bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased Risk of Lung Cancer in Men with Tuberculosis in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study
Authors: Shiels Meredith S. , Albanes Demetrius , Virtamo Jarmo , Engels Eric A. 
Published: March 2011

Abstract
Background: Lung cancer and tuberculosis cause significant morbidity and mortality worldwide. Tuberculosis may increase lung cancer risk through substantial and prolonged pulmonary inflammation. However, prospective data on tuberculosis and lung cancer risk are limited.
Methods: Our study included 29,133 Finnish male smokers followed prospectively in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (1985–2005). Lung cancers were identified through linkage with the Finnish Cancer Registry, and hospital-treated tuberculosis cases were ascertained from the National Hospital Discharge Register. We assessed the association between tuberculosis and lung cancer risk with proportional hazards regression models, adjusting for age and cigarette smoking.
Results: Forty-four lung cancer cases occurred among 273 men with tuberculosis (incidence rate = 1,786 per 100,000 person-years). Tuberculosis was associated with a two-fold elevation in lung cancer risk (HR = 1.97; 95% CI = 1.46–2.65) with significant associations observed for both incident (HR = 2.05; 95% CI = 1.42–2.96) and prevalent tuberculosis (HR = 1.82; 95% CI = 1.09–3.02). Lung cancer risk was greatest in the 2-year window after tuberculosis diagnosis (HR = 5.01; 95% CI = 2.96–8.48) but remained elevated at longer latencies (HR = 1.53; 95% CI = 1.07–2.20). Though tuberculosis was associated with an increased risk of squamous cell carcinoma (HR = 3.71), adenocarcinoma (HR = 1.71), small cell carcinoma (HR = 1.72), and lung cancer of other (HR = 1.23) and unknown histologies (HR = 1.35), only the association for squamous cell carcinoma was statistically significant.
Conclusions: Tuberculosis is associated with increased lung cancer risk in male smokers.
Impact: Our results add to the growing body of evidence implicating chronic inflammation and pulmonary scarring in the etiology of lung cancer. Cancer Epidemiol Biomarkers Prev; 20(4); 672–8. ©2011 AACR.
U.S. Geographic Distribution of Prevaccine Era Cervical Cancer Screening, Incidence, Stage, and Mortality
Authors: Horner Marie-Josèphe , Altekruse Sean F. , Zou Zhaohui , Wideroff Louise , Katki Hormuzd A. , Stinchcomb David G. 
Published: March 2011

AbstractBackground: Cervical cancer prevention programs are being reconfigured to incorporate human papillomavirus (HPV) testing and vaccination. To define priority areas for prevention efforts, we examined the geographic distribution of cervical cancer screening, incidence, stage, and mortality in the United States, prior to the introduction of HPV-based prevention technologies.Methods: County-level cervical cancer incidence data from 37 central registries were obtained from Surveillance, Epidemiology, and End Results and North American Association of Central Cancer Registries. A spatial–temporal model that accounted for demographic and behavioral attributes was used to generate a complete view of county-level incidence from 1995 to 2004, including counties with missing data. Distribution of stage at diagnosis was examined by registry. Counties with high mortality and infrequent screening were identified using vital statistics and newly available county-level screening estimates.Results: Compared with non-Hispanic whites and Asian and Pacific Islanders, incidence rates were higher among non-Hispanic black, American Indian and Alaska Native, and Hispanic women. Counties with infrequent screening often experienced elevated incidence and mortality rates and were located in states with suboptimal stage at diagnosis profiles. Affected areas included Appalachia, the southeastern Atlantic states, and the lower Mississippi Valley. Elevated death rates were experienced in central counties of large metropolitan areas.Conclusions: Geographic and racial/ethnic variability were evident in cervical cancer incidence and mortality. Women living in areas with endemic poverty would benefit from access to HPV-based prevention technologies.Impact: These findings provide a baseline for monitoring progress in cervical cancer control in the era of HPV-based prevention. Cancer Epidemiol Biomarkers Prev; 20(4); 591–9. ©2011 AACR.
Jewish Ethnicity and Pancreatic Cancer Mortality in a Large U.S. Cohort
Authors: Eldridge Ronald C. , Gapstur Susan M. , Newton Christina C. , Goodman Michael , Patel Alpa V. , Jacobs Eric J. 
Published: March 2011

Abstract
Background: An association between Jewish ethnicity and pancreatic cancer risk was suggested by analyses comparing pancreatic cancer mortality rates between Jews and non-Jews in New York in the 1950s. These analyses lacked information on potential confounding factors and the association between Jewish ethnicity and pancreatic cancer has not been examined in any contemporary U.S. population or in any cohort study.
Methods: We examined the association between Jewish ethnicity and pancreatic cancer mortality among approximately 1 million participants in the Cancer Prevention Study II cohort. Participants completed a questionnaire at enrollment in 1982 which included information on religion, smoking, obesity, and diabetes. During follow-up through 2006, there were 6,727 pancreatic cancer deaths, including 480 among Jewish participants. Proportional hazards modeling was used to calculate multivariable rate ratios (RR).
Results: After adjusting for age, sex, smoking, body mass index, and diabetes, pancreatic cancer mortality was higher among Jewish participants than among non-Jewish whites (RR = 1.43; 95% CI, 1.30–1.57). In analyses by birthplace, RRs were 1.59 (95% CI, 1.31–1.93) for North American–born Jews with North American–born parents, 1.43 (95% CI, 1.27–1.61) for North American–born Jews with 1 or more parents born outside North America, and 1.03 (0.73, 1.44) for Jews born outside North America (Pheterogeneity = 0.07).
Conclusions: These results support a higher risk of developing pancreatic cancer among U.S. Jews that is not explained by established risk factors.
Impact: Future studies may clarify the role of specific environmental or genetic factors responsible for higher risk among U.S. Jews. Cancer Epidemiol Biomarkers Prev; 20(4); 691–8. ©2011 AACR.
Serum Lycopene Concentration and Prostate Cancer Risk: Results from the Prostate Cancer Prevention Trial
Authors: Kristal Alan R. , Till Cathee , Platz Elizabeth A. , Song Xiaoling , King Irena B. , Neuhouser Marian L. , Ambrosone Christine B. , Thompson Ian M. 
Published: March 2011

Abstract
Background: Lycopene has been promoted for prostate cancer prevention, despite the inconsistency of scientific evidence.
Methods: This nested case-control study examined whether serum lycopene was associated with prostate cancer risk among participants in the Prostate Cancer Prevention Trial, a placebo-controlled trial of finasteride for prostate cancer prevention. Presence or absence of cancer was determined by prostate biopsy, recommended during the trial due to elevated prostate specific antigen (PSA) level or abnormal digital rectal examination (DRE) and offered to all men at the trial end. There were 1,683 cases (461 Gleason score ≥ 7, 125 Gleason score ≥ 8) and 1,751 controls.
Results: There were no associations of lycopene with prostate cancer risk. The odds ratios for a linear increase in lycopene (per 10 μg/dL) were 0.99 (95% CI: 0.94–1.04), 1.01 (0.94–1.08), and 1.02 (0.90–1.15) for Gleason 2 to 6, 7 to 10, and 8 to 10, respectively. In the placebo arm, a 10 μg/dL increase in lycopene was associated with a 7% (95% CI: 14–0) reduced risk of cancer diagnosed following an elevated PSA or abnormal DRE, which are cancers that best match those detected in screened populations. However, a 10 μg/dL increase in lycopene was also associated with an 8% (95% CI: 1–16) increased risk of cancer diagnosed without a biopsy prompt, which are cancers generally not detected. These findings were similar for low- and high-grade cancer.
Conclusion: This study does not support a role for lycopene in prostate cancer prevention.
Impact: Scientists and the public should understand that early studies supporting an association of dietary lycopene with reduced prostate cancer risk have not been replicated in studies using serum biomarkers of lycopene intake. Recommendations of professional societies to the public should be modified to reflect the likelihood that increasing lycopene intake will not affect prostate cancer risk. Cancer Epidemiol Biomarkers Prev; 20(4); 638–46. ©2011 AACR.
Vitamin D: Marker or Mechanism of Action?
Authors: Jacobs Elizabeth T. , Martínez María Elena , Jurutka Peter W. 
Published: March 2011

Abstract
The field of vitamin D and cancer research has been moving forward quickly. However, some challenges remain regarding the interpretation and integration of data collected from epidemiological investigations and laboratory experiments. These include consideration of vitamin D biology, a better understanding of characteristics that affect concentrations of the biomarker of vitamin D status, 25(OH)D, and elucidation of variation in response to vitamin D supplementation. To further the field of vitamin D and cancer prevention, future studies will need to bridge the gap between the epidemiology and molecular biology of vitamin D activity in carcinogenesis. Cancer Epidemiol Biomarkers Prev; 20(4); 585–90. ©2011 AACR.
Plasma Coenzyme Q10 Levels and Prostate Cancer Risk: The Multiethnic Cohort Study
Authors: Chai Weiwen , Cooney Robert V. , Franke Adrian A. , Caberto Christian P. , Wilkens Lynne R. , Le Marchand Loïc , Goodman Marc T. , Henderson Brian E. , Kolonel Laurence N. 
Published: March 2011

Abstract
Background: Coenzyme Q10 (CoQ10) is considered to be a potential anticancer agent, but epidemiologic evidence regarding CoQ10 and prostate cancer risk is lacking. We examined the association of circulating CoQ10 levels with prostate cancer risk, using prediagnostic blood samples.
Methods: Each of the 307 cases was individually matched to approximately 2 controls, for a total of 596 controls, on age, ethnicity, geographic location, date/time of specimen collection, and hours of fasting. Logistic regression was used to compute ORs and 95% CIs.
Results: There was no overall statistically significant association of plasma CoQ10 levels with prostate cancer risk (Ptrend = 0.50). However, after matched sets in which controls who had possible undiagnosed prostate cancer (prostate specific antigen value &gt;4.0) were excluded, the ORs for quintiles 2 to 5 were all less than 1.0.
Conclusions: The results suggest the possibility that moderate levels of circulating CoQ10 may be optimal for the reduction of prostate cancer risk; however, the findings were weak and not statistically significant. Because this is the first epidemiologic study of the association between CoQ10 and prostate cancer, further research on this topic is needed.
Impact: If a nutritional factor such as CoQ10 were determined to reduce prostate cancer risk, it would have considerable public health significance because of the very high incidence of this cancer. Cancer Epidemiol Biomarkers Prev; 20(4); 708–10. ©2011 AACR.
Nutrients, Food Groups, Dietary Patterns, and Risk of Pancreatic Cancer in Postmenopausal Women
Authors: Inoue-Choi Maki , Flood Andrew , Robien Kim , Anderson Kristin 
Published: March 2011

Abstract
Introduction: Identifying modifiable risk factors for pancreatic cancer is important because of its poor prognosis. Previous findings on diet are inconsistent.
Methods: Associations between intake of nutrients, food groups, dietary patterns, and pancreatic cancer risk were examined among 34,642 postmenopausal women in the Iowa Women's Health Study (IWHS).
Results: No significant associations were observed between intake of nutrients and food groups or dietary patterns and pancreatic cancer.
Conclusion: Our findings do not support the hypothesis that fruits, vegetables, and red meat are associated with risk of pancreatic cancer.
Impact: Dietary intake, assessed in multiple aspects in a large prospective cohort study, was not associated with pancreatic cancer. Cancer Epidemiol Biomarkers Prev; 20(4); 711–4. ©2011 AACR.
The Association between Prognostic Demographic and Tumor Characteristics of Breast Carcinomas with Serum 25-OH Vitamin D Levels
Authors: Peppone L , Rickles A , Huston A , Sprod L , Hicks D , Mustian K , Skinner K 
Published: March 2011

Abstract
Objective: Epidemiologic studies show that women with low 25-OH vitamin D levels have an increased risk of breast cancer incidence and mortality. However, there is a lack of research examining vitamin D levels and prognostic variables in breast cancer patients. The aim of this study is to identify the associations between 25-OH vitamin D levels, demographic variables, and prognostic pathological and genetic characteristics of breast cancers.
Method: This study cohort consists of 155 women who underwent breast cancer surgery at the University of Rochester between 1/2009 and 9/2010. Vitamin D levels were obtained in the 1-year period before and after surgery (74% of vitamin D levels within 6 months). Prognostic variables included age, race, menopausal status, Oncotype DX score, TNM staging, ER/PR status, and HER2 expression. ANCOVA, linear regression, and logistic regression were used to determine the association between prognostic variables and 25-OH vitamin D levels, while controlling for relevant covariates (age, race, and month of blood draw).
Results: Non-Caucasian (OR = 3.8; P &lt; 0.01) and premenopausal (OR = 3.5; P &lt; 0.01) breast cancer patients were significantly more likely to have suboptimal 25-OH vitamin D levels than Caucasian and postmenopausal patients, respectively. Women with invasive breast tumors were more likely to have suboptimal vitamin D levels (invasive OR = 2.4; P = 0.10) and lower mean 25-OH vitamin D levels (invasive: 30.5 ng/mL vs. in situ: 36.9 ng/mL; P = 0.04). A significant correlation (r = −0.42; P = 0.04) between decreasing vitamin D levels and increasing Oncotype score was noted. Breast cancer patients who had ER- and triple-negative breast tumors were more likely to have suboptimal levels of 25-OH vitamin D (ER-OR = 2.4; P = 0.07; triple-negative OR = 2.6; P = 0.09).
Conclusions: Breast cancer patients with suboptimal vitamin D levels were more likely to have tumors with more aggressive tumor profiles, worse prognostic markers (ER- and triple-negative tumors), and higher recurrence risk (Oncotype scores), lending support to previous research that found decreased breast cancer survival among vitamin D deficient individuals. Further research is needed to elucidate the biological relationship between vitamin D and prognostic breast cancer markers.
The Association of Serum Phthalates and Parabens with Mammographic Breast Density
Authors: Sprague B , Trentham-Dietz A , Hedman C , Hemming J , Hampton J , Buist D , Aiello Bowles E , Burnside E , Sisney G 
Published: March 2011

Abstract
Humans are exposed to a large number of environmental chemicals which have estrogenic activity, raising concern regarding potential effects on breast tissue and breast cancer risk. Phthalates are commonly found in personal care products, such as shampoos, lotions, and shaving products, and are present in many consumer plastics, adhesives, detergents, and pharmaceuticals. Parabens are also found in personal care products, and are additionally used as antimicrobials in foods. In vitro studies have demonstrated that many phthalates and parabens can bind to the estrogen receptor and initiate estrogenic cellular pathways, and a recent case-control study found that urinary concentrations of mono-ethyl-phthalate were positively associated with breast cancer risk. We examined the cross-sectional association of circulating serum levels of phthalates and parabens with mammographic breast density (a marker for breast cancer risk). A total of 261 postmenopausal women (ages 55–70, with no history of postmenopausal hormone use) were recruited from mammography clinics in Madison, Wisconsin. Patients completed a questionnaire regarding known breast cancer risk factors and provided a blood sample that was analyzed for mono-ethyl-phthalate, mono-butyl-phthalate, mono-benzyl-phthalate, butyl paraben, and propyl paraben. Percent breast density was measured from patients' mammograms as a continuous variable using a computer-assisted thresholding method (Cumulus software). After adjusting for age and body mass index, mono-ethyl-phthalate was positively associated with percent breast density. Women with detectable mono-ethyl-phthalate levels (&gt;0.4 ng/mL; N = 36) had higher percent breast density than women with no detectable mono-ethyl-phthalate (N = 225) in their serum (16.8% vs. 12.8%; P = 0.03). Serum levels of mono-butyl-phthalate and mono-benzyl-phthalate were generally below the limits of detection. Serum levels of butyl-paraben and propyl-paraben were higher (detectable in 55% and 67% of patients, respectively), but neither was associated with breast density (P &gt; 0.20). These results suggest that further investigation into the potential influence of mono-ethly-phthalate (and its parent compound diethyl-phthalate) on breast tissue is warranted.
Cervical Cancer Screening Efficacy in Older Women
Authors: Kamineni A , Weinmann S , Shy KK , Mandelson MT , Glass AG , Weiss NS 
Published: March 2011

Abstract
Although the effectiveness of cervical cancer screening, by means of the Pap smear, has been firmly established in reproductive-age women, the usefulness of cytologic screening in older women is unclear. We sought to assess the degree to which such screening in older women can reduce the incidence of cervical cancer. We conducted a case-control study to evaluate the efficacy of cervical cancer screening in older women enrolled in one of two large health maintenance organizations in the northwestern United States. Cases (n = 69) consisted of those women, 55 to 79 years of age, who were diagnosed with invasive cervical cancer during 1980 to 1999 as enumerated by regional cancer registries. Controls (n = 208) were women sampled from among enrollees who had not previously had a hysterectomy and were similar to cases in terms of age and length of enrollment in the health plan. We reviewed medical records to ascertain demographic, reproductive, and cervical screening history information during the 7 years before the reference date. Only tests which occurred during the presumed detectable preinvasive phase (DPP) of the disease, when screening could be beneficial, were considered and we evaluated results for a series of plausible estimates of this interval. Compared to cases, controls were more likely to have had a Pap test during the DPP, regardless of the estimate used. After adjustment for age and current smoking status, screening was associated with a substantial reduction in the risk of invasive cervical cancer (DPP = 72 months: OR, 0.23; 95% CI, 0.11–0.44). We observed only small differences in the odds ratio across the various estimates of the DPP that were employed. Analysis of the relative incidence of invasive cervical cancer in relation to the time following a negative screening test suggested a large reduction during the first year (OR, 0.09; 95% CI, 0.03–0.24). The incidence remained low for several years thereafter, returning to the incidence among unscreened women after 5 to 7 years. Cervical cancer screening is highly efficacious in older women. This needs to be explicitly considered in weighing the benefits and costs of such screening beyond the reproductive years.
MicroRNA-Related Genetic Variants as Predictors of Early Stage Non–Small Cell Lung Cancer Clinical Outcomes
Authors: Pu X , Lu C , Stewart DJ , Gu J , Hildebrandt MAT , Lin J , Lippman SM , Xifeng W 
Published: March 2011

Abstract
Purpose: MicroRNAs (miRNA) can function as oncogenes or tumor suppressors. In this study, we test the hypothesis that genetic variation within miRNA processing genes or miRNA binding sites in cancer-related genes may alter clinical outcomes for non–small cell cancer (NSCLC) patients.
Methods: We genotyped 72 single nucleotide polymorphisms (SNPs) from eight miRNA processing genes and 168 SNPs from 133 predicted miRNA binding sites in 535 patients with early stage (stages I, IIA, and IIB) NSCLC to determine the effect of these variations on progression risk and overall survival. We further conducted a subset analysis to exclude potential bias due to different treatment regimens.
Results: In the analysis of overall survival, an FAS SNP remained significant for decreased risk after multiple comparisons in all early patients (HR: 0.59, 95% CI: 0.44–0.77; GG: MST = 58 mos, GA + AA: MST = 118 mos) and surgery plus chemotherapy subgroup (HR: 0.19, 95% CI: 0.07–0.46, P = 1.84 × 10−5; GG: MST = 65 mos, GA + AA: MST = 137 mos). In the surgery-only patients, an FZD4 SNP (HR: 0.46, 95% CI: 0.32–0.65; GG: MST = 59 mons, GA + AA: MST = 117 mos) had a significant protective effect after multiple comparisons adjustment. For progression risk, following multiple comparison, an SP1 SNP (HR: 2.19, 95% CI: 1.45–3.32; GG: MST &gt; 270 mos, GA + AA: MST = 45 mos) and an MBD1 SNP (HR: 2.41, 95% CI: 1.45–4.0; AA: MST &gt; 270 mos, C + CC: MST = 90 mos) remained significant increased progression risk in the entire and surgery only population respectively. All the associations significant after adjusting for multiple comparisons were validated by Bootstrap resampling method. A strong cumulative effect of these variant genotypes to increase risk and dramatically decrease median event-free time was consistently observed. We also identified potential higher-order gene–gene interactions among these SNPs.
Conclusions: We identified significant association between miRNA-related genetic variants and early stage NSCLC patient clinical outcomes. With validation, our result can be used in the prognosis of clinical outcomes for early stage NSCLC patients.
The Impact of Detection and Treatment of Carcinoma In Situ on Breast Cancer Mortality
Authors: Trentham-Dietz A , Sprague BL , Alagoz O , Reaidi P , Rosenberg M , Gangnon RE , Stout NK 
Published: March 2011

Abstract
Purpose: Ductal carcinoma in situ (DCIS), a nonobligate precursor to invasive breast cancer, makes up 20% of new breast cancer diagnoses. DCIS is primarily detected by mammography and has excellent prognosis regardless of therapy choice. We aim to quantify the impact of detection and treatment of DCIS on breast cancer mortality using computer modeling.
Methods: We used a validated microsimulation model to replicate U.S. trends in breast cancer incidence and mortality from 1975 to 2000. All breast cancer tumors began in the in situ stage and progressed through more advanced stages with increasing tumor size and lymph node involvement, with a fraction of tumors assumed as nonlethal. Age-adjusted breast cancer mortality was examined under historical U.S. screening and treatment patterns and three alternative scenarios: (1) only women 50 years and older received screening and all breast cancer cases received treatment according to historical patterns, (2) all women received screening according to historical patterns but DCIS was untreated unless later detected at an invasive stage, and (3) historical screening was used but DCIS was never treated.
Results: The model predicts breast cancer mortality rates declined during the 1990s to a low of 39.9 per 100,000 in 2000, which is consistent with observed mortality based on the SEER program (38.0 per 100,000 in 2000). Delaying mammography until age 50 or postponing treatment until DCIS progressed to invasive cancer increased mortality to 42.4 and 43.2 per 100,000, respectively, by 2000. If DCIS patients did not receive any treatment, mortality remained steady (∼51.2 per 100,000) through 2000.
Conclusions: Our model results suggested detection and treatment of DCIS in the U.S. reduced breast cancer deaths in the year 2000 by about 28%. Most of this benefit (92%–94%) could also be achieved if instead mammography began at age 50 or treatment was reserved for invasive breast cancers only.