Showing papers by "Dennis Deapen published in 2010"
TL;DR: Among women at age 35 to 64 years, BMI at age 18 years is inversely associated with risk of breast cancer, but association with recent BMI varies by menopause status, race, and hormone receptor status.
Abstract: Objective: Large body size has been associated with decreased risk of breast cancer in premenopausal women but with increased risk in postmenopausal women. Limited information is available about African-American women and differences by estrogen and progesterone receptor status.
Methods: We analyzed data from the Women's Contraceptive and Reproductive Experiences Study among 3,997 white and African-American breast cancer case patients diagnosed in 1994 to 1998 and 4,041 control participants ages 35 to 64 years. We calculated multivariate odds ratios (OR) as measures of relative risk of breast cancer associated with self-reported body mass index (BMI) at age 18 and 5 years before diagnosis (recent BMI).
Results: Risk tended to decrease with increasing BMI at age 18 years in all women [ORBMI ≥ 25 kg/m2 versus < 20 kg/m2 = 0.76; 95% confidence interval (CI), 0.63-0.90; P trend = 0.005] and with recent BMI in premenopausal women (ORBMI ≥ 35 kg/m2 versus < 25 kg/m2 = 0.81; 95% CI, 0.61-1.06; P trend = 0.05), unmodified by race. Among postmenopausal white but not African-American women, there was an inverse relation between recent BMI and risk. High recent BMI was associated with increased risk of estrogen receptor– and progesterone receptor–positive tumors among postmenopausal African-American women (ORBMI ≥ 35 kg/m2 versus < 25 kg/m2 = 1.83; 95% CI, 1.08-3.09; P trend = 0.03).
Conclusion: Among women at age 35 to 64 years, BMI at age 18 years is inversely associated with risk of breast cancer, but association with recent BMI varies by menopause status, race, and hormone receptor status.
Impact: Our findings indicate that studies of BMI and breast cancer should consider breast cancer subtypes. Cancer Epidemiol Biomarkers Prev; 19(6); 1532–44. ©2010 AACR.
108 citations
TL;DR: Some epidemiologic evidence is provided that parity and age at first full-term pregnancy are involved in the development of breast cancer among postmenopausal women.
Abstract: Introduction
Although pregnancy-related factors such as nulliparity and late age at first full-term pregnancy are well-established risk factors for invasive breast cancer, the roles of these factors in the natural history of breast cancer development remain unclear.
83 citations
TL;DR: The feasibility of collecting HER2 data and its completeness in three registries in the Surveillance Epidemiology and End Results (SEER) Program was assessed and it was found that HER2 will likely be a required data element for these patients in 2010.
Abstract: The clinical importance of human epidermal growth factor receptor-2 (HER2) in breast cancer is now clearly established, given that expression of this tumor marker is used to guide therapy and as a prognostic indicator. Despite its now routine evaluation in breast cancer patients, population-based data are lacking because information on HER2 status is not routinely collected in the majority of population-based cancer registries. We assessed the feasibility of collecting HER2 data and its completeness in three registries in the Surveillance Epidemiology and End Results (SEER) Program. Among a sample of invasive first primary breast cancer patients diagnosed between June and December 2007, HER2 tests had been done on 96.5% (n = 522), and test results were available for 95.2% (n = 515) of patients. The majority of HER2 tests were performed by immunohistochemistry alone (50.9%), 35.3% by both immunohistochemistry and fluorescence in situ hybridization (FISH), and 11.8% of tests by FISH alone. As a result of these findings, SEER registries will collect HER2 data on all invasive breast cancer patients as an optional data element for those diagnosed in 2009 and HER2 will likely be a required data element for these patients in 2010.
60 citations
TL;DR: Breast cancer risks increased with longer duration of ET and EPT use, and risks were highest for continuous-combined E PT use, which underscores the need for personalized risk-benefit discussions with women contemplating HT use.
Abstract: Background: Although it is well established that combined estrogen-progestin therapy (EPT) increases breast cancer risk, questions remain regarding the effect of different formulations of hormones, whether certain women are at particularly high risk, and whether risk varies by tumor subtype.
Methods: We investigated hormone therapy (HT) use in relation to breast cancer risk in the California Teachers Study cohort; after a mean follow-up of 9.8 years, 2,857 invasive breast cancers were diagnosed.
Results: Compared with women who had never used HT, women who reported 15 or more years of estrogen therapy (ET) use had a 19% greater risk of breast cancer (95% confidence interval, 1.03-1.37), whereas women using EPT for 15 or more years had an 83% greater risk (95% confidence interval, 1.48-2.26). Breast cancer risk was highest among women using continuous combined EPT regimens. Risks associated with EPT and ET use were increased with duration of HT use for women with a body mass index (BMI) of <29.9 kg/m2 but not for women with BMI of ≥30 kg/m2. Elevated risks associated with EPT and ET use were confined to tumors that were positive for both estrogen and progesterone receptors and those that were HER2+ but were slightly diminished for HER2− tumors.
Conclusions: Breast cancer risks increased with longer duration of ET and EPT use, and risks were highest for continuous-combined EPT use. Furthermore, risks varied by BMI and tumor subtype.
Impact: These findings underscore the need for personalized risk-benefit discussions with women contemplating HT use. Cancer Epidemiol Biomarkers Prev; 19(9); OF1–13. ©2010 AACR.
50 citations
TL;DR: Stable in situ breast cancer rates imply consistent levels of screening and suggest recent declines in invasive breast cancer to be explained predominantly by changes in HT use.
Abstract: Recent, international declines in breast cancer incidence are unprecedented, and the causes remain controversial Few data sources can address breast cancer incidence trends according to pertinent characteristics like hormone therapy use history We used the prospective California Teachers Study to evaluate changes in self-reported use of menopausal hormone therapy (HT) between 1995 to 1996 and 2005 to 2006 and age-adjusted breast cancer incidence among 74,647 participants aged 50 years or older Breast cancer occurrence was determined by linkage with the California Cancer Registry During 517,286 woman years of follow up, 565 in situ and 2,668 invasive breast cancers were diagnosed In situ breast cancer incidence rates in this population did not change significantly from 2000 to 2002 to 2003 to 2005, whereas rates of invasive breast cancer declined significantly by 260% from 5280 (95% confidence intervals (CI) = 4911, 5649) per 100,000 women in 2000 to 2002 to 3906 (95% CI = 3556, 4257) in 2003 to 2005 The decline in invasive breast cancer incidence rates was restricted to estrogen receptor-positive tumors In 1996 to 1999 and 2000 to 2002 invasive breast cancer incidence was higher for women who reported current HT use especially estrogen-progestin (EP) use at baseline than for never or past users; but by 2003 to 2005 rates were comparable between these groups For women who were taking EP in 2001 to 2002,75% of whom had stopped use by 2005 to 2006, incidence had declined 306% by 2003 to 2005 (P = 0001); whereas incidence did not change significantly for those who never took HT (P = 033) Few data resources can examine prospectively individual HT use and breast cancer diagnosis Stable in situ breast cancer rates imply consistent levels of screening and suggest recent declines in invasive breast cancer to be explained predominantly by changes in HT use
45 citations
TL;DR: Among women who never used HT, risk was strongly positively related to obesity and may have been influenced more by abdominal than by overall adiposity; however, due to small numbers, this latter finding requires replication.
Abstract: To investigate whether hormone therapy (HT) and obesity are associated with endometrial cancer risk among postmenopausal women in the California Teachers Study cohort. Of 28,418 postmenopausal women, 395 developed type 1 endometrial cancer between 1995 and 2006. Multivariate Cox regression was performed to estimate relative risks (RR), stratified by HT use (never used, ever estrogen alone (ET) or exclusively estrogen-plus-progestin (EPT)). Among women who never used HT, overall and abdominal adiposity were associated with increased risk; when evaluated simultaneously, abdominal adiposity was more strongly associated (RR 2.2, 95% confidence interval (CI): 1.1–4.5 for waist ≥35 vs. <35 inches). Among women who ever used ET, risk was increased in women with BMI ≥ 25 kg/m2 (RR 1.6, 95% CI: 1.1–2.3 vs. <25 kg/m2). Neither overall nor abdominal obesity was associated with risk in women who exclusively used EPT (p-interaction <0.001 for BMI by HT use). Among women who never used HT, risk was strongly positively related to obesity and may have been influenced more by abdominal than by overall adiposity; however, due to small numbers, this latter finding requires replication. Among women who ever used ET, being overweight at baseline predicted higher risk, whereas use of EPT mitigated any effects of obesity.
36 citations
TL;DR: It is suggested that abdominal adiposity and weight gain, but not overall obesity, increase ovarian cancer risk and that there may be a threshold level beyond which additional hormones, whether exogenous or endogenous, do not result in additional elevation in risk.
Abstract: Objective
To investigate whether obesity and hormone therapy (HT) are associated with ovarian cancer risk among women in the California Teachers Study cohort.
28 citations
TL;DR: Prediagnosis meat consumption was not associated with CRC-specific mortality among 704 CRC patients (and 201 CRC- specific deaths), and regular NSAID use versus none was associated with decreased CRC- Specific mortality among patients in the lowest meat consumption tertile, but not among Patients in the higher meat intake tertiles.
Abstract: A low-meat diet and regular use of nonsteroidal anti-inflammatory drugs (NSAID) have been associated with decreased mortality among colorectal cancer (CRC) patients. Here, we investigated the association between prediagnosis usual meat consumption and CRC-specific mortality, and whether meat consumption modifies the previously noted association between NSAID use and CRC-specific mortality among women in the California Teachers Study cohort. Women joining the California Teachers Study in 1995-1996 without prior CRC diagnosis, diagnosed with incident CRC during follow-up through December 2007, were eligible for inclusion. Meat intake (frequency and serving size) and NSAID use (aspirin or ibuprofen use) were ascertained via self-administered questionnaires before diagnosis. Vital status and cause of death were determined by linkage with mortality files. Multivariable Cox proportional hazards regression models were used to estimate hazard ratios for death and 95% confidence intervals. Prediagnosis meat consumption was not associated with CRC-specific mortality among 704 CRC patients (and 201 CRC-specific deaths), comparing patients in the lowest consumption tertile (0-5.4 medium-sized servings/wk) to those in the higher consumption tertiles. Regular NSAID use (1-3 times/wk, 4-6 times/wk, daily) versus none was associated with decreased CRC-specific mortality among patients in the lowest meat consumption tertile (hazard ratio, 0.22; 95% CI, 0.06-0.82), but not among patients in the higher meat intake tertiles. The previously observed mortality risk reduction among female CRC patients associated with regular NSAID use was restricted to patients who reported low meat intake before diagnosis. These findings have implications for CRC survivorship and tertiary CRC prevention.
22 citations
TL;DR: Using a population‐based case‐control design, incidence rate ratios of fatal breast cancer in postmenopausal hormone therapy (HT) users compared to non‐users are estimated by type, duration, and recency of HT use.
Abstract: Purpose
Among unanswered questions is whether menopausal use of estrogen therapy (ET) or estrogen-plus-progestin therapy (CHT) increases risk of developing fatal breast cancer i.e., developing and dying of breast cancer. Using a population-based case-control design, we estimated incidence rate ratios of fatal breast cancer in postmenopausal hormone therapy (HT) users compared to non-users by type, duration, and recency of HT use.
Methods
HT use prior to breast cancer diagnosis in 278 women who died of breast cancer within 6 years of diagnosis (cases) was compared with use in 2224 controls never diagnosed with breast cancer using conditional logistic regression. Measures taken to address potential bias and confounding inherent in case-control studies included collecting and adjusting for detailed data on demographic and other factors potentially associated both with HT use and breast cancer.
Results
Fifty-six per cent of cases and 68% of controls reported HT use. Among current 3+ year HT users, odds ratios and 95% confidence intervals for death were 0.83 (0.50, 1.38) and 0.69 (0.44, 1.09), respectively, for exclusive use of CHT or of ET, and were 0.94 (0.59, 1.48) and 0.70 (0.45, 1.07) for any use of CHT or of ET regardless of other hormone use.
Conclusion
Point estimates suggest no increased risk of fatal breast cancer with HT use, although 50% increases in risk in longer-term current CHT users cannot be ruled out. Copyright © 2010 John Wiley & Sons, Ltd.
15 citations
TL;DR: Evaluated data suggest that ET use decreases the risk of B-cell NHL among women with both ovaries removed, but not among women retaining at least part of an ovary remaining.
Abstract: Objective: To evaluate whether use of oral contraceptives (OCs) or menopausal hormonal therapy (MHT) is associated with B-cell non-Hodgkin lymphoma (NHL).
Methods: Within the prospective California Teachers Study cohort, women under age 85 with no history of hematopoietic cancer were followed from 1995 through 2007 for diagnosis of B-cell NHL. Overall, 547 women of 116,779 women eligible for analysis of OC use and 402 of 54,758 postmenopausal women eligible for analysis of MHT use developed B-cell NHL. Relative risks (RR) and 95% confidence intervals (CI) were estimated by fitting multivariable Cox proportional hazards models.
Results: Women who used OCs had marginally lower risk of B-cell NHL than women who had never used OCs (RR = 0.86, 95% CI = 0.69-1.06). The reduced risk was most pronounced among women who started OCs before age 25, but did not decrease with increasing duration. No association with MHT was observed when MHT ever users were compared to the never users (RR = 1.05, 95% CI = 0.83-1.33); this result was consistent across formulations of MHT [unopposed estrogen therapy (ET), combined estrogen and progestin therapy (EPT)]. Among women who had never used MHT, women with a bilateral oophorectomy had three times greater risk than those with natural menopause (RR = 3.15, 95% CI = 1.62-6.13), whereas there was no association with bilateral oophorectomy among women who had used MHT. In stratified analyses according to hysterectomy and oophrectomy status, ET and EPT did not affect risk for women with natural menopause or those with hysterectomy who had at least part of an ovary remaining. Among women who had a bilateral oophorectomy, ET reduced risk of NHL (RR = 0.41, 95% CI = 0.21-0.82).
Conclusion: These data suggest that ET use decreases the risk of B-cell NHL among women with both ovaries removed, but not among women retaining at least part of an ovary. In other subgroups MHT does not influence risk. Additional study of associations of MHT and OCs with B-cell NHL are warranted.
This abstract is one of the 17 highest scoring abstracts of those submitted for presentation at the 34th Annual Meeting of the American Society of Preventive Oncology, to be held March 20-23, 2010 in Bethesda, MD.
2 citations
TL;DR: Evaluated data suggest that ET use decreases the risk of B-cell NHL among women with both ovaries removed, but not among women retaining at least part of an ovary remaining.
Abstract: Objective: To evaluate whether use of oral contraceptives (OC) or menopausal hormonal therapy (MHT) is associated with B-cell non-Hodgkin lymphoma (NHL). Methods: Within the prospective California Teachers Study cohort, women under age 85 with no history of hematopoietic cancer were followed from 1995 through 2007 for diagnosis of B-cell NHL. Overall, 547 women of 116,779 women eligible for analysis of OC use and 402 of 54,758 postmenopausal women eligible for analysis of MHT use developed B-cell NHL. Relative risks (RR) and 95% confidence intervals (CI) were estimated by fitting multivariable Cox proportional hazards models. Results: Women who used OCs had marginally lower risk of B-cell NHL than women who had never used OCs (RR=0.86, 95% CI=0.69-1.06). The reduced risk was most pronounced among women who started OCs before age 25, but did not decrease with increasing duration. No association with MHT was observed when MHT ever users were compared to the never users (RR=1.05, 95% CI=0.83-1.33); this result was consistent across formulations of MHT [unopposed estrogen therapy (ET), combined estrogen and progestin therapy (EPT)]. Among women who had never used MHT, women with a bilateral oophorectomy had three times greater risk than those with natural menopause (RR=3.15, 95% CI=1.62-6.13), whereas there was no association with bilateral oophorectomy among women who had used MHT. In stratified analyses according to hysterectomy and oophrectomy status, ET and EPT did not affect risk for women with natural menopause or those with hysterectomy who had at least part of an ovary remaining. Among women who had a bilateral oophorectomy, ET reduced risk of NHL (RR=0.41, 95% CI=0.21-0.82). Conclusion: These data suggest that ET use decreases the risk of B-cell NHL among women with both ovaries removed, but not among women retaining at least part of an ovary. In other subgroups MHT does not influence risk. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 867.