bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 658: Fruit and vegetable intake and cancer incidence in Korean men
Authors: Lee Jung Eun , Kim Dong-Hyun , Ahn Yoon-Ok 
Published: August 2012

Abstract
Few prospective cohort studies have examined the association between fruit and vegetable intake and cancer incidence in Asian population, who consume a diet rich in fruit and vegetable and experience dramatic change in their diet. We investigated whether total fruit intake, total vegetable intake, and total fruit and vegetable intake were associated with risk of incident cancers among 13,563 Korean men during 15 years of follow-up. We used the Cox proportional hazards model to calculate relative risks (RRs) and 95% confidence intervals (CIs) for incident cancers according to fruit and vegetable intake assessed by a validated food frequency-questionnaire. All statistical tests were two-sided. We identified a total of 831 incident cancers. We observed that low intake of total vegetable intake or total fruit and vegetable intake was associated with increased risk of overall cancer incidence. The risk reduction was attributable to increasing intake above a threshold of approximately 100 to 150 g/d. For example, compared with &lt;100 g/d of total fruit and vegetable intake, RRs (95% CIs) for overall cancer risk were 0.74 (0.53-1.02) for 100-&lt;300 g/d, 0.73 (0.53-1.01) for 300-&lt;500 g/d, 0.76 (0.53-1.11) for 500-&lt;600 g/d, and 0.71 (0.51-0.99) for 600 or more g/d. However, when we chose &lt;200 g/d as the referent category, we did not observe the statistically significant associations. In conclusion, our findings suggest that low levels of fruit and vegetable intake could pose an increase in risk of cancer, but the risk could be minimized with modestly increasing intake.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 658. doi:1538-7445.AM2012-658
Abstract 671: Smoking, alcohol consumption and body size measures and risk of B-cell non-Hodgkin lymphoma among women in Los Angeles
Authors: Lu Yani , Wang Sophia , Sullivan-Halley Jane , Cozen Wendy , Bernstein Leslie 
Published: August 2012

Abstract
Background: There are few known causes for non-Hodgkin lymphoma (NHL). The aim of this study is to identify if previous suggested modifiable risk factors (smoking, alcohol consumption and body size measures) are associated with B-cell NHL risk among women. Methods: We conducted a population-based case-control study among women in Los Angeles County consisting of 998 histologically confirmed B-cell NHL patients and 998 individually matched controls (matched on age, race and socioeconomic status). Conditional logistic regression was used to evaluate these associations. Results: Compared to never smokers, current smokers had 51% increased risk of B-cell NHL (odds ratio [OR] =1.51, 95% confidence interval [CI] =1.10-2.09). The risk of B-cell NHL increased with increasing smoking years (P-trend=0.03) and pack-years (P-trend=0.02). This risk pattern was observed for diffuse large B-cell lymphoma (DLBCL), follicular lymphoma, and mantle cell lymphoma although these associations were not statistically significant. Current alcohol consumption decreased B-cell NHL risk (OR=0.75, 95% CI=0.60-0.94) with risk most pronounced among women with moderate lifetime consumption (1-&lt;7 drinks/week). Women who were obese at 5 years before diagnosis had an increased risk of B-cell NHL (OR=1.70, 95% CI=1.28-2.26). Among NHL subtypes, the increased risk was most pronounced for B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) (OR=1.94, 95% CI=1.07-3.52). Conclusions: These findings add to the literature regarding the potential importance of modifiable risk factors and NHL risk. Our results suggest that smoking and obesity may increase NHL risk, but moderate alcohol consumption may reduce NHL risk.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 671. doi:1538-7445.AM2012-671
Abstract 681: Prognostic role of Perp in breast cancer
Authors: Dolfi Sonia C. , Kulkarni Diptee , Lu Shou-En , Chen Chunxia , Moore Dirk , Vazquez Alexei , Harris Sandi , Toppmeyer Deborah , Levine Arnold , Hirshfield Kim M. 
Published: August 2012

Abstract
Perp, a tetraspan plasma membrane protein, is activated by p53 during apoptosis and is also regulated by p63 where it functions as an essential component of the desmosome and contributes to epithelial integrity. A single nucleotide polymorphism (SNP) in Perp was identified by its effect on apoptotic efficiency in irradiated lymphoblastoid cell lines. Therefore, this SNP may have functional significance in clinical outcomes of cancer. In this study, this SNP in PERP was evaluated as a prognostic marker and in its relationship to other known prognostic factors. Genotyping was performed on DNA isolated from peripheral blood of 1020 patients with breast cancer and genotypes were linked with annotated clinical information. Analysis of recurrence free survival was performed on a subset limited to 790 Caucasians. Among Caucasian cases, homozygous SNP genotypes were nearly equally distributed (AA: 25% and GG: 26%). Using a COX proportional hazards survival analysis, the AA genotype was found to be an independent predictor of worse recurrence-free survival (RFS, hazard ratio [HR]: 1.95, 95% CI: 1.38-2.76, p=0.0001). RFS was similar between AG and GG carriers and was more favorable as compared to AA carriers. For patients receiving breast-conserving surgery followed by radiation, patients diagnosed at or above 51 years of age or patients with stage III disease, the deleterious effect of AA genotype on RFS was more significant. In addition, the AA genotype associated with decreased RFS in subgroups of Caucasian cases regardless of stratification by hormone receptor status, HER2 status, and whether they received chemotherapy or hormonal therapy. Adjusting for effects due to stage and chemotherapy, this association remained significant in estrogen receptor positive and progesterone receptor negative cases. We also analyzed the NCI-60 cell line panel for an association between this polymorphism and response to 132 standard chemotherapeutic drugs. A significant association was observed with respect to genotype and response to anti-mitotic agents. Collectively, cell lines with the AA genotype were more sensitive to anti-mitotic agents than the GG genotype. Clinical data suggest that the AA genotype of Perp has a functional phenotype leading to increased risk of recurrence. Further studies are needed to determine the mechanism behind this association, but ultimately this SNP may be useful as a prognostic marker in breast cancer and could be used as a tool to optimize treatment strategies.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 681. doi:1538-7445.AM2012-681
Abstract 684: Identification of biomarker genes associated with endocrine therapy responsiveness in patients with estrogen receptor positive IBC and nIBC
Authors: Van Laere Steven J. , Jansen Maurice PHM , Sas Leen , Sieuwerts Anieta , Vermeulen Peter B. , Berns Els MJJ , Dirix Luc Y. 
Published: August 2012

Abstract
Introduction: Endocrine therapy is a cornerstone in the treatment of patients with Estrogen Receptor (ER) positive (+) breast cancer. Nevertheless, resistance to endocrine treatment, either de novo or acquired, irreversably develops. In this study, we build upon the endocrine therapy resistant phenotype of patients with ER+ Inflammatory Breast Cancer (IBC) to identify and validate predictive biomarkers of endocrine therapy responsiveness. Materials and methods: Expression profiles of 21 ER+ IBC and 42 non-stage matched ER+ nIBC samples were compared using Prediction Analysis of Microarrays. The resulting gene signature was applied onto expression datasets from ER+ nIBC patients with documented intervals of relapse-free survival (RFS) for adjuvant endocrine treatment (GSE17705; N=298) or of progression-free survival (PFS) for first-line endocrine treatment (Jansen dataset (JCO, 2005), N=101). The gene signature classified samples as “IBC-like” or “nIBC-like” and Kaplan Meier and Cox regression analyses were performed. Robust biomarkers for endocrine resistance were selected using permutation analysis and validated using qRT-PCR on a series of samples from 225 ER+ nIBC patients with metastatic disease receiving first-line tamoxifen. Results: We identified a gene signature of 139 unique genes able to discriminate ER+ IBC from ER+ nIBC samples (sensitivity: 100%; specificity: 87.5%). Application of this signature onto data sets of patients with ER+ nIBC revealed significant associations with RFS (HR=1.87, P=0.001) and PFS (HR=2.04, P&lt;0.001) under endocrine therapy. Permutation analysis selected 6 genes robustly discriminating ER+ IBC from ER+ nIBC samples: ABAT, ADAMDEC1, CLEC7A, ETS1, ITK1 and STC2. Expression analysis with qRT-PCR confirmed the predictive value of ADAMDEC1 (HR=1.127, P=0.020), ABAT (HR=0.779, P&lt;0.001) and STC2 (HR=0.866, P&lt;0.001) in 225 patients with ER+ breast cancer treated with Tamoxifen. Ingenuity Pathway Analysis revealed an intricate network linking each of the core genes with ER-, NFkB- and TGFβ-signalling. Conclusion: In this study we identified and validated a gene signature predictive of response to endocrine therapy in patients with breast cancer by comparing ER+ IBC samples to ER+ nIBC samples. Within this gene signature, ADAMDEC1, ABAT and STC2 were identified as robust markers for endocrine therapy responsiveness.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 684. doi:1538-7445.AM2012-684
Abstract 686: Warburg effect in mammary atypia from high-risk women
Authors: Seewaldt Victoria L. , Hoffman Abigail , Ibarra-Drendall Catherine 
Published: August 2012

Abstract
Background: Aggressive cancers are known to consume glucose avidly and produce lactic acid (rather than fully metabolize glucose via the Tricarboxylic Acid (TCA) cycle). This shift toward lactate production, even in the presence of adequate oxygen, is termed the Warburg effect. The Warburg effect is thought to be a late event in breast cancer, however, our studies in high-risk women provide evidence that the Warburg effect occurs during cancer initiation. This is an important observation as glucose-signaling can be readily targeted for breast cancer prevention with minimal toxicity. Here we investigated the role of the Warburg effect in breast cancer initiation in young high-risk women. Methods and Results: Similar to fluorodeoxyglucose, 2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose (2-NBDG) is a fluorescent glucose analog that can be used to track glucose uptake and glycolysis. 2-NBDG spectroscopy provides a means to track glucose metabolism in live mammary epithelial cells from high-risk women. We used 2-NBDG spectroscopy to measure glucose uptake in ER- breast cancer and live atypical mammary epithelial cells from high-risk premenopausal women. We observe that both triple-negative breast cancer and a subset of atypia exhibits accumulation of 2-NBDG. There is growing recognition that phosphoprotein signaling networks (rather than single genes) play a key role in breast cancer initiation and progression. Our team used Reverse Phase Proteomic Microarray (RPPM) profiling to test for activation of phosphoprotein signaling networks in atypical RPFNA cytology from high-risk premenopausal women in our cohort. RPFNA were obtained from two independent sets of 39 and 38 high-risk premenopausal women; 45% of these women were African American. The signaling network most highly expressed in precancerous cells contained activated signaling proteins associated with the Warburg effect (AKT/mTOR/PI3K), insulin signaling (pACC, IRS1) and epithelial to mesenchymal transition (EMT) IL6/Stat3/vimentin. Conclusions: This is the first evidence that abnormal glucose uptake and the Warburg effect occurs during breast cancer initiation in high-risk premenopausal women. These studies demonstrate our ability to identify abnormal glucose and activated signaling networks associated with the Warbug effect in atypical mammary cells from high-risk women.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 686. doi:1538-7445.AM2012-686
Abstract 689: Validation of antibodies to Estrogen Receptor ≤ and quantitative assessment of ERα1 and ERα5 expression in breast cancer
Authors: Wimberly Hallie , Murphy Leigh C. , Haffty Bruce , Rimm David 
Published: August 2012

Abstract
INTRODUCTION: Estrogen receptors are members of the nuclear hormone receptor family that play an important role in breast carcinogenesis and response to endocrine therapy. Though the role of ERα in breast cancer has been studied extensively, little is known about the alternative isoform ERα. ERα has significant sequence homology to ERα but is located on a different chromosome and maintains both overlapping and unique functional attributes. Five variants resulting from alternative splicing of the C-terminal region of ERα exist. The relevance of ERα variants in breast cancer outcomes and response to therapy is difficult to assess because of conflicting results in the literature, likely due to variable methods used to assess ERα in patient tumors. METHODS: Antibodies against ERα variants (ERα1: ThermoScientific PPG5/10; ERα2/cx: Serotec Clone 57/3; ERα5: Serotec Clone 5/25) were validated for staining specificity by siRNA knockdown of ESR2 as well as staining reproducibility on FFPE tissue by quantitative immunofluorescence (QIF) using AQUA technology (HistoRx). QIF staining of validated antibodies was then assessed on two separate breast cancer cohorts. RESULTS: ERα1 and ERα5, but not ERα2/cx, antibodies were found to be sensitive, specific and reproducible, as shown by reduction in signal after siRNA knockdown in cell lines and reproducible QIF scores on a set of breast cancer control cases. ERα1 and ERα5 expression is significantly associated in both cohorts examined (R*2=.224, p&lt;0.0001). However, ERα1 does not show significant association with patient outcome or response to endocrine therapy. In contrast, ERα5 is associated with worse recurrence free survival (log rank p=0.0500) and, though it shows no association with response to tamoxifen, it predicts response to chemotherapy (log rank p=0.0393). CONCLUSIONS: Validation of ERα antibodies reveals that not all reagents are specific for the expected isoforms. Assessment of breast cancer cohorts using validated reagents show that ERα1 is not associated with outcome while ERα5 is both prognostic and predictive.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 689. doi:1538-7445.AM2012-689
Abstract 694: Characterization of a novel monoclonal antibody to Glia maturation factor-beta showing significant clinical utility in the identification of breast carcinoma
Authors: Alper Ozgul M. , Chen Cui P. , Akoa Achille , Herrmann Marille , Alper Ozge 
Published: August 2012

Abstract
Background: Glia maturation factor beta (GMF-beta) is a growth and differentiation factor of brain cells, stimulation of neural degeneration and inhibition of proliferation of tumor cells. It was recently found to involve in the progression of serous ovarian carcinoma. In the present study, we generated a novel antibody against human GMF-beta and investigated the potential of GMF-beta as a biomarker in breast cancer. Methods and findings: We generated a novel monoclonal antibody (mAb), AB-GMF-beta using hybridoma technology and native protein as an immunogen. This mAb is of IgG1 (kappa) type. It specifically recognized both native and denatured human GMF-beta protein and displayed high affinity as assessed by ELISA, immunohistochemistry assay, western blot and flow cytometry applications. Using this mAb in competitive ELISA, we showed for the first time that soluble GMF-beta level is significantly increased in metastatic breast cancer patients’ plasma which directly correlated with GMF-beta expression pattern in metastatic breast cancer tissues. Tissue expression of GMF-beta was determined by using immunohistochemical techniques. Seventy normal and 241 breast cancer tissues were included which consist of 194 ductal and 47 lobular carcinoma samples. Most of normal tissues showed negative or weak nuclear staining, while different levels of nuclear, and diffuse and weak cytoplasmic staining were observed in cancer sections. To evaluate the immunoreactivity of GMF-beta associated with tumor histological types, the staining intensity in nucleus were scored as 0, 1+, 2+ and 3+. Grade 0 and 1+ were defined as negative and 2+ and 3+ as positive. Forty four percent of ductal carcinomas showed strong staining whereas it is significantly increased to 72.3% in lobular tumors (p&lt;0.001). Conclusion: The novel AB-GMF-beta mAb showed high performance in blood and tissue assays. The circulating GMF-beta levels and expressions in breast tissues are significantly increased in breast cancer patients in comparison of normal controls. The increased tissue expressions in breast carcinoma associate with histological tumor types. Our data suggest the potential clinical use of GMF-beta as a biomarker for diagnosis and prognosis in blood and tissue as well as a therapeutic target.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 694. doi:1538-7445.AM2012-694
Abstract 696: Loss of ALCAM function as a biologic basis for ethnic disparity in breast cancer
Authors: Tan Fang , Mosunjac Marina , Adams Amy L. , Ofori-Acquah Solomon 
Published: August 2012

Abstract
Breast cancer affects African American women at a lower frequency than Caucasian women, yet progression of the tumor and mortality from the disease is higher among African Americans. The genetic and molecular contributions to this ethnic disparity are poorly understood. Activated leukocyte cell adhesion molecule (ALCAM) is a junctional adhesive molecule tethered at sites of cell-cell contact in epithelia, mesenchymal, neuronal, and connective tissues. Loss of ALCAM function, due to reduced transcript levels, and low membrane localization, is associated with increased mortality, and poor response to adjuvant therapy in breast cancer. In the current study, we tested the hypothesis that this phenomenon contributes to the ethnic disparity in breast cancer in the US. We studied cases of breast cancer in Atlanta among African American (n=90) and Caucasian (n=104) women. Immunohistochemical staining was used to study ALCAM expression in tumor and non-tumor adjacent breast tissues. Clinicopathological variables including histologic tumor grade, tumor size, lymph node involvement, estrogen receptor (ER), progesterone receptor (PR), and HER2-neu status were abstracted, and their relationship to ALCAM expression was analyzed. Membranous ALCAM (mALCAM) expression correlated significantly with tumor grade, with poorly differentiated tumors showing low ALCAM staining. In addition, mALCAM correlated positively with ER status (African American: p=0.0013; Caucasian: p=0.0008) and PR status (African American: p=0.025; Caucasian: p=0.0027) in both ethnic groups; however, there were no associations between ALCAM expression and tumor size, lymph node involvement, or HER2-neu status. Tumor expression of mALCAM in Caucasians was significantly higher than in African Americans (p&lt;0.0001), while there was no difference in expression of cytoplasmic ALCAM between the two groups. To our knowledge, this is the first study to examine ALCAM expression in African American breast cancer, and to compare this phenotype with Caucasians. Our results indicate that markedly lower ALCAM expression may contribute to the poor prognosis of breast cancer among African Americans. Future studies will examine the genetic basis of this variation.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 696. doi:1538-7445.AM2012-696
Abstract 699: The prognostic value of DNA polymerase ≤ for breast cancers
Authors: Liu Xiyong , Zhang Hang , Loera Sofia , Huang Yasheng , Deng Xutao , Liu Zheng , Zhang Suzhan , Chen Lirong , Zheng Shu , Chu Peiguo , Chou Kai-Ming , Yen Yun 
Published: August 2012

Abstract
DNA polymerase eta (Pol β, POLH) is a eukaryotic DNA polymerase involved in DNA repair by translesion synthesis. To address whether Pol ≤ impacts breast cancer survival, we conducted a retrospective outcome study on 145assessable cases of breast cancers collected from affiliated hospital of Zhejiang University (ZJU set). The results were validated on six published microarray data sets (1,154 cases) with pathoclinical and follow-up information. In the ZJU set, the protein levels of Pol ≤ were determined by IHC. The specificity of antibody against Pol ≤ was validated by using peptide blocking assay. It was shown that protein expression level of Pol ≤ positively correlates with cell proliferative marker Ki-67 (trends P=0.019). The Kaplan-Meier analysis revealed that Pol ≤ was significantly related that better overall survival in breast cancer patients who received chemotherapy or radiotherapy (Log rank p=0.003). Multivariate COX analysis further confirmed that the hazard ratio (HR) of Pol ≤ for overall and progress-free survival were 0.23(95% CI 0.05-0.95) and 0.32(0.11-0.96). Further stratification analysis demonstrated that Pol ≤ prognoses better survival in Luminal A and B molecular subtypes (HR=0.155 95% CI 0.04-0.62), but not HER 2 Positive or Triple negative breast cancer. Above findings were further validated in public microarray database. In Ivshina's dataset, the increase of POLH mRNA was significantly and negatively related with lymphnode involvement in a dose-dependent manner (trend p=0.044). The Kaplan-Meier analysis also revealed that the mRNA levels of POLH was significantly related to progress-free survival of breast cancer. In Chin's data, multivariate COX analysis also revealed that the HR increased significantly as with increase of POLH mRNA levels (HR= 0.22 95% CI 0.03-0.86, highest quartile vs. lowest quartile). Above findings suggested that the protein and mRNA expression levels of Pol ≤ prognoses better survival in breast cancer, especially in Luminal A or B breast cancers.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 699. doi:1538-7445.AM2012-699