bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B67: In vitro and in vivo inhibitory effects of cranberry proanthocyanidins against esophageal adenocarcinoma
Authors: Zeyzus-Johns Bree , Exum Amy , Howell Amy B. , Kresty Laura A. 
Published: January 2011

Abstract
This study investigated the cancer inhibitory potential of a proanthocyanidin rich cranberry extract utilizing a panel of authenticated human esophageal adenocarcinoma cell lines (EAC), a nude mouse xenograft model, and the rat esophagogastrodoudenal anastomosis (EGDA) model of EAC. PACs effects on cell morphology, global gene expression, phase of cell cycle, and cell death induction via apoptosis, autophagy, and necrosis were evaluated. Methods included RapidDiff and MDC staining, Annexin/PI and BrdU staining with flow cytometric evaluation, transmission electron microscopy (TEM), protein evaluation utilizing standard Western blot techniques, and validation of global gene expression changes by real-time PCR. PAC treatment [50-100µg/ml] of EAC cancer cell lines resulted in significant increases in apoptosis, autophagy and necrosis. Differential cell death induction was noted based upon the cell lines resistance to a bile/acid cocktail mimicking acid exposure in humans as well as the status of the apoptotic and autophagic machinery of the select cell line. PACs cell death inducing capacity correlated with altered MAPKinase signaling as evidenced by activation of P-p38 and P-JNK and inhibition of P-ERK1/2. PAC treatment induced other proapoptotic markers including cleaved PARP, BAK1, BAX, and cytochrome C, but in a cell line dependent manner. Mild increases in Beclin-1 were noted following PAC treatment, as were significant increases in LC3II, a marker of autophagasome formation which occurs during autophagy induction. Results were confirmed by TEM and MDC staining. PAC induced cell cycle arrest at the G2/M transition, increased the percent of cells in G1, caused an S-phase delay and increased P21 levels in all three cell lines. PAC administration significantly inhibited the growth of OE19 xenografts via modulation of cell cycle and MAPK signaling pathways. Oral gavage of PAC [250µg/mouse] six times a week to nude mice resulted in a 67% decrease in OE19 tumor volume, increased cytochrome C protein levels and decreased levels of P-ERK1/2, cyclin A, PCNA, and CD31 in PAC treated tumors compared to vehicle treated tumors. Lastly, a four week pilot study was performed to evaluate the safety of daily administration of PAC in the rodent EGDA model. PAC appeared well tolerated given the average daily dose of 450µg/rat/day as evidenced by normal body weight and food consumption, serology profiles and histopathology of the major organs. Further long-term studies are planned to more fully access the chemopreventive potential of PAC against esophageal adenocarcinoma and premalignancy utilizing the clinically relevant rat EGDA surgical model.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B67.
Abstract B69: Potential cancer chemopreventive compounds from Oplopanax horridus, a native North American plant
Authors: Wang Chong-Zhi , Calway Tyler D. , Yuan Chun-Su 
Published: January 2011

Abstract
Distributed throughout the west of North America, the plant Oplopanax horridus, or devil's club, belongs to the genus Oplopanax, which consists of three species (O. elatus, O. japonicus and O. horridus). Although many studies on the other two species have been performed, phytochemical and pharmacological investigations on O. horridus have been limited, especially cancer chemopreventive studies. After comparing differences of antiproliferative potentials among different plant parts of O. horridus, the root bark was selected to perform further phytochemical isolation to prepare active anticancer fractionations and compounds. The hydrophobic fractions showed potent antiproliferative effects on human HCT-116 and SW-480 colorectal cancer cells. Subsequent isolation of the hydrophobic fractions gave six polyynes and one polyene; in which two novel compounds, Oplopantriol A and Oplopantriol B, were obtained and their absolute structures were elucidated by detailed spectroscopic analyses, including 1D and 2D NMR techniques and chemical methods. The content of these seven compounds in the O. horridus root bark was determined using an on-line SPE-HPLC method. Pharmacological studies showed that two polyynes, including a novel compound (Oplopantriol A), possessed strong cancer cell inhibitory activities (P &lt; 0.001). The IC50 of these two polyynes were observed at 1-5 µM on the colorectal cancer cells. Treatment with active fraction and compounds noticeably induced apoptosis, and distinctly induced the G2/M phase arrest of the cell cycle in a time- and concentration-dependent manner. The trend of increasing cyclin A and cyclin B1 were similar to the increase of G2/M phase cells in all treated groups. These results suggested that active O. horridus fraction and selected polyynes had potential antiproliferative activities on human colorectal cancer cells. The observed cancer chemopreventive effects could be related to the induction of apoptosis and regulation of cell cycle transition. (This work was supported in part by the NIH/NCCAM grants AT003255, AT004418 and AT005362).
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B69.
Abstract B70: Physical activity and BMI in a population-based case-control study of endometrial cancer risk
Authors: Arem Hannah , Irwin Melinda L. , Zhou Yang , Lu Lingeng , Risch Harvey , Yu Herbert 
Published: January 2011

Abstract
Introduction: Endometrial (uterine corpus) cancer is the fourth most common incident cancer among women in the United States. Recent systematic reviews have published summary data suggesting an inverse association between physical activity and risk of endometrial cancer. However, studies show conflicting results, many do not report on reliability or validity of physical activity questionnaires, and few studies have examined the combination of physical activity and BMI on endometrial cancer risk. Thus, we evaluated the independent association between physical activity, BMI and endometrial cancer risk, as well as the combination of physical activity and BMI on risk.
Methods: We identified 668 incident cases of endometrial cancer through the population-based Rapid Case Ascertainment Shared Resource at the Yale Cancer Center and age-matched 665 controls using random digit dialing. Research staff interview-administered structured questionnaires, collecting information on demographic features, environmental exposures and lifestyle factors. We performed unconditional logistic regression to examine the relationship between moderate- to vigorous-intensity sports/recreational physical activity (MV PA) and endometrial cancer risk.
Results: We found, compared to women reporting 0 Metabolic Equivalent (MET) hours per week of MV PA, those who reported 7.5 MET hr/wk or more of MV PA had a 34% lower endometrial cancer risk (Odds Ratio (OR) = 0.66, 95% CI: 0.50-0.87) after adjusting for other risk factors including BMI. We created a composite measure of physical activity (inactive ≤ 7.5 MET hr/wk, active &gt; 7.5 MET hr/wk) and BMI (normal weight &lt; 25 kg/m,2 overweight ≥ 25 kg/m2), and found that women who were normal weight and active had a 73% lower endometrial cancer risk (OR = 0.27, 95% CI: 0.19-0.38) compared to the reference group of overweight and inactive. Women who were normal weight but inactive had a 55% lower endometrial cancer risk (OR = 0.45, 95% CI: 0.31-0.65) and women who were overweight but active had a 38% lower risk of endometrial cancer (OR= 0.62, 95% CI: 0.47-0.83).
Conclusion: Our data support an inverse, independent association between physical activity and endometrial cancer risk after adjusting for BMI and other risk factors. However, the combination of physical activity and BMI appears to further impact risk of endometrial cancer. Programs to increase physical activity levels to the current recommendation of 150 minutes per week may lower the incidence of endometrial cancer.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B70.
Abstract B72: Clinical and morphological traits of patients with triple-negative breast cancer
Authors: Petrova Valentina Dmitriyevna , Sinkina Tatiyana Vladimirovna , Selezneva Inna Anatolievna , Dimitriady Julia Nicolaevna , Boyarskikh Uljana Aleksandrovna , Ermolenko Natalya Aleksandrovna , Filipenko Maxim Leonidovich , Lazarev Alexander Fedorovich 
Published: January 2011

Abstract
Background: Breast cancer (BC) is the most prevalent cause of mortality from cancer in women aged 40-69 years in Russian Federation. There are results of clinical researches about triple negative BC [ER(-); PR(-); HER2/neu (-)].
Materials and Methods: The register consisted of 1428 Caucasian women with BC aged 20-79 years (756 — familial and 672 — sporadic BC), control group composed 1581 Caucasian women aged 19-84 years without of cancer. The questioning including data of pheno- and genotype. BRCA or other mutations were performed to all patients. The researching morphological traits of tumor were histological type, estrogen receptor (ER), progesterone receptor (PR) and HER2/neu.
Results: Triple negative BC was found out by 21 BRCA positive patients, 32 BRCA negative patients and 27 patients with sporadic BC. Some of reproductive and clinical factors differed in two groups: triple negative and non-triple negative BC. Among triple negative BC patients, women with sporadic BC were older and had clinical stage higher. Specific gravity of rare tumors was higher by patients with BRCA mutations.
Conclusion: The women with BC can be divided into two groups: having triple negative phenotype and all the rest. Considering these factors let us prognosticate progress notes and form an individual plan of special treatment.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B72.
Abstract B73: Body mass index modifies the association between SMAD7 polymorphism rs4939827 and colorectal cancer risk
Authors: Coghill Anna E. , Passarelli Michael N. , Makar Karen W. , Zheng Yingye , Potter John D. , Wernli Karen J. , Hutter Carolyn M. , Newcomb Polly A. 
Published: January 2011

Abstract
Introduction: SMAD7 inhibits the activity of transforming growth factor beta (TGF-β), an anti-inflammatory molecule that acts as a tumor suppressor and might be important for colorectal cancer incidence. We investigated the association between the risk of colorectal cancer and two common polymorphisms in SMAD7 (rs4939827, rs4464148) previously identified in GWAS as potentially associated with colorectal cancer. We further investigated these relationships across strata of environmental factors related to inflammation, including non-steroidal anti-inflammatory drug (NSAID) use and body mass index (BMI).
Methods: Incident cases of invasive colorectal cancer diagnosed from 1997-2002 in Caucasian, post-menopausal women residing in 13 counties in western Washington State were identified from SEER reports. Community-based controls were randomly selected from population lists, matched on 5-year age intervals to the cases. Women completed a baseline interview and provided a blood or buccal sample, which was genotyped for rs4939827 and rs4464148. Logistic regression was used to generate odds ratios (OR) and 95% confidence intervals (CI) for the association between SMAD7 polymorphisms and colorectal cancer risk. Interaction terms for body mass index (BMI) and non-steroidal anti-inflammatory drug (NSAID) use were included in logistic regression models to investigate potential effect modification.
Results: We did not observe evidence for any association between rs4464148 and colorectal cancer risk. However, the minor allele for rs4939827 (C allele) was associated with a significantly decreased risk of colorectal cancer overall (CT: OR: 0.81; 95% CI 0.62-1.06; CC OR: 0.73; 95% CI 0.53-1.01), p-trend=0.05. We observed significant heterogeneity for the association between rs4939827 and colorectal cancer (p-interaction=0.02) according to body mass index. Reductions in colorectal cancer risk associated with rs4939827 were limited to only non-obese women. No differences in the association of either SMAD7 polymorphism with colorectal cancer according to NSAID use were observed.
Conclusion: Our results support a role for genetic variation in SMAD7 in altering colorectal cancer risk among women. SMAD7 likely alters the risk of colorectal carcinogenesis through its regulatory role in the TGF-β pathway, which is involved in both cellular proliferation and inflammation. Our findings also suggest that exogenous and modifiable risk factors that affect inflammation, such as body mass index, may have the potential to alter the association between endogenous factors such as SMAD7 and colorectal cancer.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B73.
Abstract B84: Prospective study of self-reported diabetes and risk of upper gastrointestinal cancers
Authors: Lin Shih-Wen , Freedman Neal , Hollenbeck Albert , Abnet Christian 
Published: January 2011

Abstract
While gastric non-cardia adenocarcinoma (GNCA) incidence rates in the United States have decreased, the rates of gastric cardia adenocarcinoma (GCA) and esophageal adenocarcinomas (EADC) have increased. Obesity increases the risks of GCA and EADC, and the associations may be partially mediated by insulin resistance. A few case-control studies have shown an association between diabetes and an increased risk of EADC. We examined the association between self-reported diabetes and GCA, GNCA, EADC, and esophageal squamous cell carcinoma (ESCC) in a prospective cohort of approximately 500,000 people in the United States, ages 50-69 at baseline, using Cox proportional hazards regression to estimate the hazard ratios (HR) and 95% confidence intervals (CIs), controlling for multiple potential confounders. In contrast with previous case-control studies, the results of our prospective analysis showed no association with risk of EADC, HR (95% CI) = 0.98 (0.73-1.31). Furthermore, self-reported diabetes showed no association with ESCC, HR (95% CI) = 1.02 (0.60-1.74), or GNCA, HR (95% CI) = 0.98 (0.70-1.37). However, diabetes was significantly associated with an increased risk of GCA, HR (95% CI) = 1.89 (1.43-2.50). The association between diabetes and risk of GCA remained after adjustment for body mass index (BMI), HR (95% CI) = 1.70 (1.28-2.26). Analyses stratified on World Health Organization BMI categories yielded similar estimates. Our results suggest that the metabolic and hormonal changes related to diabetes may play an important role in the etiology of GCA independently from BMI.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B84.
Abstract B86: Changes in social inequalities in male smoking-attributable mortality in two European countries
Authors: Singhal Sonica , Jha Prabhat , Zatonski Witold , Menvielle Gwenn , Boreham Jill , Peto Richard 
Published: January 2011

Abstract
Background: Past studies have assessed trends in smoking prevalence among different social strata in developed countries. However, we know of no study that quantifies changes in social inequalities in smoking-attributable mortality rates over time. The aim of this study was to assess changes in social inequalities for smoking-attributable male mortality rates by educational level between two time periods in France and Poland.
Methods: The contribution of smoking to adult male mortality in each population was estimated indirectly from disease-specific death rates in that population (using absolute lung cancer rates to indicate proportions due to smoking of mortality from certain other diseases). We applied these methods to male death rates at ages 35-69 years from three different social strata in France and Poland, based on a total of 202,779 deaths. The social strata were low, middle, and high based on completed years of education (less than 12 years, 12 years, and more than 12 years, respectively). For France, the comparison periods were 1990-94 and 1995-99; for Poland, 1995 was compared to 2002.
Results: Smoking-attributable mortality rates were 3 to 6 times higher in the lowest education group as compared to the highest education group in both countries. In France, smoking-attributable mortality rates within each education group remained similar between 1990-94 and 1995-99. Between 1995 and 2002, Poland showed a reduction in smoking-attributable mortality rates by 15%, 4%, and 52% in the low, middle, and high education group, respectively.
Conclusion: Although men in the lowest education group in France were around four times more likely to die from smoking as compared to those in the highest education group, there was little change between the periods studied for this country. While smoking-attributable mortality rates in the highest education group of Polish males decreased much more compared to the lower education groups; declines were seen in all education groups. Mortality rates from more recent years, when tobacco control efforts have accelerated in both countries, will be of interest to confirm these trends.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B86.
Abstract B87: Cigarette smoking, lifetime exposure to passive smoking, and the risk of non-Hodgkin lymphoma in the California Teachers Study
Authors: Lu Yani , Wang Sophia S. , Reynolds Peggy , Sullivan-Halley Jane , Chang Ellen T. , Clarke Christina A. , Ma Huiyan , Bernstein Leslie 
Published: January 2011

Abstract
Background: Overall, epidemiological studies conducted to date do not support a causal relationship between smoking and non-Hodgkin lymphoma (NHL) risk. However, previous studies did not account for passive smoking in the referent group of never smokers, which may have masked subtle effects. We therefore examined the effects of cigarette smoking and passive smoking on NHL risk in the prospective California Teachers Study (CTS) cohort.
Methods: The CTS collected lifetime smoking and household passive smoking exposures in 1995 and lifetime passive smoking exposures in three settings (household, workplace, and social) in 1997-1998. Multivariable-adjusted relative risks (RRs) and 95% confidence intervals (CI) were estimated by fitting Cox proportional hazards models for NHL risk with follow-up through 2007.
Results: Compared to never smokers, ever smokers had a 1.11-fold elevated NHL risk (95% CI=0.94-1.30) which increased to 1.22 (95% CI=0.95-1.57) when women with household passive smoking were excluded from the reference category. Statistically significant dose-response trends were observed for lifetime cumulative smoking exposures (intensity and pack-years) when women with household passive smoking were excluded from the reference category (both p-trend=0.02). Among never smokers, NHL risk increased with increasing lifetime passive smoking exposure [RR=1.51 (95% CI=1.03-2.22) for more than 40 vs. less than or equal to 5 years, p-trend=0.03]. Both smoking and passive smoking were associated with increased risk of follicular lymphoma, but not other NHL subtypes.
Conclusion: Our study provides evidence that smoking and passive smoking may play a role in NHL etiology, particularly for follicular lymphoma. Studies evaluating the effect of smoking should consider the effects of passive smoking.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B87.
Abstract B88: Smoking and survival after breast cancer diagnosis: Role of molecular subtype, body mass index, and menopausal status
Authors: Braithwaite Dejana , Tammemagi Martin , Moore Dan H. , Hiatt Robert A. , Nair Seena , Caan Bette 
Published: January 2011

Abstract
Background: Cigarette smoke has been found to affect the metastatic potential of tumor cells and stimulate angiogenesis but its effect on survival among women diagnosed with breast cancer remains poorly understood.
Methods: In a cohort of 2265 multiethnic women diagnosed with breast cancer between 1997 and 2000 and followed for the median of 9 years, we examined whether smoking affected death from breast cancer, non-breast cancer-related causes and all causes. Proportional-hazards models were used to determine whether smoking was associated with time to death while taking into account baseline age, education, body mass index, tumor characteristics and adjuvant treatment. All statistical tests were two-sided.
Results: There were 164 deaths from breast cancer and 120 deaths from non-breast cancer causes during the median follow up of 9 years. Compared with never smokers, women who were current or past smokers had a 39% higher rate of dying from breast cancer [hazard ratio (HR)=1.39, 95% confidence interval (CI) 1.05-1.84] and a two-fold higher rate of dying from competing (non-breast cancer) causes (HR=2.16, 95%CI 1.57-3.00). Subgroup analyses revealed that the adverse effect of smoking on breast cancer survival was highest among women with HER2 negative tumors (HR=1.61, 95%CI 1.12-2.32), body mass index of &lt;25kg/m2 (HR=1.83, 95%CI 1.10-3.04) and postmenopausal status (HR=1.47, 95%CI 1.08-1.99).
Conclusions: In this prospective cohort study, smoking was associated with an important increased in the risk of death from all causes, competing and breast cancer-specific causes independently of clinical, sociodemographic and other lifestyle-related factors. Molecular breast cancer subtype, body mass index and menopausal status modified the effect of smoking on breast cancer-specific survival.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B88.
Abstract B9: Is delayed diagnosis of lung cancer preventable?
Authors: Hassan Wafaa 
Published: January 2011

Abstract
Background: Major efforts have been made worldwide to speed the process of referral for patients with suspected lung cancer. Delay in diagnosis of cancer is recognized as an important factor in the overall outcome of treatment.
Aim: The purpose of this study was to test if the symptom history of patients with operable disease differs from that of patients with inoperable disease.
Methods: 39 men and women recently diagnosed with lung cancer at Assiut University Hospital during the period from August 2009-June 2010 were included in this study. The main outcome measures were the symptoms leading up to a diagnosis of lung cancer in operable and inoperable cases.
Results: Patients recalled having new symptoms for many months, typically over the year before their diagnosis, irrespective of their disease stage once diagnosed.
In the time interval between appearance of the first symptom and operation, a significantly shorter median delay was found for patients with operable and inoperable lung cancer (P=0.028). Concerning the interval from first contact with the healthcare system to operation a significantly shorter median delay was found for the group of patients in operable compared to the inoperable patients (P=0.019).
Conclusion: Our findings, although preliminary, suggest that the widely held view that lung cancer is silent until far advanced may be inaccurate. Encouragement to present early with signs of lung cancer should be considered alongside other efforts to speed up diagnosis and treatment. A few months delay before final treatment of a non-small-cell lung cancer seems to have an impact on the perioperative stage of the cancer, and thereby on the patients prognosis. A screening of asymptomatic risk-group patients will result in recognition of early lung cancer.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B9.