prostate cancer diagnosis to the end of first 12 calendar months after diagnosis. The relative risks of suicide and cardiovascular death were calculated as standardized mortality ratios (SMRs) comparing corresponding incidences among prostate cancer patients with those of the general US male population, with adjustment for age, calendar period, and state of residence. We compared risks in the first year and months after a prostate cancer diagnosis. The analyses were further stratified by calendar period at diagnosis, tumor characteristics, and other variables.</p><p>Results: During follow-up, 148 men died of suicide (mortality rate = 0.5 per 1000 person-years) and 6845 died of cardiovascular diseases (mortality rate = 21.8 per 1000 person-years). Patients with prostate cancer were at increased risk of suicide during the first year (SMR = 1.4, 95% confidence interval [CI] = 1.2 to 1.6), especially during the first 3 months (SMR = 1.9, 95% CI = 1.4 to 2.6), after diagnosis. The elevated risk was apparent in pre-prostate-specific antigen (PSA) (1979-1986) and peri-PSA (1987-1992) eras but not since PSA testing has been widespread (1993-2004). The risk of cardiovascular death was slightly elevated during the first year (SMR = 1.09, 95% CI = 1.06 to 1.12), with the highest risk in the first month (SMR = 2.05, 95% CI = 1.89 to 2.22), after diagnosis. The first-month risk was statistically significantly elevated during the entire study period, and the risk was higher for patients with metastatic tumors (SMR = 3.22, 95% CI = 2.68 to 3.84) than for those with local or regional tumors (SMR = 1.57, 95% CI = 1.42 to 1.74).</p><p>Conclusion: A diagnosis of prostate cancer may increase the immediate risks of suicide and cardiovascular death.</p>
  •  
54.
  • Mucci, Lorelei A., et al. (författare)
  • Circadian dysrhythm and advanced prostate cancer
  • 2014
  • Ingår i: Journal of Clinical Oncology. - 0732-183X .- 1527-7755. ; 32:4
  • Tidskriftsartikel (övrigt vetenskapligt)abstract
    • <p><strong><strong>Background:</strong> </strong> The circadian rhythm regulates diverse biologic pathways including tumor oncogenes, metabolism, and cell proliferation. Dysregulation of the circadian rhythm arises from faulty input signals such as exposure to light at night, variability in core circadian rhythm genes, and variation in outputs that regulate circadian behavior including melatonin. There is compelling biologic rationale, but little human data, on circadian dysrhythm and advanced prostate cancer.</p><p><strong><strong>Methods:</strong> </strong> We undertook an integrative molecular epidemiology study of circadian dysrhythm and advanced prostate cancer among men in the Icelandic AGES-Reykjavik cohort and the U.S. Health Professionals Follow-up Study, which allowed integration of questionnaire data, biorepositories, and long-term follow-up. We characterized circadian dysrhythm using complimentary approaches: information on sleep problems from questionnaires, prediagnostic melatonin (6-sulfatoxymelatonin) measured on first morning void urine samples, and genetic variation across twelve circadian clock genes. We used multivariable regression models to estimate relative risks (RR) and 95% confidence intervals (CI) of associations with advanced prostate cancer, adjusted for potential confounders.</p><p><strong><strong>Results:</strong> </strong> Twenty percent of men reported sleep problems. Men who had trouble falling asleep (RR = 2.1; 95% CI 0.7-6.2) and staying asleep (RR=3.2, 95% CI 1.1-9.7) had an increased risk of developing advanced prostate cancer. Men with sleep problems had significantly lower melatonin levels compared to those without. Low melatonin levels were associated with a statistically significant 4-fold higher risk of advanced prostate cancer compared to those with high levels (95% CI: 1.25-10.0). Variant alleles in two SNPs in <em>cryptochrome</em> (<em>CRY1</em>), involved in generating and maintaining circadian rhythms, were significantly associated with risk of advanced prostate cancer in both cohorts, with a gene-level p-value&lt;0.01.</p><p><strong><strong>Conclusions:</strong> </strong> Our results suggest there are multiple nodes in the circadian rhythm that are associated with an increased risk of advanced prostate cancer. As such, there is the potential for complimentary strategies to target circadian disruption and reduce the risk of advanced prostate cancer.</p>
  •  
55.
  • Mucci, Lorelei A., et al. (författare)
  • Nine-gene molecular signature is not associated with prostate cancer death in a watchful waiting cohort
  • 2008
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 17:1, s. 249-251
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Tumor molecular markers hold promise to distinguish potentially lethal from indolent prostate cancer and to guide treatment choices. A previous study identified a nine-gene molecular signature in tumors associated with prostate-specific antigen relapse after prostatectomy. We examined this molecular model in relation to prostate cancer death among 172 men with initially localized disease. We quantified protein expression of the nine genes in tumors to classify progression risk. Accounting for clinical prognostic factors, the nine-gene model did not provide discrimination to predict lethal and indolent prostate cancer.</p>
  •  
56.
  • Mucci, Lorelei A., et al. (författare)
  • Nine-gene molecular signature is not associated with prostate cancer death in a watchful waiting cohort
  • 2008
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Baltimore : Waverly Press. - 1055-9965 .- 1538-7755. ; 17:1, s. 249-251
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Tumor molecular markers hold promise to distinguish potentially lethal from indolent prostate cancer and to guide treatment choices. A previous study identified a nine-gene molecular signature in tumors associated with prostate-specific antigen relapse after prostatectomy. We examined this molecular model in relation to prostate cancer death among 172 men with initially localized disease. We quantified protein expression of the nine genes in tumors to classify progression risk. Accounting for clinical prognostic factors, the nine-gene model did not provide discrimination to predict lethal and indolent prostate cancer.</p>
  •  
57.
  • Mucci, Lorelei A., et al. (författare)
  • Testing a multigene signature of prostate cancer death in the Swedish Watchful Waiting Cohort
  • 2008
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 17:7, s. 1682-8
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Although prostate cancer is a leading cause of cancer death, most men die with and not from their disease, underscoring the urgency to distinguish potentially lethal from indolent prostate cancer. We tested the prognostic value of a previously identified multigene signature of prostate cancer progression to predict cancer-specific death. The Orebro Watchful Waiting Cohort included 172 men with localized prostate cancer of whom 40 died of prostate cancer. We quantified protein expression of the markers in tumor tissue by immunohistochemistry and stratified the cohort by quintiles according to risk classification. We accounted for clinical variables (age, Gleason, nuclear grade, and tumor volume) using Cox regression and calculated receiver operator curves to compare discriminatory ability. The hazard ratio of prostate cancer death increased with increasing risk classification by the multigene model, with a 16-fold greater risk comparing highest-risk versus lowest-risk strata, and predicted outcome independent of clinical factors (P = 0.002). The best discrimination came from combining information from the multigene markers and clinical data, which perfectly classified the lowest-risk stratum where no one developed lethal disease; using the two lowest-risk groups as reference, the hazard ratio (95% confidence interval) was 11.3 (4.0-32.8) for the highest-risk group and difference in mortality at 15 years was 60% (50-70%). The combined model provided greater discriminatory ability (area under the curve = 0.78) than the clinical model alone (area under the curve = 0.71; P = 0.04). Molecular tumor markers can add to clinical variables to help distinguish lethal and indolent prostate cancer and hold promise to guide treatment decisions.</p>
  •  
58.
  • Mucci, Lorelei A., et al. (författare)
  • Testing a multigene signature of prostate cancer death in the Swedish Watchful Waiting Cohort
  • 2008
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Philadelphia : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 17:7, s. 1682-1688
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Although prostate cancer is a leading cause of cancer death, most men die with and not from their disease, underscoring the urgency to distinguish potentially lethal from indolent prostate cancer. We tested the prognostic value of a previously identified multigene signature of prostate cancer progression to predict cancer-specific death. The Örebro Watchful Waiting Cohort included 172 men with localized prostate cancer of whom 40 died of prostate cancer. We quantified protein expression of the markers in tumor tissue by immunohistochemistry and stratified the cohort by quintiles according to risk classification. We accounted for clinical variables (age, Gleason, nuclear grade, and tumor volume) using Cox regression and calculated receiver operator curves to compare discriminatory ability. The hazard ratio of prostate cancer death increased with increasing risk classification by the multigene model, with a 16-fold greater risk comparing highest-risk versus lowest-risk strata, and predicted outcome independent of clinical factors (P = 0.002). The best discrimination came from combining information from the multigene markers and clinical data, which perfectly classified the lowest-risk stratum where no one developed lethal disease; using the two lowest-risk groups as reference, the hazard ratio (95% confidence interval) was 11.3 (4.0-32.8) for the highest-risk group and difference in mortality at 15 years was 60% (50-70%). The combined model provided greater discriminatory ability (area under the curve = 0.78) than the clinical model alone (area under the curve = 0.71; P = 0.04). Molecular tumor markers can add to clinical variables to help distinguish lethal and indolent prostate cancer and hold promise to guide treatment decisions. </p>
  •  
59.
  • Penney, Kathryn L., et al. (författare)
  • mRNA Expression Signature of Gleason Grade Predicts Lethal Prostate Cancer
  • 2011
  • Ingår i: Journal of Clinical Oncology. - 0732-183X .- 1527-7755. ; 29:17, s. 2391-2396
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Purpose Prostate-specific antigen screening has led to enormous overtreatment of prostate cancer because of the inability to distinguish potentially lethal disease at diagnosis. We reasoned that by identifying an mRNA signature of Gleason grade, the best predictor of prognosis, we could improve prediction of lethal disease among men with moderate Gleason 7 tumors, the most common grade, and the most indeterminate in terms of prognosis. Patients and Methods Using the complementary DNA-mediated annealing, selection, extension, and ligation assay, we measured the mRNA expression of 6,100 genes in prostate tumor tissue in the Swedish Watchful Waiting cohort (n = 358) and Physicians' Health Study (PHS; n = 109). We developed an mRNA signature of Gleason grade comparing individuals with Gleason &lt;= 6 to those with Gleason &gt;= 8 tumors and applied the model among patients with Gleason 7 to discriminate lethal cases. Results We built a 157-gene signature using the Swedish data that predicted Gleason with low misclassification (area under the curve [AUC] = 0.91); when this signature was tested in the PHS, the discriminatory ability remained high (AUC = 0.94). In men with Gleason 7 tumors, who were excluded from the model building, the signature significantly improved the prediction of lethal disease beyond knowing whether the Gleason score was 4 + 3 or 3 + 4 (P = .006). Conclusion Our expression signature and the genes identified may improve our understanding of the de-differentiation process of prostate tumors. Additionally, the signature may have clinical applications among men with Gleason 7, by further estimating their risk of lethal prostate cancer and thereby guiding therapy decisions to improve outcomes and reduce overtreatment. J Clin Oncol 29:2391-2396.</p>
  •  
60.
  • Setlur, Sunita R., et al. (författare)
  • Estrogen-dependent signaling in a molecularly distinct subclass of aggressive prostate cancer
  • 2008
  • Ingår i: Journal of the National Cancer Institute. - Oxford : Oxford univ. press. - 0027-8874 .- 1460-2105. ; 100:11, s. 815-825
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>BACKGROUND: The majority of prostate cancers harbor gene fusions of the 5'-untranslated region of the androgen-regulated transmembrane protease serine 2 (TMPRSS2) promoter with erythroblast transformation-specific transcription factor family members. The common fusion between TMPRESS2 and v-ets erythroblastosis virus E26 oncogene homolog (avian) (ERG) is associated with a more aggressive clinical phenotype, implying the existence of a distinct subclass of prostate cancer defined by this fusion. METHODS: We used complementary DNA-mediated annealing, selection, ligation, and extension to determine the expression profiles of 6144 transcriptionally informative genes in archived biopsy samples from 455 prostate cancer patients in the Swedish Watchful Waiting cohort (1987-1999) and the United States-based Physicians(') Health Study cohort (1983-2003). A gene expression signature for prostate cancers with the TMPRSS2-ERG fusion was determined using partitioning and classification models and used in computational functional analysis. Cell proliferation and TMPRSS2-ERG expression in androgen receptor-negative (NCI-H660) prostate cancer cells after treatment with vehicle or estrogenic compounds were assessed by viability assays and quantitative polymerase chain reaction, respectively. All statistical tests were two-sided. RESULTS: We identified an 87-gene expression signature that distinguishes TMPRSS2-ERG fusion prostate cancer as a discrete molecular entity (area under the curve = 0.80, 95% confidence interval [CI] = 0.792 to 0.81; P &lt; .001). Computational analysis suggested that this fusion signature was associated with estrogen receptor (ER) signaling. Viability of NCI-H660 cells decreased after treatment with estrogen (viability normalized to day 0, estrogen vs vehicle at day 8, mean = 2.04 vs 3.40, difference = 1.36, 95% CI = 1.12 to 1.62) or ERbeta agonist (ERbeta agonist vs vehicle at day 8, mean = 1.86 vs 3.40, difference = 1.54, 95% CI = 1.39 to 1.69) but increased after ERalpha agonist treatment (ERalpha agonist vs vehicle at day 8, mean = 4.36 vs 3.40, difference = 0.96, 95% CI = 0.68 to 1.23). Similarly, expression of TMPRSS2-ERG decreased after ERbeta agonist treatment (fold change over internal control, ERbeta agonist vs vehicle at 24 hours, NCI-H660, mean = 0.57- vs 1.0-fold, difference = 0.43-fold, 95% CI = 0.29- to 0.57-fold) and increased after ERalpha agonist treatment (ERalpha agonist vs vehicle at 24 hours, mean = 5.63- vs 1.0-fold, difference = 4.63-fold, 95% CI = 4.34- to 4.92-fold). CONCLUSIONS: TMPRSS2-ERG fusion prostate cancer is a distinct molecular subclass. TMPRSS2-ERG expression is regulated by a novel ER-dependent mechanism.</p>
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 51-60 av 67
  • Föregående 12345[6]7Nästa
Åtkomst
fritt online (13)
Typ av publikation
tidskriftsartikel (66)
forskningsöversikt (1)
Typ av innehåll
refereegranskat (66)
övrigt vetenskapligt (1)
Författare/redaktör
Stampfer, Meir J. (47)
Albanes, Demetrius (38)
Le Marchand, Loïc (34)
Giles, Graham G (29)
Travis, Ruth C (27)
Gaziano, J Michael (27)
visa fler...
Kraft, Peter (26)
Giovannucci, Edward (26)
Ma, Jing (26)
Haiman, Christopher ... (25)
Kolonel, Laurence N (24)
Severi, Gianluca (23)
Bueno-de-Mesquita, H ... (23)
Stevens, Victoria L (22)
Mucci, Lorelei A (22)
Hunter, David J. (22)
Trichopoulos, Dimitr ... (20)
Stampfer, Meir (20)
Kaaks, Rudolf (19)
Johansson, Mattias (19)
Riboli, Elio (18)
Berndt, Sonja I (18)
Allen, Naomi E. (18)
Weinstein, Stephanie ... (18)
Stattin, Pär, (17)
Henderson, Brian E (17)
Chanock, Stephen J (17)
Key, Timothy J (16)
Hoover, Robert N. (16)
Virtamo, Jarmo (16)
Yeager, Meredith (16)
Boeing, Heiner (15)
Schumacher, Fredrick ... (15)
Stram, Daniel O (15)
Siddiq, Afshan (15)
Sesso, Howard D (15)
Ziegler, Regina G. (14)
Buring, Julie E (14)
Shu, Xiao-Ou (14)
Tjonneland, Anne (13)
Canzian, Federico (13)
Hayes, Richard B (13)
Visvanathan, Kala (13)
Gapstur, Susan M (12)
Thun, Michael J. (12)
Black, Amanda (12)
Zheng, Wei (12)
Brennan, Paul, (12)
Cai, Qiuyin (12)
Lindstrom, Sara (12)
visa färre...
Lärosäte
Umeå universitet (29)
Uppsala universitet (16)
Örebro universitet (14)
Lunds universitet (7)
Linköpings universitet (1)
Språk
Engelska (67)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (61)
Naturvetenskap (1)

År

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy