Rowan T Chlebowski

Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, United States

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Publications (379)3611.31 Total impact

  • Rowan T Chlebowski
    The Lancet Oncology 06/2015; DOI:10.1016/S1470-2045(15)00052-2 · 24.73 Impact Factor
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    ABSTRACT: Importance The use of menopausal hormone therapy (HT) continues in clinical practice, but reports are conflicting concerning the longer-term breast cancer effects of relatively short-term use.Objective To report the longer-term influence of menopausal HT on breast cancer incidence in the 2 Women’s Health Initiative (WHI) randomized clinical trials.Design, Setting, and Participants A total of 27 347 postmenopausal women aged 50 to 79 years were enrolled at 40 US centers from 1993 to 1998 and followed up for a median of 13 years through September 2010.Interventions A total of 16 608 women with a uterus were randomized to conjugated equine estrogens (0.625 mg/d [estrogen]) plus medroxyprogesterone acetate (2.5 mg/d [progestin]) (E + P) or placebo with a median intervention duration of 5.6 years, and 10 739 women with prior hysterectomy were randomized to conjugated equine estrogens alone (0.625 mg/d) or placebo with a median intervention duration of 7.2 years.Main Outcomes and Measures Time-specific invasive breast cancer incidence rates and exploratory analyses of breast cancer characteristics by intervention and postintervention phases in the 2 HT trials.Results In the E + P trial, hazard ratios (HRs) for the influence of combined HT on breast cancer were lower than 1 for 2 years (HR, 0.71; 95% CI, 0.47-1.08) and steadily increased throughout intervention, becoming significantly increased for the entire intervention phase (HR, 1.24; 95% CI, 1.01-1.53). In the early postintervention phase (within 2.75 years from intervention), there was a sharp decrease in breast cancer incidence in the combined HT group, though the HR remained higher than 1 (HR, 1.23; 95% CI, 0.90-1.70). During the late postintervention phase (requiring patient re-consent), the HR for breast cancer risk remained higher than 1 through 5.5 years (median) of additional follow-up (HR, 1.37; 95% CI, 1.06-1.77). In the estrogen alone trial, the HR for invasive breast cancer risk was lower than 1 throughout the intervention phase (HR, 0.79; 95% CI, 0.61-1.02) and remained lower than 1 in the early postintervention phase (HR, 0.55; 95% CI, 0.34-0.89), but risk reduction was not observed during the late postintervention follow-up (HR, 1.17; 95% CI, 0.73-1.87). Characteristics of breast cancers diagnosed during early and late postintervention phases differed in both trials.Conclusions and Relevance In the E + P trial, the higher breast cancer risk seen during intervention was followed by a substantial drop in risk in the early postintervention phase, but a higher breast cancer risk remained during the late postintervention follow-up. In the estrogen alone trial, the lower breast cancer risk seen during intervention was sustained in the early postintervention phase but was not evident during the late postintervention follow-up.
    06/2015; 1(3). DOI:10.1001/jamaoncol.2015.0494
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    ABSTRACT: In an invited editorial, Dr Shapiro proposes that vaginal bleeding leading to unblinding and subsequent detection bias explains the breast cancer increase seen with estrogen plus progestin in the Women's Health Initiative (WHI) clinical trial (1) . In the context of a uniform detection program of protocol-mandated annual mammography and breast examinations, such a proposal is medically implausible. Dr Shapiro suggests detection bias would identify a larger number of 'slowly growing tumors that would otherwise remain clinically silent'. The findings of more advanced cancers with increased deaths from breast cancer in the estrogen plus progestin group refute this conjecture. During early post-intervention phases of both WHI hormone therapy trials, when breast cancer detection bias is asserted by Dr Shapiro because participants had been informed of randomization assignment, breast cancer incidence rates were lower (rather than higher) than during intervention. Thus, Dr Shapiro's claims are directly refuted by findings from the WHI randomized clinical trials. Health-care providers should be aware that randomized clinical trial evidence supports estrogen plus progestin increasing breast cancer incidence and deaths from breast cancer. In contrast, among women with prior hysterectomy, randomized clinical trial evidence supports estrogen alone reducing breast cancer incidence and deaths from breast cancer.
    Climacteric 06/2015; 18(3):336-8. DOI:10.3109/13697137.2015.1038770 · 2.24 Impact Factor
  • Cancer Research 05/2015; 75(9 Supplement):P6-10-04-P6-10-04. DOI:10.1158/1538-7445.SABCS14-P6-10-04 · 9.28 Impact Factor
  • Cancer Research 05/2015; 75(9 Supplement):PD4-2-PD4-2. DOI:10.1158/1538-7445.SABCS14-PD4-2 · 9.28 Impact Factor
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    ABSTRACT: BACKGROUND The preponderance of observational studies describe an association between the use of estrogen alone and a lower incidence of colorectal cancer. In contrast, no difference in the incidence of colorectal cancer was seen in the Women's Health Initiative (WHI) randomized, placebo-controlled trial with estrogen alone after a mean intervention of 7.1 years and cumulative follow-up of 13.2 years. This study extends these findings by providing detailed analyses of the effects of estrogen alone on the histology, grade, and stage of colorectal cancer, relevant subgroups, and deaths from and after colorectal cancer.METHODS The WHI study was a randomized, double-blind, placebo-controlled trial involving 10,739 postmenopausal women with prior hysterectomy. Participants were assigned to conjugated equine estrogen at 0.625 mg/d (n = 5279) or a matching placebo (n = 5409). Rates of colorectal cancer diagnoses and deaths from and after colorectal cancer were assessed throughout the study.RESULTSColorectal cancer rates in the estrogen-alone and placebo groups were comparable: 0.14% and 0.12% per year, respectively (hazard ratio [HR], 1.13; 95% confidence interval [CI], 0.83-1.58; P = .43). Bowel screening examinations were comparable between the 2 groups throughout the study. The grade, stage, and location of colorectal cancer did not differ between the randomization groups. There were more colorectal cancer deaths in the estrogen-alone group (34 [0.05%] vs 24 [0.03%]; HR, 1.46, 95% CI, 0.86-2.46; P = .16), but the difference was not statistically significant. The colorectal cancer incidence was higher for participants with a history of colon polyp removal in the estrogen-alone group (0.23% vs 0.02%; HR, 13.47; nominal 95% CI, 1.76-103.0; P < .001).CONCLUSIONS The use of estrogen alone in postmenopausal women with prior hysterectomy does not influence the incidence of colorectal cancer or deaths from or after colorectal cancer. A possibly higher risk of colorectal cancer in women with prior colon polyp removal who use estrogen alone requires confirmation. Cancer 2015. © 2015 American Cancer Society.
    Cancer 05/2015; DOI:10.1002/cncr.29464 · 4.90 Impact Factor
  • 04/2015; 2(2):88. DOI:10.17294/2330-0698.1079
  • Rowan T Chlebowski, Garnet L Anderson
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    ABSTRACT: The Women’s Health Initiative (WHI) has conducted two randomized, placebo-controlled clinical trials to evaluate the influence of menopausal hormone therapy on chronic disease risk. Estrogen plus progestin was evaluated in 16,608 postmenopausal women without prior hysterectomy during 5.6 years’ intervention. In that setting, combined hormone therapy use significantly increased breast cancer incidence and interfered with breast cancer detection. The breast cancers were not limited to estrogen receptor positive, favorable prognosis cancers and were identified at more advanced stage. As a result, deaths from breast cancer were significantly increased by estrogen plus progestin use. While the absolute breast cancer risk for relatively short term (2-4 years) use of combined hormone therapy is small, on a population basis a therapy which nearly doubles deaths from breast cancer requires cautious use. Estrogen alone was evaluated in 10,739 postmenopausal women with prior hysterectomy during 7.1 years’ intervention. There was an overall reduction of breast cancer incidence seen with estrogen alone use and a suggestion that the effect on risk was more pronounced in women initiating hormone therapy further from menopause. Nonetheless, women with prior hysterectomy can be assured that short duration estrogen alone use for climacteric symptom management is relatively safe. Neither estrogen plus progestin nor estrogen alone should be used for chronic disease risk reduction. The safety of duration of use on chronic disease risk longer than in the WHI clinical trials is not defined.
    04/2015; 6(2). DOI:10.1177/2042098614568300
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    ABSTRACT: Results from the Women's Health Initiative (WHI) clinical trials (CT) demonstrated no increase in the risk of lung cancer in postmenopausal women treated with hormone therapy. We conducted a joint analysis of the WHI observational study data and CT data to further explore the association between estrogen and estrogen-related reproductive factors and lung cancer risk. Reproductive history, oral contraceptive (OC) use, and postmenopausal hormone therapy (HT) was evaluated in 160,855 women with known HT exposures. Follow-up for lung cancer was through September 17, 2012; 2,467 incident lung cancer cases were ascertained, with median follow-up of 14 years. For all lung cancers, women with previous use of estrogen plus progestin of < 5 years (HR=0.84; 95% CI 0.71-0.99) were at reduced risk. A limited number of reproductive factors demonstrated associations with risk. There was a trend towards decreased risk with increasing age at menopause (ptrend=0.04) and a trend towards increased risk with increasing number of live births (ptrend=0.03). Reduced risk of non-small cell lung cancer was associated with age 20-29 at first live birth. Risk estimates varied with smoking history, years of HT use and previous bilateral oophorectomy. Indirect measures of estrogen exposure to lung tissue, as used in this study, provide only weak evidence for an association between reproductive history or HT use and risk of lung cancer. More detailed mechanistic studies and evaluation of risk factors in conjunction with ER expression in the lung should continue as a role for estrogen can't be ruled out and may hold potential for prevention and treatment strategies.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 04/2015; DOI:10.1097/JTO.0000000000000558 · 5.80 Impact Factor
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    ABSTRACT: The risks of both endometrial cancer and postmenopausal breast cancer are increased by obesity and higher endogenous estrogen levels. Although aromatase inhibitors reduce breast cancer incidence, their influence on endometrial cancer is uncertain. The authors investigated this issue in a cohort of 17,064 women who were diagnosed with hormone receptor-positive breast cancer in an integrated group practice health plan. Information on demographics, comorbidities, and the receipt of adjuvant endocrine therapy was available from electronic medical records and pharmacy records, respectively. Endometrial cancer information was obtained from the health plan's Surveillance, Epidemiology, and End Results-affiliated tumor registry, and rates were compared across endocrine therapy groups (aromatase inhibitor, n = 5303; tamoxifen, n = 5155; switchers: both [n = 3787] or none [n = 2819]) using multivariable adjusted Cox proportional-hazards models. Endometrial cancer incidence was a statistically significant 48% lower in the aromatase inhibitor group versus the tamoxifen group (hazard ratio, 0.52; 95% confidence interval, 0.31-0.87; P = .01). Endometrial cancer incidence was 29% lower in the aromatase inhibitor group versus the no endocrine therapy group (hazard ratio, 0.71; 95% confidence interval, 0.37-1.35; P = .30) and 33% lower in the aromatase inhibitor group versus the tamoxifen group (hazard ratio, 0.67; 95% confidence interval, 0.42-1.06; P = .08), but neither difference was statistically significant. Associations were stronger among those with good drug adherence. In a community-based, integrated health plan setting, endometrial cancer incidence was lower in women who were receiving an aromatase inhibitor compared with those who were receiving tamoxifen. In addition, aromatase inhibitors may mitigate the incidence of tamoxifen-associated endometrial cancer. Although there were somewhat fewer endometrial cancers in the aromatase inhibitor group versus the no endocrine therapy group, further studies are needed for the definitive assessment of this potential association. Cancer 2015. © 2015 American Cancer Society. © 2015 American Cancer Society.
    Cancer 03/2015; DOI:10.1002/cncr.29332 · 4.90 Impact Factor
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    ABSTRACT: To evaluate the association between statins and breast cancer stage and mortality in the Women's Health Initiative. The study population included 128,675 postmenopausal women aged 50-79 years, out of which there were 7,883 newly diagnosed cases of in situ (19 %), local (61 %)-, regional (19 %)- and distant (1 %)-stage breast cancer and 401 deaths due to breast cancer after an average of 11.5 (SD = 3.7) years of follow-up. Stage was coded using SEER criteria and was stratified into early (in situ and local)- versus late (regional and distant)-stage disease. Information on statins and other risk factors were collected by self- and interviewer-administered questionnaires. Cause of death was based on medical record review. Multivariable-adjusted hazards ratios (HR) and 95 % confidence intervals (CIs) evaluating the relationship between statin use (at baseline only and in a time-dependent manner) and diagnosis of late-stage breast cancer and breast cancer-specific mortality were computed from Cox proportional hazards analyses after adjusting for appropriate confounders. Statins were used by 10,474 women (8 %) at baseline. In the multivariable-adjusted time-dependent model, use of lipophilic statins was associated with a reduction in diagnosis of late-stage breast cancer (HR 0.80, 95 % CI 0.64-0.98, p = 0.035) which was also significant among women with estrogen receptor-positive disease (HR 0.72, 95 % CI 0.56-0.93, p = 0.012). Breast cancer mortality was marginally lower in statin users compared with nonusers (HR 0.59, 95 % CI 0.32-1.06, p = 0.075). Prior statin use is associated with lower breast cancer stage at diagnosis.
    Cancer Causes and Control 03/2015; 26(4). DOI:10.1007/s10552-015-0530-7 · 2.96 Impact Factor
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    ABSTRACT: Bisphosphonates are common medications used for the treatment of osteoporosis and are also used to reduce metastases to bone in patients with cancer. Several studies, including the Women's Health Initiative (WHI), have found that use of bisphosphonates is associated with reduced risk of developing breast cancer, but less is known about associations with other common malignancies. This study was aimed at examining the effects of bisphosphonates on the risk of endometrial cancer. We evaluated the relationship between use of oral bisphosphonates and endometrial cancer risk in a cohort of 89,918 postmenopausal women participating in the WHI. A detailed health interview was conducted at baseline, and bisphosphonate use was ascertained from an inventory of regularly used medications at baseline and over follow-up. All women had an intact uterus at the time of study entry. During a median follow-up of 12.5 years, 1,123 women were diagnosed with incident invasive endometrial cancer. Ever use of bisphosphonates was associated with reduced endometrial cancer risk (adjusted hazard ratio, 0.80; 95% CI, 0.64 to 1.00; P = .05), with no interactions observed with age, body mass index, or indication for use. In this large prospective cohort of postmenopausal women, bisphosphonate use was associated with a statistically significant reduction in endometrial cancer risk. © 2015 by American Society of Clinical Oncology.
    Journal of Clinical Oncology 02/2015; 33(10). DOI:10.1200/JCO.2014.58.6842 · 17.88 Impact Factor
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    ABSTRACT: We investigated if metformin lowers breast, endometrial, and ovarian cancer risk in women with type 2 diabetes mellitus compared with women who used other antidiabetic medications. We followed a cohort of 66 778 female patients with diabetes for a maximum of 12 years (median 6 years). We examined breast, endometrial, and ovarian cancer risk, and the composite cancer risk. We examined drug categories using pharmacy records: metformin only; metformin combination regimens; non-metformin regimens; and non-users. We used χ(2) analyses to examine categorical variables. We conducted multivariable Cox regression models with time-dependent drug use status. Women who used metformin combination regimens versus metformin only had a 15% lower breast cancer risk (adjusted HR=0.85, 95% CI 0.69 to 1.04). After stratifying by glycated hemoglobin (HbA1c), the association attenuated in those who had poorly controlled HbA1c (adjusted HR=1.06, 95% CI 0.73 to 1.55). Given the small numbers of ovarian and endometrial cancer outcomes, we examined these as a composite. The risk of all cancers combined was similar in those who used metformin combination regimens versus metformin only (adjusted HR=0.92, 95% CI 0.78 to 1.10). We found no significant differences for breast cancer or all cancers combined when we compared risks in non-metformin users versus metformin only users. Women who used metformin and other antidiabetic drugs had a lower breast cancer risk compared with women who used metformin only, but the results were not significant. We also found no difference in overall cancer risks when we compared women who used other antidiabetic drugs (no metformin) versus metformin users.
    01/2015; 3(1):e000049. DOI:10.1136/bmjdrc-2014-000049
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    ABSTRACT: Atypical hyperplasia of the breast (AH) is associated with increased risk of subsequent invasive breast cancer, yet little is known about the etiology of AH. Insulin-like growth factor binding protein 2 (IGFBP-2) may contribute to the development of AH due to its proliferative effects on mammary tissue. We conducted a nested case-control study of postmenopausal women enrolled in Women’s Health Initiative-Clinical Trial. Cases were 275 women who developed incident AH during follow-up, individually (1 : 1) matched to controls. Levels of IGFBP-2 were determined from fasting serum collected at baseline. Multivariable conditional logistic regression models were used to estimate odds ratios for the association of IGFBP-2 with risk of AH. Serum IGFBP-2 was associated with a nonsignificant decrease in risk for AH, when comparing the highest quartile to lowest quartile (OR = 0.65; 95% CI = 0.32-1.31). This decrease in risk was most evident when analyses were restricted to nondiabetic, nonusers of hormone therapy (OR = 0.33, 95% CI = 0.13-0.86, ptrend = 0.06) and nondiabetic women who were overweight or obese (OR = 0.43, 95% CI = 0.18-1.03, ptrend = 0.05). Results from this study provide some support for an inverse association between serum IGFBP2 levels and risk of AH, particularly in nondiabetic women who are overweight or obese. Further studies are required to confirm these results.
    Journal of Cancer Epidemiology 01/2015; 2015:1-7. DOI:10.1155/2015/203284
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    ABSTRACT: Importance More than two-thirds of US women are overweight or obese, placing them at increased risk for postmenopausal breast cancer.Objective To investigate in this secondary analysis the associations of overweight and obesity with risk of postmenopausal invasive breast cancer after extended follow-up in the Women’s Health Initiative (WHI) clinical trials.Design, Setting, and Participants The WHI clinical trial protocol incorporated measured height and weight, baseline and annual or biennial mammography, and adjudicated breast cancer end points in 67 142 postmenopausal women ages 50 to 79 years at 40 US clinical centers. The women were enrolled from 1993 to 1998 with a median of 13 years of follow-up through 2010; 3388 invasive breast cancers were observed.Main Outcomes and Measures Height and weight were measured at baseline, and weight was measured annually thereafter. Data were collected on demographic characteristics, personal and family medical history, and personal habits (smoking, physical activity). Women underwent annual or biennial mammograms. Breast cancers were verified by medical records reviewed by physician adjudicators.Results Women who were overweight and obese had an increased invasive breast cancer risk vs women of normal weight. Risk was greatest for obesity grade 2 plus 3 (body mass index [BMI], calculated as weight in kilograms divided by height in meters squared, >35.0) (hazard ratio [HR] for invasive breast cancer, 1.58; 95% CI, 1.40-1.79). A BMI of 35.0 or higher was strongly associated with risk for estrogen receptor-positive and progesterone receptor-positive breast cancers (HR, 1.86; 95% CI, 1.60-2.17) but was not associated with estrogen receptor-negative cancers. Obesity grade 2 plus 3 was also associated with advanced disease, including larger tumor size (HR, 2.12; 95% CI, 1.67-2.69; P = .02), positive lymph nodes (HR, 1.89; 95% CI, 1.46-2.45; P = .06), regional and/or distant stage (HR, 1.94; 95% CI, 1.52-2.47; P = .05), and deaths after breast cancer (HR, 2.11; 95% CI, 1.57-2.84; P < .001). Women with a baseline BMI of less than 25.0 who gained more than 5% of body weight over the follow-up period had an increased breast cancer risk (HR, 1.36; 95% CI, 1.1-1.65), but among women already overweight or obese we found no association of weight change (gain or loss) with breast cancer during follow-up. There was no effect modification of the BMI-breast cancer relationship by postmenopausal hormone therapy, and the direction of association across BMI categories was similar for never, past, and current hormone therapy use.Conclusions and Relevance Obesity is associated with increased invasive breast cancer risk in postmenopausal women. These clinically meaningful findings should motivate programs for obesity prevention.Trial Registration clinicaltrials.gov Identifier: NCT00000611
    01/2015; DOI:10.1001/jamaoncol.2015.1546
  • Rowan T Chlebowski
    The Lancet Oncology 12/2014; 16(1). DOI:10.1016/S1470-2045(14)71184-2 · 24.73 Impact Factor
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    ABSTRACT: A body shape index (ABSI) has been proposed as a possible improvement over waist circumference (WC) as a marker of abdominal adiposity because it removes the correlation of WC with body mass index (BMI) and with height. We assessed the association of ABSI with four obesity-related cancers compared to that of other anthropometric measures of adiposity. We used data from the Women's Health Initiative, a large cohort of postmenopausal women, recruited between 1993 and 1998 and followed until September 2013, to assess the associations of ABSI and other anthropometric measures with risk of cancers of the breast, endometrium, colorectum, and kidney. The four comparison anthropometric measures were BMI, WC, waist circumference-to-height ratio (WHtR), and waist-hip ratio (WHR). Over a median of 12.7 years of follow-up, among 143,901 women, we identified 7,039 invasive breast cancers, 1,157 endometrial cancers, 1,908 colorectal cancers, and 376 kidney cancers. We used Cox proportional hazards models to estimate the association of quintiles of the five measures with risk of the four cancers. Unlike the other anthropometric indices, ABSI was not associated with increased risk of breast or endometrial cancer. BMI and WC were comparable as predictors of breast and endometrial cancer, and these associations were unchanged after mutual adjustment. For colorectal and kidney cancers, ABSI was a significant predictor comparable to BMI; however, WC showed the strongest association with colorectal cancer, and WC, WHtR, and WHR all showed stronger associations with kidney cancer. In contrast to other anthropometric measures, ABSI showed no association with risk of breast or endometrial cancer and was more weakly associated with risk of colorectal and kidney cancers compared to more established measures of central adiposity.
    Cancer Causes and Control 11/2014; 26(2). DOI:10.1007/s10552-014-0501-4 · 2.96 Impact Factor
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    ABSTRACT: Positive associations between dog ownership and physical activity in older adults have been previously reported. The objective of this study was to examine cross-sectional associations between dog ownership and physical activity measures in a well-characterized, diverse sample of postmenopausal women. Analyses included 36,984 dog owners (mean age: 61.5years), and 115,645 non-dog owners (mean age: 63.9years) enrolled in a clinical trial or the observational study of the Women's Health Initiative between 1993 and 1998. Logistic regression models were used to test for associations between dog ownership and physical activity, adjusted for potential confounders. Owning a dog was associated with a higher likelihood of walking ≥150min/wk (Odds Ratio, 1.14; 95% Confidence Interval, 1.10-1.17) and a lower likelihood of being sedentary ≥8h/day (Odds Ratio, 0.86; 95% Confidence Interval, 0.83-0.89) as compared to not owning a dog. However, dog owners were less likely to meet ≥7.5MET-h/wk of total physical activity as compared to non-dog owners (Odds Ratio, 1.03; 95% Confidence Interval, 1.00-1.07). Dog ownership is associated with increased physical activity in older women, particularly among women living alone. Health promotion efforts aimed at older adults should highlight the benefits of regular dog walking for both dog owners and non-dog owners. Copyright © 2014 Elsevier Inc. All rights reserved.
    Preventive Medicine 11/2014; 70C:33-38. DOI:10.1016/j.ypmed.2014.10.030 · 2.93 Impact Factor
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    ABSTRACT: Lung cancer is the leading cause of worldwide cancer deaths. While smoking is its leading risk factor, few prospective cohort studies have reported on the association of lung cancer with both active and passive smoking. This study aimed to determine the relationship between lung cancer incidence with both active and passive smoking (childhood, adult at home, and at work).
    Annals of Oncology 10/2014; DOI:10.1093/annonc/mdu470 · 6.58 Impact Factor
  • Rowan T Chlebowski, Kathy Pan
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    ABSTRACT: To the Editor: In a planned subgroup analysis of the Tamoxifen and Exemestane Trial (TEXT) and the Suppression of Ovarian Function Trial (SOFT) reported by Pagani et al. (July 10 issue),(1) an interaction between human epidermal growth factor receptor 2 (HER2) status and treatment is shown (see Fig. S1 in the Supplementary Appendix, available with the full text of the article at NEJM.org), with apparently no benefit of exemestane plus ovarian suppression versus tamoxifen plus ovarian suppression in patients with HER2-positive tumors. This finding is unexpected considering that HER2 status is prognostic but not predictive of the efficacy of aromatase . . .
    New England Journal of Medicine 10/2014; 371(14):1357-1359. DOI:10.1056/NEJMc1409366#SA2 · 54.42 Impact Factor

Publication Stats

17k Citations
3,611.31 Total Impact Points

Institutions

  • 1987–2015
    • Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
      • Department of Medicine
      Torrance, California, United States
  • 1979–2015
    • Harbor-UCLA Medical Center
      • Department of Pediatrics
      Torrance, California, United States
  • 2012–2014
    • Torrance Memorial Medical Center
      Torrance, California, United States
  • 1980–2014
    • University of California, Los Angeles
      • • Division of Hematology and Medical Oncology
      • • Department of Medicine
      Los Angeles, California, United States
  • 2013
    • University of Balamand
      • Faculty of Health Sciences
      Amiun, Liban-Nord, Lebanon
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
    • University of Alabama at Birmingham
      • Department of Epidemiology
      Birmingham, AL, United States
  • 2007–2011
    • Fred Hutchinson Cancer Research Center
      • Division of Public Health Sciences
      Seattle, Washington, United States
  • 2010
    • Albert Einstein College of Medicine
      • Department of Epidemiology & Population Health
      New York City, NY, United States
  • 2006–2010
    • Stanford University
      • Department of Medicine
      Palo Alto, California, United States
    • University at Buffalo, The State University of New York
      • Department of Social and Preventive Medicine
      Buffalo, NY, United States
  • 2008
    • Maine Medical Center
      Portland, Maine, United States
  • 2003
    • University of South Carolina
      • Department of Epidemiology & Biostatistics
      Columbia, SC, United States
    • The Ohio State University
      Columbus, Ohio, United States
  • 1999
    • American Society of Clinical Oncology
      Alexandria, Virginia, United States
  • 1982
    • University of Southern California
      • Department of Medicine
      Los Angeles, California, United States