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Amy Berrington de Gonzalez

Bio: Amy Berrington de Gonzalez is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Cancer & Breast cancer. The author has an hindex of 6, co-authored 7 publications receiving 1620 citations. Previous affiliations of Amy Berrington de Gonzalez include National Institutes of Health & City of Hope National Medical Center.

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Journal ArticleDOI
21 Aug 2006-Vaccine
TL;DR: The causal role of human papillomavirus in all cancers of the uterine cervix has been firmly established biologically and epidemiologically and co-infection with Chlamydia trachomatis and herpes simplex virus type-2 have been identified as established cofactors.

1,267 citations

Journal ArticleDOI
TL;DR: Results show a favorable decrease of 3% per year for CBC incidence in the United States since 1985, driven by declining CBC rates after an ER-positive cancer, possibly because of the widespread usage of adjuvant hormone therapies, after the results of the Nolvadex Adjuvant Trial Organisation were published in 1983, and/or other adjUvant treatments.
Abstract: Purpose Contralateral breast cancer (CBC) is the most frequent new malignancy among women diagnosed with a first breast cancer. Although temporal trends for first breast cancers have been well studied, trends for CBC are not so well established. Patients and Methods We examined temporal trends in CBC incidence using US Surveillance, Epidemiology, and End Results database (1975 to 2006). Data were stratified by estrogen receptor (ER) status of the first breast cancer for the available time period (1990+). We estimated the annual percent change (EAPC) in CBC rates using Poisson regression models adjusted for the age at and time since first breast cancer diagnosis. Results Before 1985, CBC incidence rates were stable (EAPC, 0.27% per year; 95% CI, −0.4 to 0.9), after which they declined with an EAPC of −3.07% per year (95% CI, −3.5 to −2.7). From 1990 forward, the declines were restricted to CBC after an ER-positive cancer (EAPC, −3.18%; 95% CI, −4.2 to −2.2) with no clear decreases after an ER-negative canc...

217 citations

Journal ArticleDOI
TL;DR: The results suggest that there would be no net benefit from annual mammographic screening of BRCA mutation carriers at age 25-29 years; the net benefit would be zero or small at age 30-34 years, but there should be some net benefit at age 35 or older.
Abstract: BRCA mutation carriers are recommended to start mammographic screening for breast cancer as early as age 25-30 years. We used an excess relative risk model (based on a pooled analysis of three cohorts with 7600 subjects who received radiation exposure) to estimate the lifetime risk of radiation-induced breast cancer from five annual mammographic screenings in young (<40 years) BRCA mutation carriers. We then estimated the reduction in breast cancer mortality required to outweigh the radiation risk. Breast cancer rates for mutation carriers were based on a pooled analysis of 22 pedigree studies with 8139 subjects. For BRCA1 mutation carriers, the estimated lifetime risk of radiation-induced breast cancer mortality per 10,000 women resulting from annual mammography was 26 (95% confidence interval [CI] = 14 to 49) for screening at age 25-29 years, 20 (95% CI = 11 to 39) for screening at age 30-34 years, and 13 (95% CI = 7 to 23) for screening at age 35-39 years. To outweigh these risks, screening would have to reduce breast cancer mortality by 51% (95% CI = 27% to 96%) at age 25-29 years, by 12% (95% CI = 6% to 23%) at age 30-34 years, and by 4% (95% CI = 2% to 7%) at age 35-39 years; estimates were similar for BRCA2 mutation carriers. If we assume that the mortality reduction from mammography is 15%-25% or less for young women, these results suggest that there would be no net benefit from annual mammographic screening of BRCA mutation carriers at age 25-29 years; the net benefit would be zero or small at age 30-34 years, but there should be some net benefit at age 35 or older. These results depend on a number of assumptions due to the absence of empiric data. The impact of varying these assumptions was therefore examined.

117 citations

Journal ArticleDOI
TL;DR: The association with elevated liver enzyme levels is a novel finding that warrants further investigation and is found previously to be associated with pancreatic cancer risk in this cohort of men and women.
Abstract: There is increasing evidence that type 2 diabetes mellitus and glucose intolerance are a cause, not just a consequence, of pancreatic cancer. We examined whether other factors that characterize the insulin resistance syndrome are also risk factors for pancreatic cancer in a prospective cohort study of 631,172 men and women (ages 45+ years) who received health insurance from the Korean Medical Insurance Corporation. The biennial medical evaluations from 1992 to 1995 provided the baseline information for this study. Relative risks (RR) were estimated using proportional hazards models adjusted for age, sex, smoking, and fasting serum glucose (after excluding the first 2 years of follow-up). There were 2,194 incident cases of pancreatic cancer diagnosed in the cohort over a median follow-up of 12 years. There was no evidence that pancreatic cancer risk was associated with total cholesterol, systolic blood pressure, WBC count, or body mass index. Abnormal levels of aspartate aminotransferase and alanine aminotransferase were both associated with a moderately increased risk of developing the disease (40+ versus <20; RR, 1.33; 95% CI, 1.14-1.55; P trend = 0.05 and RR, 1.34; 95% CI, 1.16-1.56; P trend = 0.02, respectively). Excluding 6 years of follow-up reduced this RR (95% CI) for aspartate aminotransferase to 1.22 (1.01-1.49), but even after excluding 10 years follow-up the RR (95% CI) for alanine aminotransferase was unchanged [1.36 (1.01-1.83)]. Although fasting serum glucose has been found previously to be associated with pancreatic cancer risk in this cohort, most other factors that characterize insulin resistance syndrome were not associated with pancreatic cancer risk. The association with elevated liver enzyme levels is a novel finding that warrants further investigation. (Cancer Epidemiol Biomarkers Prev 2008;17(2):359–64)

54 citations

Journal ArticleDOI
TL;DR: The cumulative risk of radiation-induced cancer from repeated lung CT scans for patients with cystic fibrosis is relatively small (less than 0.5%).
Abstract: Rationale: Computed tomography (CT) is being considered as a tool for routine monitoring of lung damage in people with cystic fibrosis. Concern has been raised, however, about the associated risk of radiation-induced cancer. Objectives: To estimate the risk of radiation-induced cancer from lung CT for patients with cystic fibrosis, assuming annual monitoring starting at age 2 years. Methods: Radiation risk models (derived primarily from the study of Japanese atomic bomb survivors) were used to estimate the excess risk of radiation-induced cancer for the organs that receive measurable doses from lung CT. Two scenarios were considered: median survival to age 36 years (approximate current median survival) and median survival to age 50 years (projected median survival by 2030). Measurements and Main Results: The estimated risk of radiationinduced cancer from annual lung CT was 0.02% for males and 0.07% for females assuming median survival to age 36 years. The estimated risks increased to 0.08% for males and 0.46% for females assuming median survival increases to age 50 years. The risks are higher for females because of the risk of radiation-induced breast cancer (50% of total risk) and higher risk of thyroid cancer. Conclusions: The cumulative risk of radiation-induced cancer from repeated lung CT scans for patients with cystic fibrosis is relatively small (less than 0.5%). However, routine monitoring should not be recommended until there is a demonstrated benefit that will outweigh these risks.

50 citations


Cited by
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Journal ArticleDOI
TL;DR: The new HPV-oriented model of cervical carcinogenesis should gradually replace older morphological models based only on cytology and histology, and can minimise the incidence of cervical cancer, and the morbidity and mortality it causes, even in low-resource settings.

2,429 citations

Journal ArticleDOI
20 Nov 2012-Vaccine
TL;DR: The high-risk HPV types are a cause of several important human cancers, including almost all cases of cervical cancer, a large proportion of other anogenital cancers and a growing number of head and neck tumours.

1,108 citations

Journal ArticleDOI
TL;DR: These cross-protection results complement the vaccine's prophylactic efficacy against disease associated with HPV-6, -11, -16, and -18 and are needed to fully ascertain the population-based impact and public health significance of these findings.
Abstract: Background. Human papillomavirus (HPV)-6/11/16/18 vaccine reduces the risk of HPV-6/11/16/18-related cervical intraepithelial neoplasia (CIN) 1-3 or adenocarcinoma in situ (AIS). Here, its impact on CIN1-3/AIS associated with nonvaccine oncogenic HPV types was evaluated. Methods. We enrolled 17,622 women aged 16-26 years. All underwent cervicovaginal sampling and Pap testing at regular intervals for up to 4 years. HPV genotying was performed for biopsy samples, and histological diagnoses were determined by a pathology panel. Analyses were conducted among subjects who were negative for 14 HPV types on day 1. Prespecified analyses included infection of >= 6 months' duration and CIN1-3/AIS due to the 2 and 5 most common HPV types in cervical cancer after HPV types 16 and 18, as well as all tested nonvaccine types. Results. Vaccination reduced the incidence of HPV-31/45 infection by 40.3% (95% confidence interval [CI], 13.9% to 59.0%) and of CIN1-3/AIS by 43.6% (95% CI, 12.9% to 64.1%), respectively. The reduction in HPV-31/33/45/52/58 infection and CIN1-3/AIS was 25.0% (95% CI, 5.0% to 40.9%) and 29.2% (95% CI, 8.3% to 45.5%), respectively. Efficacy for CIN2-3/AIS associated with the 10 nonvaccine HPV types was 32.5% (95% CI, 6.0% to 51.9%). Reductions were most notable for HPV-31. Conclusions. HPV-6/11/16/18 vaccine reduced the risk of CIN2-3/AIS associated with nonvaccine types responsible for similar to 20% of cervical cancers. The clinical benefit of cross-protection is not expected to be fully additive to the efficacy already observed against HPV-6/11/16/18-related disease, because women may have >1 CIN lesion, each associated with a different HPV type. (Less)

612 citations

Journal ArticleDOI
TL;DR: HP16, HPV18, HPV31, and HPV33 infection and especially HPV16 persistence were associated with high absolute risks for progression to high-grade cervical lesions and the results indicate the potential value of genotyping in cervical cancer screening.
Abstract: Background Infection with high-risk human papillomavirus (HPV) is the main cause of high-grade cervical intraepithelial neoplasia (CIN) and cancer. It has been suggested that information about high-risk HPV type–specific infection might make cervical cancer screening more effective. Persistent HPV infection could also be a useful screening marker. We estimated the long-term risk of high-grade CIN after one-time detection of high-risk HPV DNA and after persistent infection with individual high-risk HPV types.

481 citations