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Dive into the research topics where Maureen Hatch is active.

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Featured researches published by Maureen Hatch.


Health Psychology | 2000

Depressive symptomatology during pregnancy: evidence for an association with decreased fetal growth in pregnancies of lower social class women.

Susie Hoffman; Maureen Hatch

The relationship between depressive symptom scores on the Center for Epidemiological Studies Depression Scale (CES-D; L. S. Radloff, 1977) at each trimester of pregnancy and a decrement in either fetal growth or gestational duration was evaluated among 666 pregnant women. There was no association overall, but among 222 women from lower occupational status households, each unit increase on the CES-D at 28 weeks gestation was associated with a reduction of 9.1 g (95% confidence interval [CI] = -16.0, -2.3) in gestational-age-adjusted birth weight. When missing data were multiply imputed, the estimate was -4.6 g (95% CI = - 10.7, 1.5). CES-D score was unrelated to fetal growth or gestational duration in analyses among other potentially high-risk subgroups: smokers, women with a history of adverse outcome, and women with social vulnerabilities. These results raise the possibility that among lower status women, depressive mood may be associated with restricted fetal growth.


Epidemiology | 1996

Do stressful life events affect duration of gestation and risk of preterm delivery

Morten Hedegaard; Tine Brink Henriksen; Niels Jørgen Secher; Maureen Hatch; Svend Sabroe

&NA; The present study was designed to test the relation between stressful life events experienced during pregnancy and the risk of preterm delivery and shortened duration of pregnancy. We collected data prospectively in a general population sample, including repeated questionnaire measures of exposure to stressful life events during pregnancy. Between August 1989 and September 1991, 8,719 Danish‐speaking women with singleton pregnancies attended antenatal care. Of these women, 5,873 (67%) completed all questionnaires. When indicating an event, the woman was asked to rate the amount of stress induced by this event. Measurement of gestational duration was primarily based on early ultrasound scan. When we evaluated life events independently of the individuals appraisal, we found no association with duration of gestation or risk of preterm delivery. In contrast, life events assessed by the subject as highly stressful were associated with shorter mean duration of gestation and increased risk of preterm delivery. This association was observed primarily with events experienced between the 16th and 30th week of gestation. Women who had one or more highly stressful life events had a risk of preterm delivery 1.76 times greater than those without stressful events (95% confidence interval = 1.15‐2.71). We found no evidence for a buffering effect of social support. (Epidemiology 1996;7:339‐345)


International Journal of Cancer | 1996

Aflatoxin exposure and risk of hepatocellular carcinoma in Taiwan

Li-Yu Wang; Maureen Hatch; Chien-Jen Chen; Bruce Levin; San-Lin You; Sheng-Nan Lu; Mei-Huei Wu; Wei-Pin Wu; Lian-Wen Wang; Qiao Wang; Guan-Tarn Huang; Pei-Ming Yang; Hsuan-Shu Lee; Regina M. Santella

To investigate the carcinogenic effect of environmental aflatoxin exposure, 56 cases of hepatocellular carcinoma (HCC) diagnosed between 1991 and 1995 were identified and individually matched by age, sex, residence and date of recruitment to 220 healthy controls from the same large cohort in Taiwan. Blood samples were analyzed for hepatitis B and C viral markers and for aflatoxin‐albumin adducts; urine was tested for aflatoxin metabolites. We obtained information about socio‐demographic characteristics, habitual alcohol drinking, cigarette smoking and diet in a structured interview. Hepatitis B virus surface antigen (HBsAg) carriers had a significantly increased risk for HCC. After adjustment for HBsAg serostatus, the matched odds ratio (ORm) was significantly elevated for subjects with high levels of urinary aflatoxin metabolites. When stratified into tertiles, a dose‐response relationship with HCC was observed. The ORm for detectable aflatoxin‐albumin adducts was not significant after adjustment for HBsAg serostatus. HBsAg‐seropositive subjects with high aflatoxin exposure had a higher risk than subjects with high aflatoxin exposure only or HBsAg seropositivity only. In male HBsAg‐seropositive subjects, adjusted ORs were 2.8 (95% confidence interval [Cl] = 0.9–9.1) for detectable compared with non‐detectable aflatoxin‐albumin adducts and 5.5 (Cl = 1.3–23.4) for high compared with low urinary aflatoxin metabolite levels. Our results suggest that environmental aflatoxin exposure may enhance the hepatic carcinogenic potential of hepatitis B virus. A large‐scale study will be needed to evaluate the effect of aflatoxin exposure on HBsAg non‐carriers.


Breast Cancer Research and Treatment | 2002

The Long Island Breast Cancer Study Project: Description of a multi-institutional collaboration to identify environmental risk factors for breast cancer

Marilie D. Gammon; Alfred I. Neugut; Regina M. Santella; Susan L. Teitelbaum; Julie A. Britton; Mary Beth Terry; Sybil M. Eng; Mary S. Wolff; Steven D. Stellman; Geoffrey C. Kabat; Bruce Levin; H. Leon Bradlow; Maureen Hatch; Jan Beyea; David Camann; Martin Trent; Ruby T. Senie; Gail C. Garbowski; Carla Maffeo; Pat Montalvan; Ger trud S. Berkowitz; Margaret Kemeny; Marc L. Citron; Freya Schnabel; Allan Schuss; Steven I. Hajdu; Vincent Vincguerra; Gwen W. Collman; G. Iris Obrams

The Long Island Breast Cancer Study Project is a federally mandated, population-based case-control study to determine whether breast cancer risk among women in the counties of Nassau and Suffolk, NY, is associated with selected environmental exposures, assessed by blood samples, self-reports, and environmental home samples. This report describes the collaborative projects background, rationale, methods, participation rates, and distributions of known risk factors for breast cancer by case-control status, by blood donation, and by availability of environmental home samples. Interview response rates among eligible cases and controls were 82.1% (n, = 1,508) and 62.8% (n = 1,556), respectively. Among case and control respondents who completed the interviewer-administered questionnaire, 98.2 and 97.6% self-completed the food frequency questionnaire; 73.0 and 73.3% donated a blood sample; and 93.0 and 83.3% donated a urine sample. Among a random sample of case and control respondents who are long-term residents, samples of dust (83.6 and 83.0%); soil (93.5 and 89.7%); and water (94.3 and 93.9%) were collected. Established risk factors for breast cancer that were found to increase risk among Long Island women include lower parity, late age at first birth, little or no breast feeding, and family history of breast cancer. Factors that were found to be associated with a decreased likelihood that a respondent would donate blood include increasing age and past smoking; factors associated with an increased probability include white or other race, alcohol use, ever breastfed, ever use of hormone replacement therapy, ever use of oral contraceptives, and ever had a mammogram. Long-term residents (defined as 15+ years in the interview home) with environmental home samples did not differ from other long-term residents, although there were a number of differences in risk factor distributions between long-term residents and other participants, as anticipated.


Cancer Epidemiology, Biomarkers & Prevention | 2002

Environmental Toxins and Breast Cancer on Long Island. I. Polycyclic Aromatic Hydrocarbon DNA Adducts

Marilie D. Gammon; Regina M. Santella; Alfred I. Neugut; Sybil M. Eng; Susan L. Teitelbaum; Andrea Paykin; Bruce Levin; Mary Beth Terry; Tie Lan Young; Lian Wen Wang; Qiao Wang; Julie A. Britton; Mary S. Wolff; Steven D. Stellman; Maureen Hatch; Geoffrey C. Kabat; Ruby T. Senie; Gail C. Garbowski; Carla Maffeo; Pat Montalvan; Gertrud S. Berkowitz; Margaret Kemeny; Marc L. Citron; Freya Schnabel; Allan Schuss; Steven I. Hajdu; Vincent Vinceguerra

Polycyclic aromatic hydrocarbons (PAH) are potent mammary carcinogens in rodents, but their effect on breast cancer development in women is not clear. To examine whether currently measurable PAH damage to DNA increases breast cancer risk, a population-based case-control study was undertaken on Long Island, NY. Cases were women newly diagnosed with in situ and invasive breast cancer; controls were randomly selected women frequency matched to the age distribution of cases. Blood samples were donated by 1102 (73.0%) and 1141 (73.3%) of case and control respondents, respectively. Samples from 576 cases and 427 controls were assayed for PAH-DNA adducts using an ELISA. The geometric mean (and geometric SD) of the log-transformed levels of PAH-DNA adducts on a natural scale was slightly, but nonsignificantly, higher among cases [7.36 (7.29)] than among controls [6.21 (4.17); P = 0.51]. The age-adjusted odds ratio (OR) for breast cancer in relation to the highest quintile of adduct levels compared with the lowest was 1.51 [95% confidence interval (CI), 1.04-2.20], with little or no evidence of substantial confounding (corresponding multivariate-adjusted OR, 1.49; 95% CI, 1.00-2.21). There was no consistent elevation in risk with increasing adduct levels, nor was there a consistent association between adduct levels and two of the main sources of PAH, active or passive cigarette smoking or consumption of grilled and smoked foods. These data indicate that PAH-DNA adduct formation may influence breast cancer development, although the association does not appear to be dose dependent and may have a threshold effect.


Journal of Radiological Protection | 2006

Cancer consequences of the Chernobyl accident: 20 years on

Elisabeth Cardis; Geoffrey R. Howe; Elaine Ron; Vladimir Bebeshko; Tetyana I. Bogdanova; André Bouville; Zhanat Carr; Vadim V. Chumak; Scott Davis; Yuryi Demidchik; Vladimir Drozdovitch; Norman E Gentner; Natalya Gudzenko; Maureen Hatch; V. K. Ivanov; Peter Jacob; Eleonora Kapitonova; Yakov Kenigsberg; Ausrele Kesminiene; Kenneth J. Kopecky; Victor Kryuchkov; Anja Loos; Aldo Pinchera; Christoph Reiners; Michael Repacholi; Yoshisada Shibata; Roy E. Shore; Gerry Thomas; Margot Tirmarche; Shunichi Yamashita

26 April 2006 marks the 20th anniversary of the Chernobyl accident. On this occasion, the World Health Organization (WHO), within the UN Chernobyl Forum initiative, convened an Expert Group to evaluate the health impacts of Chernobyl. This paper summarises the findings relating to cancer. A dramatic increase in the incidence of thyroid cancer has been observed among those exposed to radioactive iodines in childhood and adolescence in the most contaminated territories. Iodine deficiency may have increased the risk of developing thyroid cancer following exposure to radioactive iodines, while prolonged stable iodine supplementation in the years after exposure may reduce this risk. Although increases in rates of other cancers have been reported, much of these increases appear to be due to other factors, including improvements in registration, reporting and diagnosis. Studies are few, however, and have methodological limitations. Further, because most radiation-related solid cancers continue to occur decades after exposure and because only 20 years have passed since the accident, it is too early to evaluate the full radiological impact of the accident. Apart from the large increase in thyroid cancer incidence in young people, there are at present no clearly demonstrated radiation-related increases in cancer risk. This should not, however, be interpreted to mean that no increase has in fact occurred: based on the experience of other populations exposed to ionising radiation, a small increase in the relative risk of cancer is expected, even at the low to moderate doses received. Although it is expected that epidemiological studies will have difficulty identifying such a risk, it may nevertheless translate into a substantial number of radiation-related cancer cases in the future, given the very large number of individuals exposed.


Epidemiology | 1995

MATERNAL SMOKING, ALCOHOL DRINKING, CAFFEINE CONSUMPTION, AND FETAL GROWTH: RESULTS FROM A PROSPECTIVE STUDY

Xiao-Ou Shu; Maureen Hatch; James L. Mills; John D. Clemens; Mervyn Susser

In a prospective study of 712 pregnancies, we examined associations between maternal smoking, alcohol, and caffeine consumption and fetal growth. We interviewed patients at entry into care [12.9 ± 4.3 (standard deviation) weeks], and at 28 and 36 weeks of gestation. We found the expected reductions in adjusted birthweight among women who smoked throughout pregnancy: 168 gm [95% confidence limits (CL) = −326, −10] for low/moderate amounts (≤15 cigarettes per day); 288 gm (95% CL = −491, −84) for heavy smoking (>15 cigarettes per day). We also found a decrease in birthweight ( - 179 gm; 95% CL = −364, 7) among smokers who reported quitting early in pregnancy. First trimester alcohol consumption (average: four drinks per week) was associated with a 155-gm reduction in fetal growth (95% CL = −324, 15), even after adjustment for number of cigarettes smoked. The association, observed with all types of alcohol consumption, was stronger among smokers ( - 270 gm) but was also present in nonsmokers ( - 115 gm). Caffeine consumption showed no relation to fetal growth, even among heavy consumers, although they were relatively few. This study implicates heavy maternal smoking at any point in pregnancy, including solely in the early months, and possibly moderate alcohol drinking as causes of low birthweight.


Environmental Health Perspectives | 2011

I-131 dose response for incident thyroid cancers in Ukraine related to the Chornobyl accident.

Alina V. Brenner; Mykola Tronko; Maureen Hatch; Tetyana I. Bogdanova; Valery A. Oliynik; Jay H. Lubin; Lydia B. Zablotska; Valery P. Tereschenko; Robert J. McConnell; Galina A. Zamotaeva; Patrick O'Kane; André Bouville; Ludmila V. Chaykovskaya; Ellen Greenebaum; Ihor P. Paster; Victor Shpak; Elaine Ron

Background: Current knowledge about Chornobyl-related thyroid cancer risks comes from ecological studies based on grouped doses, case–control studies, and studies of prevalent cancers. Objective: To address this limitation, we evaluated the dose–response relationship for incident thyroid cancers using measurement-based individual iodine-131 (I-131) thyroid dose estimates in a prospective analytic cohort study. Methods: The cohort consists of individuals < 18 years of age on 26 April 1986 who resided in three contaminated oblasts (states) of Ukraine and underwent up to four thyroid screening examinations between 1998 and 2007 (n = 12,514). Thyroid doses of I-131 were estimated based on individual radioactivity measurements taken within 2 months after the accident, environmental transport models, and interview data. Excess radiation risks were estimated using Poisson regression models. Results: Sixty-five incident thyroid cancers were diagnosed during the second through fourth screenings and 73,004 person-years (PY) of observation. The dose–response relationship was consistent with linearity on relative and absolute scales, although the excess relative risk (ERR) model described data better than did the excess absolute risk (EAR) model. The ERR per gray was 1.91 [95% confidence interval (CI), 0.43–6.34], and the EAR per 104 PY/Gy was 2.21 (95% CI, 0.04–5.78). The ERR per gray varied significantly by oblast of residence but not by time since exposure, use of iodine prophylaxis, iodine status, sex, age, or tumor size. Conclusions: I-131–related thyroid cancer risks persisted for two decades after exposure, with no evidence of decrease during the observation period. The radiation risks, although smaller, are compatible with those of retrospective and ecological post-Chornobyl studies.


British Journal of Cancer | 2011

Thyroid cancer risk in Belarus among children and adolescents exposed to radioiodine after the Chornobyl accident

Lydia B. Zablotska; Elaine Ron; Alexander Rozhko; Maureen Hatch; Olga N. Polyanskaya; Alina V. Brenner; Jay H. Lubin; G N Romanov; Robert J. McConnell; Patrick O'Kane; V V Evseenko; Vladimir Drozdovitch; N Luckyanov; Viktor Minenko; André Bouville; V B Masyakin

Background:Previous studies showed an increased risk of thyroid cancer among children and adolescents exposed to radioactive iodines released after the Chornobyl (Chernobyl) accident, but the effects of screening, iodine deficiency, age at exposure and other factors on the dose–response are poorly understood.Methods:We screened 11 970 individuals in Belarus aged 18 years or younger at the time of the accident who had estimated 131I thyroid doses based on individual thyroid activity measurements and dosimetric data from questionnaires. The excess odds ratio per gray (EOR/Gy) was modelled using linear and linear–exponential functions.Results:For thyroid doses <5 Gy, the dose–response was linear (n=85; EOR/Gy=2.15, 95% confidence interval: 0.81–5.47), but at higher doses the excess risk fell. The EOR/Gy was significantly increased among those with prior or screening-detected diffuse goiter, and larger for men than women, and for persons exposed before age 5 than those exposed between 5 and 18 years, although not statistically significant. A somewhat higher EOR/Gy was estimated for validated pre-screening cases.Conclusion:10–15 years after the Chornobyl accident, thyroid cancer risk was significantly increased among individuals exposed to fallout as children or adolescents, but the risk appeared to be lower than in other Chornobyl studies and studies of childhood external irradiation.


Cancer | 2014

ETV6-NTRK3 is a common chromosomal rearrangement in radiation-associated thyroid cancer.

Rebecca J. Leeman-Neill; Lindsey M. Kelly; Pengyuan Liu; Alina V. Brenner; Mark P. Little; Tetiana Bogdanova; Viktoria N. Evdokimova; Maureen Hatch; Liudmyla Y. Zurnadzy; Marina N. Nikiforova; Ning J. Yue; Miao Zhang; Kiyohiko Mabuchi; Mykola Tronko; Yuri E. Nikiforov

In their previous analysis of papillary thyroid carcinomas (PTCs) from an Ukrainian‐American cohort that was exposed to iodine‐131 (131I) from the Chernobyl accident, the authors identified RET/PTC rearrangements and other driver mutations in 60% of tumors.

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Alina V. Brenner

National Institutes of Health

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André Bouville

National Institutes of Health

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Mark P. Little

National Institutes of Health

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Vladimir Drozdovitch

National Institutes of Health

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Kiyohiko Mabuchi

Radiation Effects Research Foundation

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Marilie D. Gammon

University of North Carolina at Chapel Hill

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Susan L. Teitelbaum

Icahn School of Medicine at Mount Sinai

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