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Eva S. Schernhammer

Bio: Eva S. Schernhammer is an academic researcher from Medical University of Vienna. The author has contributed to research in topics: Shift work & Breast cancer. The author has an hindex of 68, co-authored 265 publications receiving 19787 citations. Previous affiliations of Eva S. Schernhammer include University of Vienna & Duke University.


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Journal ArticleDOI
TL;DR: Converging results from epidemiological research and in vivo carcinogenesis models indicate that high levels of circulating IGF1 are associated with increased risk of several common cancers, and ongoing research seeks to clarify the mechanisms underlying these observations.
Abstract: The insulin-like growth factor 1 (IGF1) signalling pathway has important roles in regulating cellular proliferation and apoptosis. Converging results from epidemiological research and in vivo carcinogenesis models indicate that high levels of circulating IGF1 are associated with increased risk of several common cancers. Ongoing research seeks to clarify the mechanisms underlying these observations and to determine the extent to which IGF physiology influences patterns of cancer incidence. Various therapeutic strategies that target the IGF1 receptor have demonstrated impressive antineoplastic activity in laboratory models, and clinical trials of several novel drug candidates are planned.

1,477 citations

Journal ArticleDOI
Ganna Chornokur, Hui-Yi Lin, Jonathan Tyrer1, Kate Lawrenson2  +155 moreInstitutions (51)
19 Jun 2015-PLOS ONE
TL;DR: Associations between inherited cellular transport gene variants and risk of EOC histologic subtypes are revealed on a large cohort of women.
Abstract: BACKGROUND: Defective cellular transport processes can lead to aberrant accumulation of trace elements, iron, small molecules and hormones in the cell, which in turn may promote the formation of reactive oxygen species, promoting DNA damage and aberrant expression of key regulatory cancer genes. As DNA damage and uncontrolled proliferation are hallmarks of cancer, including epithelial ovarian cancer (EOC), we hypothesized that inherited variation in the cellular transport genes contributes to EOC risk. METHODS: In total, DNA samples were obtained from 14,525 case subjects with invasive EOC and from 23,447 controls from 43 sites in the Ovarian Cancer Association Consortium (OCAC). Two hundred seventy nine SNPs, representing 131 genes, were genotyped using an Illumina Infinium iSelect BeadChip as part of the Collaborative Oncological Gene-environment Study (COGS). SNP analyses were conducted using unconditional logistic regression under a log-additive model, and the FDR q<0.2 was applied to adjust for multiple comparisons. RESULTS: The most significant evidence of an association for all invasive cancers combined and for the serous subtype was observed for SNP rs17216603 in the iron transporter gene HEPH (invasive: OR = 0.85, P = 0.00026; serous: OR = 0.81, P = 0.00020); this SNP was also associated with the borderline/low malignant potential (LMP) tumors (P = 0.021). Other genes significantly associated with EOC histological subtypes (p<0.05) included the UGT1A (endometrioid), SLC25A45 (mucinous), SLC39A11 (low malignant potential), and SERPINA7 (clear cell carcinoma). In addition, 1785 SNPs in six genes (HEPH, MGST1, SERPINA, SLC25A45, SLC39A11 and UGT1A) were imputed from the 1000 Genomes Project and examined for association with INV EOC in white-European subjects. The most significant imputed SNP was rs117729793 in SLC39A11 (per allele, OR = 2.55, 95% CI = 1.5-4.35, p = 5.66x10-4). CONCLUSION: These results, generated on a large cohort of women, revealed associations between inherited cellular transport gene variants and risk of EOC histologic subtypes.

1,100 citations

Journal ArticleDOI
TL;DR: Women who work on rotating night shifts with at least three nights per month, in addition to days and evenings in that month, appear to have a moderately increased risk of breast cancer after extended periods of working rotating night shift.
Abstract: Background: Melatonin shows poten-tial oncostatic action,and light expo-sure during night suppresses melatoninproduction. There is little information,however,about the direct effect ofnight work on the risk of cancer. Weinvestigated the effect of night work inbreast cancer. Methods: We examinedthe relationship between breast cancerand working on rotating night shiftsduring 10 years of follow-up in 78562women from the Nurses’ Health Study.Information was ascertained in 1988about the total number of years duringwhich the nurses had worked rotatingnight shifts with at least three nightsper month. From June 1988 throughMay 1998,we documented 2441 inci-dent breast cancer cases. Logistic re-gression models were used to calculaterelative risks (RRs) and 95% confi-dence intervals (CIs),adjusted for con-founding variables and breast cancerrisk factors. All statistical tests weretwo-sided. Results: We observed a mod-erate increase in breast cancer riskamong the women who worked 1–14years or 15–29 years on rotating nightshifts (multivariate adjusted RR = 1.08[95% CI = 0.99 to 1.18] and RR = 1.08[95% CI = 0.90 to 1.30],respectively).The risk was further increased amongwomen who worked 30 or more yearson the night shift (RR = 1.36; 95% CI =1.04 to 1.78). The test for trend was sta-tistically significant ( P = .02).Conclu-sions: Women who work on rotatingnight shifts with at least three nightsper month,in addition to days and eve-nings in that month,appear to have amoderately increased risk of breastcancer after extended periods of work-ing rotating night shifts. [J Natl CancerInst 2001;93:1563–8]The suprachiasmatic nucleus in the hy-pothalamus, one of the most importantphysiologic determinants of alertness andperformance, drives a circadian pace-maker in mammals, with an intrinsic pe-riod averaging 24 hours. Light is the pri-mary stimulus to disrupt and reset thispacemaker, which is expressed in chang-ing melatonin rhythms. Light exposure atnight may, therefore, be related to a vari-ety of behavioral changes and associatedhealth problems not yet well explored.Studies (1)have suggested an increasedrisk of coronary heart disease among ro-tating night shift workers, not fully ex-plained by an increased prevalence ofcoronary risk factors. Others have linkednight work to an increased breast cancerrisk among women (2).Melatonin, the “hormone of the dark-ness,” has only recently gained substantialattention from the scientific communitywith regard to its potential oncostatic ac-tions and its possible effect on breast can-cer risk (3–10).Melatonin serum levels inhumans decrease when people are ex-posed to light at night (11).Suppressedserum melatonin levels might enhance tu-mor development (12).Observationalstudies (2,13–15)are compatible with aneffect of melatonin on breast cancer risk,reporting meaningful increases in breastcancer risk among postmenopausal womenexposed to shiftwork. Recently, a tumor-promoting effect of light exposure wasdemonstrated on chemically induced tu-mors in rodents (16).To date, melatoninhas been shown to be oncostatic for a va-riety of tumor cells in experimental car-cinogenesis (17–26).The evidence of arelation between melatonin and oncogen-esis in humans is conflicting (27),butthe majority of reports indicate protectiveaction (28).Several mechanisms have been hy-pothesized to explain an association be-tween melatonin and breast cancer. Cohenet al. (29)proposed that loss of pinealfunction and the resulting decreased mel-atonin serum levels may increase repro-ductive hormone levels and, in particular,estradiol levels, thereby increasing thegrowth and proliferation of hormone-sensitive cells in the breast. More recentresearch focuses on potential mechanismsthrough which melatonin is directly onco-static. Melatonin is believed to have anti-mitotic activity by affecting directly hor-mone-dependent proliferation throughinteraction with nuclear receptors (4).An-other explanation is that melatonin in-creases the expression of the tumor sup-pressor gene p53 (3).Cells lacking p53have been shown to be genetically un-stable and thus more prone to tumors (30).Breast cancer is the most common can-cer among women in the United States.To date, the relationship between nightwork and breast cancer risk has not beenevaluated in prospective cohort studies. Acausal link between the two would be ofpublic health importance, because smallchanges in shift patterns may create a sub-stantial decrease of disease burden amongwomen.In this report, we evaluate the relation-ship between night work, as a surrogatefor light exposure at night, and breastcancer risk in a large prospective cohortof premenopausal and postmenopausalwomen. Our analysis is based on 10 yearsof follow-up in 78562 women participat-ing in the Nurses’ Health Study.

1,061 citations

Journal ArticleDOI
TL;DR: It is suggested that working a rotating night shift at least three nights per month for 15 or more years may increase the risk of colorectal cancer in women.
Abstract: Exposure to light at night suppresses the physiologic production of melatonin, a hormone that has antiproliferative effects on intestinal cancers. Although observational studies have associated night-shift work with an increased risk of breast cancer, the effect of night-shift work on the risk of other cancers is not known. We prospectively examined the relationship between working rotating night shifts and the risk of colorectal cancers among female participants in the Nurses' Health Study. We documented 602 incident cases of colorectal cancer among 78 586 women who were followed up from 1988 through 1998. Compared with women who never worked rotating night shifts, women who worked 1-14 years or 15 years or more on rotating night shifts had multivariate relative risks of colorectal cancer of 1.00 (95% confidence interval [CI] = 0.84 to 1.19) and 1.35 (95% CI = 1.03 to 1.77), respectively (P(trend) =.04). These data suggest that working a rotating night shift at least three nights per month for 15 or more years may increase the risk of colorectal cancer in women.

748 citations

Journal ArticleDOI
TL;DR: Studies on physicians' suicide collectively show modestly (men) to highly (women) elevated suicide rate ratios, and larger studies should help clarify whether female Physicians' suicide rate is truly elevated or can be explained by publication bias.
Abstract: OBJECTIVE: Physicians’ suicide rates have repeatedly been reported to be higher than those of the general population or other academics, but uncertainty remains. In this study, physicians’ suicide rate ratios were estimated with a meta-analysis and systematic quality assessment of recent studies. METHOD: Studies of physicians’ suicide rates were located in MEDLINE, PsycINFO, AARP Ageline, and the EBM Reviews: Cochrane Database of Systematic Reviews with the terms “physicians,” “doctors,” “suicide,” and “mortality.” Studies were included if they were published in or after 1960 and gave estimates of age-standardized suicide rates of physicians and their reference population or reported extractable data on physicians’ suicide; 25 studies met the criteria. Reviewers extracted data and scored each study for quality. The studies were tested for heterogeneity and publication bias and were stratified by publication year, follow-up, and study quality. Effect sizes were pooled by using fixed-effects (women) and ran...

700 citations


Cited by
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Book ChapterDOI
01 Jan 2010

5,842 citations

Journal ArticleDOI
TL;DR: In a meta-analysis, Julianne Holt-Lunstad and colleagues find that individuals' social relationships have as much influence on mortality risk as other well-established risk factors for mortality, such as smoking.
Abstract: Background The quality and quantity of individuals' social relationships has been linked not only to mental health but also to both morbidity and mortality. Objectives This meta-analytic review was conducted to determine the extent to which social relationships influence risk for mortality, which aspects of social relationships are most highly predictive, and which factors may moderate the risk. Data Extraction Data were extracted on several participant characteristics, including cause of mortality, initial health status, and pre-existing health conditions, as well as on study characteristics, including length of follow-up and type of assessment of social relationships. Results Across 148 studies (308,849 participants), the random effects weighted average effect size was OR = 1.50 (95% CI 1.42 to 1.59), indicating a 50% increased likelihood of survival for participants with stronger social relationships. This finding remained consistent across age, sex, initial health status, cause of death, and follow-up period. Significant differences were found across the type of social measurement evaluated (p<0.001); the association was strongest for complex measures of social integration (OR = 1.91; 95% CI 1.63 to 2.23) and lowest for binary indicators of residential status (living alone versus with others) (OR = 1.19; 95% CI 0.99 to 1.44). Conclusions The influence of social relationships on risk for mortality is comparable with well-established risk factors for mortality. Please see later in the article for the Editors' Summary

5,070 citations

Journal ArticleDOI
TL;DR: Interest in the topic of tumour metabolism has waxed and waned over the past century, but it has become clear that many of the signalling pathways that are affected by genetic mutations and the tumour microenvironment have a profound effect on core metabolism, making this topic once again one of the most intense areas of research in cancer biology.
Abstract: Interest in the topic of tumour metabolism has waxed and waned over the past century of cancer research. The early observations of Warburg and his contemporaries established that there are fundamental differences in the central metabolic pathways operating in malignant tissue. However, the initial hypotheses that were based on these observations proved inadequate to explain tumorigenesis, and the oncogene revolution pushed tumour metabolism to the margins of cancer research. In recent years, interest has been renewed as it has become clear that many of the signalling pathways that are affected by genetic mutations and the tumour microenvironment have a profound effect on core metabolism, making this topic once again one of the most intense areas of research in cancer biology.

4,169 citations

Journal ArticleDOI
TL;DR: Panitumumab monotherapy efficacy in mCRC is confined to patients with WT KRAS tumors, and KRAS status should be considered in selecting patients withmCRC as candidates for panitumuab mon Therapy.
Abstract: Purpose Panitumumab, a fully human antibody against the epidermal growth factor receptor (EGFR), has activity in a subset of patients with metastatic colorectal cancer (mCRC). Although activating mutations in KRAS, a small G-protein downstream of EGFR, correlate with poor response to anti-EGFR antibodies in mCRC, their role as a selection marker has not been established in randomized trials. Patients and Methods KRAS mutations were detected using polymerase chain reaction on DNA from tumor sections collected in a phase III mCRC trial comparing panitumumab monotherapy to best supportive care (BSC). We tested whether the effect of panitumumab on progression-free survival (PFS) differed by KRAS status. Results KRAS status was ascertained in 427 (92%) of 463 patients (208 panitumumab, 219 BSC). KRAS mutations were found in 43% of patients. The treatment effect on PFS in the wild-type (WT) KRAS group (hazard ratio [HR], 0.45; 95% CI: 0.34 to 0.59) was significantly greater (P .0001) than in the mutant group (HR, 0.99; 95% CI, 0.73 to 1.36). Median PFS in the WT KRAS group was 12.3 weeks for panitumumab and 7.3 weeks for BSC. Response rates to panitumumab were 17% and 0%, for the WT and mutant groups, respectively. WT KRAS patients had longer overall survival (HR, 0.67; 95% CI, 0.55 to 0.82; treatment arms combined). Consistent with longer exposure, more grade III treatment-related toxicities occurred in the WT KRAS group. No significant differences in toxicity were observed between the WT KRAS group and the overall population. Conclusion Panitumumab monotherapy efficacy in mCRC is confined to patients with WT KRAS tumors. KRAS status should be considered in selecting patients with mCRC as candidates for panitumumab monotherapy.

3,040 citations