Institution
Cancer Epidemiology Unit
About: Cancer Epidemiology Unit is a based out in . It is known for research contribution in the topics: Population & Cancer. The organization has 669 authors who have published 1725 publications receiving 93979 citations.
Topics: Population, Cancer, Breast cancer, European Prospective Investigation into Cancer and Nutrition, Prospective cohort study
Papers published on a yearly basis
Papers
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TL;DR: In this paper, a simple approach using study-specific quantiles or percentage increases can provide substantial information on the relationship of the biomarker with cancer risk, even when the studies do not have standardized methods.
Abstract: Large numbers of observations are needed to provide adequate power in epidemiological studies of biomarkers and cancer risk. However, there are currently few large mature studies with adequate numbers of cases with biospecimens available. Therefore pooling biomarker measures from different studies is a valuable approach, enabling investigators to make robust estimates of risk and to examine associations in subgroups of the population. The ideal situation is to have standardized methods in all studies so that the biomarker data can be pooled in their original units. However, even when the studies do not have standardized methods, as with existing studies on hormones and cancer, a simple approach using study-specific quantiles or percentage increases can provide substantial information on the relationship of the biomarker with cancer risk.
34 citations
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University of Tromsø1, Heidelberg University2, German Cancer Research Center3, Imperial College London4, Utrecht University5, National and Kapodistrian University of Athens6, Cancer Epidemiology Unit7, Aarhus University8, Lund University9, University of Naples Federico II10, University Medical Center11, Umeå University12, University of Granada13, Prevention Institute14, International Agency for Research on Cancer15
TL;DR: The rate of overall mortality, as well as mortality from ischaemic heart disease and cancer in relation to the intake of total fish, lean fish, and fatty fish in a large prospective cohort including ten European countries is examined.
Abstract: Fish is a source of important nutrients and may play a role in preventing heart diseases and other health outcomes. However, studies of overall mortality and cause-specific mortality related to fish consumption are inconclusive. We examined the rate of overall mortality, as well as mortality from ischaemic heart disease and cancer in relation to the intake of total fish, lean fish, and fatty fish in a large prospective cohort including ten European countries. More than 500,000 men and women completed a dietary questionnaire in 1992–1999 and were followed up for mortality until the end of 2010. 32,587 persons were reported dead since enrolment. Hazard ratios and their 99 % confidence interval were estimated using Cox proportional hazard regression models. Fish consumption was examined using quintiles based on reported consumption, using moderate fish consumption (third quintile) as reference, and as continuous variables, using increments of 10 g/day. All analyses were adjusted for possible confounders. No association was seen for fish consumption and overall or cause-specific mortality for both the categorical and the continuous analyses, but there seemed to be a U-shaped trend (p < 0.000) with fatty fish consumption and total mortality and with total fish consumption and cancer mortality (p = 0.046).
34 citations
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International Agency for Research on Cancer1, French Institute of Health and Medical Research2, University of Paris-Sud3, Aarhus University4, Aalborg University5, Institut Gustave Roussy6, Université Paris-Saclay7, German Cancer Research Center8, National and Kapodistrian University of Athens9, University of Naples Federico II10, Prevention Institute11, Utrecht University12, University of Tromsø13, University of Granada14, Umeå University15, University of Gothenburg16, Lund University17, Cancer Epidemiology Unit18, University of Cambridge19, Imperial College London20
TL;DR: The role of metabolic pathways associated with steroid metabolism and immunity and specific dietary and environmental exposures in HCC development are emphasized and replicate previous observations made in Asian and Scandinavian populations.
Abstract: Hepatocellular carcinoma (HCC) development entails changes in liver metabolism. Current knowledge on metabolic perturbations in HCC is derived mostly from case-control designs, with sparse information from prospective cohorts. Our objective was to apply comprehensive metabolite profiling to detect metabolites whose serum concentrations are associated with HCC development, using biological samples from within the prospective European Prospective Investigation into Cancer and Nutrition (EPIC) cohort (>520 000 participants), where we identified 129 HCC cases matched 1:1 to controls. We conducted high-resolution untargeted liquid chromatography-mass spectrometry-based metabolomics on serum samples collected at recruitment prior to cancer diagnosis. Multivariable conditional logistic regression was applied controlling for dietary habits, alcohol consumption, smoking, body size, hepatitis infection and liver dysfunction. Corrections for multiple comparisons were applied. Of 9206 molecular features detected, 220 discriminated HCC cases from controls. Detailed feature annotation revealed 92 metabolites associated with HCC risk, of which 14 were unambiguously identified using pure reference standards. Positive HCC-risk associations were observed for N1-acetylspermidine, isatin, p-hydroxyphenyllactic acid, tyrosine, sphingosine, l,l-cyclo(leucylprolyl), glycochenodeoxycholic acid, glycocholic acid and 7-methylguanine. Inverse risk associations were observed for retinol, dehydroepiandrosterone sulfate, glycerophosphocholine, γ-carboxyethyl hydroxychroman and creatine. Discernible differences for these metabolites were observed between cases and controls up to 10 years prior to diagnosis. Our observations highlight the diversity of metabolic perturbations involved in HCC development and replicate previous observations (metabolism of bile acids, amino acids and phospholipids) made in Asian and Scandinavian populations. These findings emphasize the role of metabolic pathways associated with steroid metabolism and immunity and specific dietary and environmental exposures in HCC development.
34 citations
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TL;DR: A randomised clinical trial was recently conducted in very low birth weight pre-term neonates given bLF alone or with the probiotic Lactobacillus GG to assess the ability of bLf to prevent late-onset sepsis of any origin in the studied infants during their stay in the NICU.
34 citations
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University of Birmingham1, Cancer Epidemiology Unit2, Institut Gustave Roussy3, Semmelweis University4, Boston Children's Hospital5, Lund University6, University of Milano-Bicocca7, University of Bern8, Newcastle upon Tyne Hospitals NHS Foundation Trust9, University of Oslo10, Turku University Hospital11, Aarhus University12
TL;DR: Risk estimates of specific STS subtypes following childhood cancers are provided for the first time and evidence that risks of MPNSTs, leiomyosarcomas, and fibromatous neoplasms are particularly increased is given.
Abstract: Background
Childhood cancer survivors are at risk of subsequent primary soft-tissue sarcomas (STS), but the risks of specific STS histological subtypes are unknown. We quantified the risk of STS histological subtypes after specific types of childhood cancer.
Methods
We pooled data from 13 European cohorts, yielding a cohort of 69 460 five-year survivors of childhood cancer. Standardized incidence ratios (SIRs) and absolute excess risks (AERs) were calculated.
Results
Overall, 301 STS developed compared with 19 expected (SIR = 15.7, 95% confidence interval [CI] = 14.0 to 17.6). The highest standardized incidence ratios were for malignant peripheral nerve sheath tumors (MPNST; SIR = 40.6, 95% CI = 29.6 to 54.3), leiomyosarcomas (SIR = 29.9, 95% CI = 23.7 to 37.2), and fibromatous neoplasms (SIR = 12.3, 95% CI = 9.3 to 16.0). SIRs for MPNST were highest following central nervous system tumors (SIR = 80.5, 95% CI = 48.4 to 125.7), Hodgkin lymphoma (SIR = 81.3, 95% CI = 35.1 to 160.1), and Wilms tumor (SIR = 76.0, 95% CI = 27.9 to 165.4). Standardized incidence ratios for leiomyosarcoma were highest following retinoblastoma (SIR = 342.9, 95% CI = 245.0 to 466.9) and Wilms tumor (SIR = 74.2, 95% CI = 37.1 to 132.8). AERs for all STS subtypes were generally low at all years from diagnosis (AER < 1 per 10 000 person-years), except for leiomyosarcoma following retinoblastoma, for which the AER reached 52.7 (95% CI = 20.0 to 85.5) per 10 000 person-years among patients who had survived at least 45 years from diagnosis of retinoblastoma.
Conclusions
For the first time, we provide risk estimates of specific STS subtypes following childhood cancers and give evidence that risks of MPNSTs, leiomyosarcomas, and fibromatous neoplasms are particularly increased. While the multiplicative excess risks relative to the general population are substantial, the absolute excess risk of developing any STS subtype is low, except for leiomyosarcoma after retinoblastoma. These results are likely to be informative for both survivors and health care providers.
34 citations
Authors
Showing all 669 results
Name | H-index | Papers | Citations |
---|---|---|---|
Richard Peto | 183 | 683 | 231434 |
Kay-Tee Khaw | 174 | 1389 | 138782 |
Silvia Franceschi | 155 | 1340 | 112504 |
Timothy J. Key | 146 | 808 | 90810 |
Hans-Olov Adami | 145 | 908 | 83473 |
Alicja Wolk | 135 | 778 | 66239 |
Paolo Vineis | 134 | 1088 | 86608 |
Lars Klareskog | 131 | 697 | 63281 |
Eva Negri | 129 | 1010 | 66735 |
John A. Baron | 128 | 609 | 61182 |
Jack Cuzick | 128 | 754 | 79979 |
Anders Ekbom | 116 | 613 | 51430 |
C. La Vecchia | 115 | 817 | 53460 |
Valerie Beral | 114 | 471 | 53729 |
Carlo La Vecchia | 112 | 1265 | 56282 |