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Breast Cancer Incidence (breast + cancer_incidence)
Selected AbstractsBreast Cancer Incidence in a Cohort of Women with Benign Breast Disease from a Multiethnic, Primary Health Care PopulationTHE BREAST JOURNAL, Issue 2 2007Maria J. Worsham PhD Abstract:, Women with benign breast diseases (BBD), particularly those with lesions classified as proliferative, have previously been reported to be at increased risk for subsequent development of breast cancer (BC). A cohort of 4970 women with biopsy-proven BBD, identified after histopathology review of BBD biopsies, was studied for determination of subsequent development of BC. We report on 4537 eligible women, 28% of whom are African-American, whose BBD mass was evaluable for pathologic assessment of breast tissue. Ascertainment of subsequent progression to BC from BBD was accomplished through examination of the tumor registries of the Henry Ford Health system, the Detroit SEER registry, and the State of Michigan cancer registry. Incidence rates (IR) are reported per 100,000 person years at risk (100 k pyr). Poisson regression models were used to evaluate the association of demographic and lesion characteristics with BC incidence, using person years at the time of BBD diagnosis as the offset variable. The estimated overall BC IR for this cohort is 452 (95% confidence interval [CI] = 394,519) per 100 k pyr. Incidence for women age 50 and older is 80% greater than for younger women (p = 0.007, IRR = 1.8, 95% CI = 1.36,2.36). Neither marital status (p = 0.91, IRR = 0.97, 95% CI = 0.73,1.29) nor race (p = 0.67, IRR = 0.9, 95% CI = 0.54,1.48) is associated with differences in BC IR. Compared with women having nonproliferative lesions, the risk for BC is greater for women with atypical ductal hyperplasia of (IRR = 5.0; 95%CI = 2.26,11.0; p < 0.001) and other proliferative lesions (IR = 1.7, 95% CI = 1.02,2.95; p = 0.04). BC risk for woman with atypical lesions is significantly higher than for women with proliferative lesions without atypia (IRR = 2.58, 95% CI = 1.35,4.90; p = 0.0039). Neither race nor marital status was a factor for BC incidence from BBD in this cohort. Age retained its importance as a predictor of risk. BBD lesion histopathology in the outcome categories of either proliferative without atypia or proliferative with atypia are significant risk factors for BC, even when adjusted for the influence of demographic characteristics. The risks associated with BBD histological classifications were not different across races. [source] Differences in breast cancer incidence in Australia and England by age, extent of disease and deprivation status: women diagnosed 1980,2002AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 2 2010Laura M. Woods Abstract Objective: To compare breast cancer incidence in England and Australia by age, extent of disease and deprivation. Methods: We analysed data for women aged 15,99 years diagnosed with breast cancer in England or Australia during the period 1990 to 1994, and in West Midlands or New South Wales during the period 1980 to 2002. We calculated three-year rolling average incidence rates and incidence rate ratios (IRR) between West Midlands and New South Wales by age, extent of disease and category of deprivation. Results: Breast cancer incidence was higher in England than in Australia, and in West Midlands than in New South Wales but became more similar over time. Socio-economic differences in incidence were greater in New South Wales than in West Midlands. The most deprived women in West Midlands were diagnosed at a later stage of disease than the most deprived women in New South Wales. Incidence among elderly women was higher in West Midlands than in New South Wales. There were also high proportions of tumours with unknown stage among elderly women in West Midlands. Conclusions: Although the overall incidence of breast cancer is similar, differences by age, extent of disease and deprivation exist. Implications: The underlying reasons for these patterns require further examination. [source] Breast cancer incidence among American Indian and Alaska Native women: US, 1999,2004,,§CANCER, Issue S5 2008Phyllis A. Wingo PhD Abstract BACKGROUND. Breast cancer is a leading cause of cancer morbidity and mortality among American Indian and Alaska Native (AI/AN) women. Although published studies have suggested that breast cancer rates among AI/AN women are lower than those among other racial and ethnic populations, accurate determinations of the breast cancer burden have been hampered by misclassification of AI/AN race. METHODS. Cancer incidence data from the National Program of Cancer Registries and the Surveillance, Epidemiology, and End Results Program were combined to estimate age-adjusted rates for the diagnosis years 1999 through 2004. Several steps were taken to reduce the misclassification of AI/AN race: linking cases to Indian Health Service (IHS) patient services database, restricting analyses to Contract Health Service Delivery Area counties, and stratifying results by IHS region. RESULTS. Breast cancer incidence rates among AI/AN women varied nearly 3-fold across IHS regions. The highest rates were in Alaska (134.8) and the Plains (Northern, 115.9; Southern, 115.7), and the lowest rates were in the Southwest (50.8). The rate in Alaska was similar to the rate among non-Hispanic white (NHW) women in Alaska. Overall, AI/AN women had lower rates of breast cancer than NHW women, but AI/AN women were more likely to be diagnosed with late-stage disease. CONCLUSIONS. To the authors' knowledge, this report provides the most comprehensive breast cancer incidence data for AI/AN women to date. The wide regional variation indicates an important need for etiologic and health services research, and the large percentage of AI/AN women with late-stage disease demands innovative approaches for increasing access to screening. Cancer 2008;113(5 suppl):1191,202. Published 2008 by the American Cancer Society. [source] Increased death risk and altered cancer incidence pattern in patients with isolated or combined autoimmune primary adrenocortical insufficiencyCLINICAL ENDOCRINOLOGY, Issue 5 2008Sophie Bensing Summary Objectives, Primary adrenocortical insufficiency is mostly caused by an autoimmune destruction of the adrenal cortex. The disease may appear isolated or as a part of an autoimmune polyendocrine syndrome (APS). APS1 is a rare hereditary disorder with a broad spectrum of clinical manifestations. In APS2, primary adrenocortical insufficiency is often combined with autoimmune thyroid disease and/or type 1 diabetes. We analysed mortality and cancer incidence in primary adrenocortical insufficiency patients during 40 years. Data were compared with the general Swedish population. Design and patients, A population based cohort study including all patients with autoimmune primary adrenocortical insufficiency (3299) admitted to Swedish hospitals 1964,2004. Measurements, Mortality risk was calculated as the standardized mortality ratio (SMR) and cancer incidence as the standardized incidence ratio (SIR). Results, A more than 2-fold increased mortality risk was observed in both women (SMR 2·9, 95% CI 2·7,3·0) and men (SMR 2·5, 95% CI 2·3,2·7). Highest risks were observed in patients diagnosed in childhood. SMR was higher in APS1 patients (SMR 4·6, 95% CI 3·5,6·0) compared with patients with APS2 (SMR 2·1, 95% CI 1·9,2·4). Cancer incidence was increased (SIR 1·3, 95% CI 1·2,1·5). When tumours observed during the first year of follow-up were excluded, only the cancer risk among APS1 patients remained increased. Cause-specific cancer incidence analysis revealed significantly higher incidences of oral cancer, nonmelanoma skin cancer, and male genital system cancer among patients. Breast cancer incidence was lower than in the general population. Conclusions, Our study shows a reduced life expectancy and altered cancer incidence pattern in patients with autoimmune primary adrenocortical insufficiency. [source] Recent trends in breast cancer incidence among 6 Asian groups in the Greater Bay Area of Northern California,INTERNATIONAL JOURNAL OF CANCER, Issue 6 2007Theresa H.M. Keegan Abstract Asians and Pacific Islanders are typically aggregated in United States (US) cancer statistics even though the few studies that have considered subgroups separately have found marked differences in cancer incidence. The objective of this study was to evaluate trends in breast cancer incidence rates separately for US Chinese, Japanese, Filipino, Korean, South Asian and Vietnamese women overall and by age at diagnosis, histologic subtype and stage at diagnosis. Age-adjusted incidence rates and annual percent changes (APC) of new, primary breast cancer diagnosed in the Greater Bay Area Cancer Registry of Northern California (1990,2002) were calculated using SEER*Stat. In women under 50 years of age, annual incidence rates decreased for Japanese (APC = ,4.1, p = 0.02) and Filipinas (APC = ,1.9, p = 0.11), and increased or fluctuated in other subgroups over the study period. In women 50 years or older, rates of invasive breast cancer increased for most subgroups, except Filipinas (APC = ,1.3, p = 0.32), and in Japanese until 1998,2000. Rates of breast cancer in situ increased in most subgroups from 1990 to 2002, as did rates of lobular breast cancer for Chinese (APC = +7.46, p < 0.01) women. In Japanese women, rates of lobular breast cancer were highest in 1995,1997 and decreased thereafter. Our data support the notion that the prevalence of established risk factors influence breast cancer incidence, as breast cancer rates increased for more recently immigrated groups and decreased among more established groups, and may suggest leads into other avenues of research, such as genetic differences, that may explain differences in incidence rates among Asian subgroups. © 2006 Wiley-Liss, Inc. [source] The contribution of hepatic steroid metabolism to serum estradiol and estriol concentrations in nonylphenol treated MMTVneu mice and its potential effects on breast cancer incidence and latencyJOURNAL OF APPLIED TOXICOLOGY, Issue 5 2005Ricardo Acevedo Abstract The two major pathways for the metabolism of estradiol-17, (E2) are the 2- and 16-hydroxylase pathways. Research has suggested that the increased production of the estrogenically active 16-hydroxy products such as estriol (E3) may be involved in increased susceptibility to breast cancer. 4-Nonylphenol (4-NP) is an environmental estrogen that also can activate the pregnane-X receptor (PXR) and induce P-450 enzymes responsible for the production of E3. It is hypothesized that 4-NP may act in part as an environmental estrogen by increasing E3 production. Based on its affinity for the estrogen receptor (ER) alone, 4-NP may be more potent than predicted at increasing mammary cancer incidence in the MMTVneu mouse. Female mice were treated per os for 7 days at 0, 25, 50 or 75 mg kg,1 day,1 4-NP to investigate the effects of 4-NP on hepatic estrogen metabolism after an acute treatment. 4-Nonylphenol increased the hepatic formation of E3 in a dose-dependent manner. However, serum E3 concentrations were only increased at 25 mg kg,1 day,1 presumably due to direct inhibition of E3 formation by 4-NP. MMTVneu mice were then treated for 32 weeks at 0, 30 or 45 mg kg,1 day,1 4-NP to determine its effects on mammary cancer formation and estrogen metabolism. 4-Nonylphenol increased mammary cancer formation in the MMTVneu mice at 45 mg kg,1 day,1 but not at 30 mg kg,1 day,1. Mice treated with an equipotent dose of E2, 10 µg kg,1 day,1, based on the relative binding affinities of nonylphenol and estradiol for ER,, did not develop mammary cancer. This suggests that nonylphenol is more potent than predicted based on its affinity for the estrogen receptor. However, no changes in serum E3 concentrations or hepatic E3 production were measured after the chronic treatment. Changes in E3 formation were correlated with increased CYP2B levels after the 7 day 4-NP treatment, and repression of CYP2B and CYP3A after 32 weeks of 4-NP treatment. Microarray analysis and Q-PCR of liver mRNA from the mice treated for 32 weeks demonstrated a decrease in RXR,, the heterodimeric partner of the PXR, which may in part explain the repressed transcription of the P450s measured. In conclusion, 4-NP treatment for 32 weeks increased mammary cancer formation at a dose of 45 mg kg,1 day,1. However, chronic treatment with 4-NP did not increase hepatic E3 formation or serum E3 concentrations. The transient induction by 4-NP of hepatic E3 formation and serum concentrations is most likely not involved in the increased incidence of mammary cancer in MMTVneu mice since E3 serum concentrations were only increased at 25 mg kg,1 day,1, a dose that was not sufficient to induce mammary tumor formation. Nevertheless, the induced hepatic E3 production in the acute exposures to 4-NP was indicative of an increase in mammary cancer incidence after the chronic exposure. Copyright © 2005 John Wiley & Sons, Ltd. [source] 4-Hydroxytamoxifen sulfation metabolismJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 6 2002Guangping Chen Abstract Tamoxifen (TAM) is an important chemotherapeutic agent for the treatment of breast cancer. It has also been shown to decrease breast cancer incidence in healthy women at high risk for the disease. The increased risk of endometrial cancer in women has raised concerns in the use of the drug. Tamoxifen has also been shown to be a potent hepatocarcinogen in rats. The oxidative metabolites of TAM include ,-hydroxytamoxifen (,-OH-TAM) and 4-hydroxytamoxifen (4-OH-TAM). The studies on the sulfation of these metabolites are very limited. It has been reported that ,-OH-TAM is a substrate for rat hydroxysteroid sulfotransferase a (STa). Our studies on the sulfation of 4-OH-TAM demonstrated that 4-hydroxytamoxifen can be sulfated by human liver and human intestinal cytosols. Human phenol-sulfating sulfotransferase and human estrogen sulfotransferase are the major enzymes for the sulfation of 4-OH-TAM. Human dopamine-sulfating sulfotransferase also has sulfation activity for 4-OH-TAM. In contrast, rat liver and intestine cytosols have no detectable sulfation activity for 4-OH-TAM. The results suggest that the ,-OH-TAM sulfation pathway leads to bioactivation of TAM, and the 4-OH-TAM sulfation pathway leads to detoxification of TAM. This agrees with the fact that TAM is more toxic for rats than for human beings. © 2002 Wiley Periodicals, Inc. J Biochem Mol Toxicol 16:279,285, 2002; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10048 [source] A possible link between prenatal exposure to famine and breast cancer: A preliminary study,AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 6 2006R.C. Painter In a study of 475 women born around the 1944,1945 Dutch famine, women exposed to prenatal famine more often reported a history of breast cancer than nonexposed women (hazard ratio, 2.6; 95% confidence interval, 0.9,7.7). They also had alterations in reproductive risk factors. Prenatal famine may increase breast cancer incidence. Am. J. Hum. Biol. 18:853,856, 2006. © 2006 Wiley-Liss, Inc. [source] Risk factors for breast cancer in East Asian women relative to women in the WestASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY, Issue 4 2009Christine S PERRY Abstract The incidence of breast cancer in women of East Asian ancestry (Chinese, Japanese and Korean) is lower than in women of European ancestry but is currently rising. This review explores potential reasons for this inter-ethnic difference in incidence by profiling breast cancer risk factors reported for East Asian and Western women. Factors such as endogenous hormone exposure, lifestyle choices, diet and genetic predisposition are associated with breast cancer risk in both East Asian and Western women. However, the relative exposure to these risk factors may vary according to a woman's geographical ancestry and culture. For example, age at menarche and menopause, parity, breast-feeding history, low fat and high soy consumption as well as the prevalence of high risk genetic alleles may vary with a woman's geographical ancestry and/or culture. Differences in exposure to these risk factors in East Asian and Western women are consistent with the inter-ethnic differences in breast cancer incidence observed. Understanding the underlying factors contributing to differences in the profile of breast cancer across populations is important when considering screening and prevention programs for East Asian women resident in the East or the West. [source] Differences in breast cancer incidence in Australia and England by age, extent of disease and deprivation status: women diagnosed 1980,2002AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 2 2010Laura M. Woods Abstract Objective: To compare breast cancer incidence in England and Australia by age, extent of disease and deprivation. Methods: We analysed data for women aged 15,99 years diagnosed with breast cancer in England or Australia during the period 1990 to 1994, and in West Midlands or New South Wales during the period 1980 to 2002. We calculated three-year rolling average incidence rates and incidence rate ratios (IRR) between West Midlands and New South Wales by age, extent of disease and category of deprivation. Results: Breast cancer incidence was higher in England than in Australia, and in West Midlands than in New South Wales but became more similar over time. Socio-economic differences in incidence were greater in New South Wales than in West Midlands. The most deprived women in West Midlands were diagnosed at a later stage of disease than the most deprived women in New South Wales. Incidence among elderly women was higher in West Midlands than in New South Wales. There were also high proportions of tumours with unknown stage among elderly women in West Midlands. Conclusions: Although the overall incidence of breast cancer is similar, differences by age, extent of disease and deprivation exist. Implications: The underlying reasons for these patterns require further examination. [source] Breast cancer survivors in the United StatesCANCER, Issue 9 20092005-201, Geographic Variability, Time Trends Abstract BACKGROUND: Breast cancer continues to place a significant burden on the healthcare system. Regional prevalence measures are instrumental in the development of cancer control policies. Very few population-based cancer registries are able to provided local, long-term incidence and follow-up information that permits the direct calculation of prevalence. Model-based prevalence estimates are an alternative when this information is lacking or incomplete. The current work represents a comprehensive collection of female breast cancer prevalence from 2005 to 2015 in the United States and the District of Columbia (DC). METHODS: Breast cancer prevalence estimates were derived from state-specific cancer mortality and survival data using a statistical package called the Mortality-Incidence Analysis Model or MIAMOD. Cancer survival models were derived from the Surveillance, Epidemiology, and End Results Program data and were adjusted to represent state-specific survival. Comparisons with reported incidence for 39 states and DC had validated estimates. RESULTS: By the year 2010, 2.9 million breast cancer survivors are predicted in the US, equaling 1.85% of the female population. Large variability in prevalent percentages was reported between states, ranging from 1.4% to 2.4% in 2010. Geographic variability was reduced when calculating age-standardized prevalence proportions or cancer survivors by disease duration, including 0 to 2 years and 2 to 5 years. The residual variability in age-adjusted prevalence was explained primarily by the state-specific, age-adjusted breast cancer incidence rates. State-specific breast cancer survivors are expected to increase from 16% to 51% in the decennium from 2005 to 2015 and by 31% at the national level. CONCLUSIONS: To the authors' knowledge, the current study is the first to provide systematic estimations of breast cancer prevalence in all US states through 2015. The estimated levels and time trends were consistent with the available population-based data on breast cancer incidence, prevalence, and population aging. Cancer 2009. © 2009 American Cancer Society. [source] | |||||||||||||