bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1872: Plasma carotenoids and breast cancer risk in the Cancer Prevention Study II Nutrition Cohort
Authors: Wang Ying , Gapstur Susan M. , Gaudet Mia M. , Furtado Jeremy D. , Campos Hannia , McCullough Marjorie L. 
Published: August 2015

Abstract
Background: Several plasma carotenoids have been inversely associated with postmenopausal breast cancer risk in large cohort studies and a pooled analysis. Whether associations differ by tumor or participant characteristics is unclear. We investigated the associations of plasma carotenoids with postmenopausal breast cancer risk overall and by estrogen receptor (ER) status, tumor stage, smoking status and body mass index in a case-control study nested in the Cancer Prevention Study II Nutrition Cohort.
Methods: A total of 561 breast cancer cases diagnosed between blood draw in 1998-2001 and June 30, 2007 and matched 1:1 with controls on race, birth date and blood draw date were included. Multivariable-adjusted conditional and unconditional logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs).
Results: Plasma α-carotene was inversely associated with breast cancer risk even after adjustment for total fruit and vegetable intake (4th vs. 1st quartile OR = 0.58, 95% CI: 0.40, 0.85, P-trend = 0.03). This inverse association was stronger among ever smokers (P-interaction&lt;0.05), and obese women (P-interaction = 0.02), but did not differ by tumor stage (P-heterogeneity = 0.61). Although there was an inverse trend between α-carotene and ER+ (P-trend = 0.01) but not ER- breast cancer (P-trend = 0.99), the test for heterogeneity by ER status was not statistically significant (P-heterogeneity = 0.28). There was some evidence of an inverse association with total carotenoids but this association was nonlinear.
Conclusions: These results suggest that higher plasma α-carotene is associated with lower risk of breast cancer, and this association was even stronger in smokers and obese women.
Citation Format: Ying Wang, Susan M. Gapstur, Mia M. Gaudet, Jeremy D. Furtado, Hannia Campos, Marjorie L. McCullough. Plasma carotenoids and breast cancer risk in the Cancer Prevention Study II Nutrition Cohort. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1872. doi:10.1158/1538-7445.AM2015-1872
Abstract 1876: Adolescent and mid-life diet: risk of pancreatic cancer in the NIH-AARP Diet and Health Study
Authors: Moy Kristin A. , Potischman Nancy , Thompson Frances E. , Subar Amy , Ruder Elizabeth H. , Thiebaut Anne C.M. , Stolzenberg-Solomon Rachael Z. 
Published: August 2015

Abstract
Background: To date, the data concerning diet and pancreatic cancer risk has focused on diet assessed during adulthood. Given the long latency period of this malignancy, examining diet during adolescence and midlife may shed light on the diet - pancreatic cancer association. Methods: We examined the associations between diet at ages 12-13 years, 10 years before baseline (ages 40-61 years), and the joint effects of both with risk of pancreatic cancer in the NIH-AARP Diet and Health Study. Six months after baseline, 303,094 individuals (175,991 men and 127,103 women) completed two 37-item food frequency questionnaires that assessed diet at ages 12-13 years and 10 years previously. Cox proportional hazards regression was used to estimate smoking, body mass index, and diabetes adjusted multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) for pancreatic cancers (n = 1,322 by the end of 2006). Results: Comparing highest to the lowest tertile (T3 vs. T1), carbohydrate intake at age 12-13 (HR (95% CI): 0.86 (0.75, 0.98), P-trend = 0.06) and 10 years before baseline (HR (95% CI): 0.87 (0.76, 1.00), P-trend = 0.05) were inversely associated with pancreatic cancer. Intake of total fat at ages 12-13 (HR (95% CI): 1.15 (1.00, 1.33), P-trend = 0.07) and 10 years before baseline (HR (95% CI): 1.18 (1.03, 1.35), P-trend = 0.02) were positively associated with risk. High intake of fat in both adolescence and midlife was positively associated with risk (HR (95% CI): 1.32 (1.08, 1.62)). Calcium intake 10 years before baseline was associated with reduced risk (T3 vs T1 HR (95% CI): 0.88 (0.77, 1.00), P-trend = 0.05) as was changing from low intake in adolescence to high intake in midlife (HR (95% CI): 0.71 (0.54, 0.93)). Solid fat (butter and margarine) intake 10 years before baseline was associated with increased risk (T3 vs T1 HR (95% CI): 1.23 (1.06, 1.42), P-trend = 0.005) as was consumption of solid fats at both time points (HR (95% CI): 1.31 (1.08, 1.60)). Conclusion: Diet during adolescence and midlife may play a role in the etiology of pancreatic cancer.
Citation Format: Kristin A. Moy, Nancy Potischman, Frances E. Thompson, Amy Subar, Elizabeth H. Ruder, Anne C.M. Thiebaut, Rachael Z. Stolzenberg-Solomon. Adolescent and mid-life diet: risk of pancreatic cancer in the NIH-AARP Diet and Health Study. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1876. doi:10.1158/1538-7445.AM2015-1876
Abstract 1889: Paleolithic and Mediterranean diet pattern scores and their associations with biomarkers of inflammation and oxidative balance
Authors: Whalen Kristine , McCullough Marji , Flanders W. Dana , Hartman Terryl J. , Judd Suzanne , Bostick Roberd M. 
Published: August 2015

Abstract
Chronic inflammation is associated with poor diet quality as well as risk for cancer and other chronic diseases. A diet-inflammation association may relate to evolutionary discordance. We investigated associations of two diet pattern scores, the “Paleolithic” and the Mediterranean, with circulating levels of two inflammation-related biomarkers, C-reactive protein (CRP), an acute inflammatory protein, and F2-isoprostanes, a reliable marker of lipid peroxidation in vivo, in a colonoscopy-based, pooled case-control study of incident sporadic colorectal adenomas (N = 646). We created diet scores from responses on a modified Willett food-frequency questionnaire, and measured plasma levels of CRP and F2-isoprostanes by ELISA and GCMS, respectively. Both diet scores were calculated and categorized into quintiles, and their associations with the biomarker levels were estimated using unconditional logistic regression. The multivariable-adjusted odds ratios (OR) comparing those in the highest relative to those in the lowest quintiles of the Paleolithic and Mediterranean diet scores, were, respectively, 0.73 (95% confidence interval [CI] 0.39, 1.36; Ptrend = 0.35) and 0.71 (95% CI 0.36, 1.40; Ptrend = 0.12) for CRP levels, and 0.35 (95% CI 0.17, 0.74; Ptrend &lt;0.01) and 0.64 (95% CI 0.29, 1.40; Ptrend = 0.03) for F2-isoprostanes levels. These findings, which are particularly strong for the inverse Paleolithic diet score-F2-isoprostanes association, suggest that diets that are more “Paleolithic-” or Mediterranean-like may be associated with lower levels of systemic inflammation and oxidative stress.
Citation Format: Kristine Whalen, Marji McCullough, W. Dana Flanders, Terryl J. Hartman, Suzanne Judd, Roberd M. Bostick. Paleolithic and Mediterranean diet pattern scores and their associations with biomarkers of inflammation and oxidative balance. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1889. doi:10.1158/1538-7445.AM2015-1889
Abstract 1925: Streamlined analysis and interpretation of RNA editing variants from melanoma cancer samples
Authors: Joecker Anika , Yip Rupert , Arens Anne , Oester Bodil , Basset Douglas , Macy Bryant 
Published: August 2015

Abstract
Of special interest in a clinical setting is the identification and interpretation of somatic variants from the DNA of a tumor/normal matched pair.
Studies have shown that a large proportion of variants present in DNA are not present in the RNA and vice versa due to RNA-Editing and other unknown molecular processes1. In addition, recent publications show that RNA-editing plays an important role in cancer2,3. These findings can have strong implications for clinical diagnostics where the correct identification and interpretation of somatic variants from tumor/normal matched samples is essential.
We took a published Whole Trancriptome/Whole Exome Sequencing dataset of tumor and peripheral blood from two patients with uveal melanomas5. We looked for somatic variants present in the RNA, but absent in the DNA using CLC Cancer Research Workbench. A strong mutation signature for C-T, A-G changes was found, which result from Adenosine to Inosine changes, a typical RNA-Editing event, which was recently published to be common in human and is mediated by ADAR proteins.
By running Ingenuity Variant Analysis directly from CLC Cancer Research Workbench we found RNA-Editing found in these two patients is highly associated with cancer and more specifically with Melanoma directly. Some of the variants directly associated with Melanoma were classified as likely pathogenic and were not described in COSMIC, but present in Ingenuity's large Knowledge Base.
1) Widespread RNA and DNA Sequence Differences in the Human Transcriptome. Mingyao Li, Isabel X. Wang, Yun Li, Alan Bruzel, Allison L. Richards, Jonathan M. Toung, and Vivian G. Cheung. Science 1 July 2011: 333 (6038), 53-58.
2) RNA editing in RHOQ promotes invasion potential in colorectal cancer. Sae-Won Han et al. J Exp Med 2014 211:613-621.
3) A disrupted RNA editing balance mediated by ADARs (Adenosine DeAminases that act on RNA) in human hepatocellular carcinoma. Tim Hon Man Chan et al.Gut 2014;63:5 832-843
4) A-to-I RNA editing occurs at over a hundred million genomic sites, located in a majority of human genes.Genome Res. March 2014 24: 365-376
5) Harbour JW et al., “Frequent mutation of BAP1 in metastasizing uveal melanomas.”, Science, 2010 Nov 4;330(6009)
Citation Format: Anika Joecker, Rupert Yip, Anne Arens, Bodil Oester, Douglas Basset, Bryant Macy. Streamlined analysis and interpretation of RNA editing variants from melanoma cancer samples. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1925. doi:10.1158/1538-7445.AM2015-1925
Abstract 1927: Evolutionary novel genes expressed in fish tumors determine progressive evolutionary characters
Authors: Matyunina Ekaterina , Emelyanov Alexander , Kozlov Andrei 
Published: August 2015

Abstract
The origin of evolutionary novel genes is connected with the origin and evolution of the novel organismal functions and the increase in morphological complexity of multicellular organisms. Novel gene acquire new or altered functions. Here we describe that evolutionary novel genes, expressed predominantly in transgenic fish tumors after their induced regression, determine progressive evolutionary characters and are conserved in human.
We used a sample of genes, which were activated in inducible krasV12 transgenic zebrafish tumors according to the results of RNASeq data. Genes from our sample were expressed after HCC regression upon kras inactivation. The search of orthologs by different tools, such as blastx and psiblast, with e-value cut off not less than 10-3 and query coverage more than 50%, discovered that considerable proportion of tumor-specifically expressed genes are evolutionary novel, i.e. their orthologs are not found in Lamprey. 63 of these novel genes have orthologs in humans. Gene ontology (GO) data were used to analyze their functions. According to the results of GO some of the genes have functions not characteristic to fish. Among known functions of the human orthologues of evolutionary novel genes of zebrafish (vs. Lamprey) there are some important morphogenetic functions. For example, genes ccdc40, lmx1ba and lepa acquired functions in lung, embryonic utera and placenta, i.e. organs originated in taxa higher than fish. A large proportion of genes from our sample are connected with retina type eye, heart and brain development.
Citation Format: Ekaterina Matyunina, Alexander Emelyanov, Andrei Kozlov. Evolutionary novel genes expressed in fish tumors determine progressive evolutionary characters. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1927. doi:10.1158/1538-7445.AM2015-1927
Abstract 1944: NFκB: Activation by EGF requires TLR4 and activation by LPS requires EGFR
Authors: De Sarmishtha , Zhou Hao , Li Xiaoxia , Stark George 
Published: August 2015

Abstract
In normal cells, quiescent NFκB is activated by inflammatory stimuli, whereas the abnormal constitutive activation of NFκB is important for the survival of most cancer cells. NFκB activation is regulated by several different pathways. Recently we showed that EGFR is an important mediator of NFκB activation, in both non-malignant and malignant cells. We now provide additional mechanistic insight into this pathway by further investigating whether signaling to NFκB in response to EGF depends solely on EGFR, or involves another receptor known to activate NFκB. Knockdown experiments revealed that TLR4 and two downstream components in the canonical TLR4 pathway, MYD88 and TAK1, are all required for EGF-dependent NFκB activation. Conversely, the ability of TLR4 to activate NFκB in response to LPS was impaired by down regulating EGFR expression or by use of the EGFR inhibitor erlotinib. PP2, a general inhibitor of SRC-family kinases, blocked EGF-induced NFκB activation, and the SRC family member LYN became bound to EGFR upon LPS stimulation. Erlotinib blocked this LPS-dependent association, indicating a key role for LYN in EGFR-TLR4 cross signaling. In mice, erlotinib blocked the LPS-induced, NFκB-dependent expression of TNFα and IL-6, indicating that EGFR is essential for LPS-induced NFκB activation in vivo.
Citation Format: Sarmishtha De, Hao Zhou, Xiaoxia Li, George Stark. NFκB: Activation by EGF requires TLR4 and activation by LPS requires EGFR. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1944. doi:10.1158/1538-7445.AM2015-1944
Abstract 1959: 15-lipoxygenase-1 suppression of colitis-associated colon cancer through inhibition of the IL-6/STAT3 signaling pathway
Authors: Zuo Xiangsheng , Mao Fei , Xu Min , Xu Weiguo , Tian Rui , Micheline J. Moussalli Micheline J. , Elias Elias , Li Haiyan S. , Watowich Stephanie S. , Shureiqi Imad 
Published: August 2015

Abstract
The IL-6/STAT3 pathway is a critical signaling pathway for colitis-associated colorectal cancer (CAC). PPAR-delta (PPAR-d), a lipid nuclear receptor, upregulates IL-6. 15-Lipoxygenase-1 (15-LOX-1) is crucial to produce lipid signaling mediators to terminate inflammation. 15-LOX-1 downregulates PPAR-d. 15-LOX-1 effects on IL-6/STAT3 signaling and CAC tumorigenesis are unknown. We here report that intestinally targeted transgenic 15-LOX-1 expression in mice (15-LOX-1-Gut mice) inhibited azoxymethane and dextran sodium sulfate-induced CAC, IL-6 expression, STAT3 phosphorylation, and IL-6/STAT3 downstream target expression (Notch and MUC1). 15-LOX-1 downregulation was associated with IL-6 upregulation in human colon cancer mucosa. Re-expression of 15-LOX-1 in human colon cancer cells suppressed IL-6 mRNA expression, STAT3 phosphorylation, IL-6 promoter activity, and PPAR-d mRNA and protein expression. PPAR-d overexpression in colonic epithelial cells (PPAR-d-Gut mice) promoted CAC tumorigenesis in mice and increased IL-6 expression and STAT3 phosphorylation, whereas concomitant 15-LOX-1 expression in colonic epithelial cells (15-LOX-1-PPAR-d-Gut mice) suppressed these effects [e.g., tumor number per mouse (mean ± SE) was 4.22 ± 0.68 in wild-type littermates, 6.67 ± 0.83 in PPAR-d-Gut mice (p = 0.026), and 2.25 ± 0.25 in 15-LOX-1-PPAR-d-Gut mice (p = 0.0006)]. Identification of 15-LOX-1 suppression of PPAR-d to inhibit IL-6/STAT3 signaling-driven CAC tumorigenesis provides mechanistic insights that can be utilized to molecularly target CAC.
Citation Format: Xiangsheng Zuo, Fei Mao, Min Xu, Weiguo Xu, Rui Tian, Micheline J. Micheline J. Moussalli, Elias Elias, Haiyan S. Li, Stephanie S. Watowich, Imad Shureiqi. 15-lipoxygenase-1 suppression of colitis-associated colon cancer through inhibition of the IL-6/STAT3 signaling pathway. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1959. doi:10.1158/1538-7445.AM2015-1959
Abstract 1977: Elucidating heterogeneity within cancer cell populations using single cell RNA detection
Authors: Weldon Don , Williams Yuko , Koong Victor , Ko Alex 
Published: August 2015

Abstract
As researchers continue to analyze the relationships between gene expression and biological processes involved in the development and progression of cancer, increasing importance is being placed on the study of genetic variation across single cells. However, traditional methods tend to measure RNA expression globally, with cell lysis and fixation steps resulting in a loss of key information about individual cells, making it challenging to properly assay the genetic heterogeneity within cell populations. We demonstrate the use of a single cell RNA detection technology that specifically measures gene expression in live cells without altering their viability or inherent biology. This enables researchers to not only detect heterogeneity within their samples, but also separate, enrich, and further characterize cell subpopulations based on RNA expression variation, when using techniques such as Fluorescent Activated Cell Sorting (FACS).
Here, we describe live cell detection of cancer biomarkers within heterogeneous cell models. First, we co-cultured MCF-7 and SK-BR3 breast cancer cell lines in specific ratios to mimic heterogeneous breast cancer populations. Subsequent characterization of the populations was performed by both flow cytometry using fluorescent live-cell RNA detection probes, and quantitative real-time PCR. Next, we analyzed miR-221 expression in a mixture of T47D and MDA-MB-231 breast cancer cell lines, which allowed us to sort the two cell types based on differential expression of this microRNA and perform downstream immunohistochemical analysis of vimentin and E-cadherin, two protein markers known to be associated with the epithelial-to-mesenchymal transition during tumor progression.
Use of a live cell RNA detection methodology in gene expression experiments allows scientists to formulate novel questions and design experiments that better address the importance of gene expression heterogeneity in normal and disease states, particularly in cancer, where individual cells within the tumor microenvironment may exhibit aberrant RNA expression profiles that render them invasive or metastatic.
Note: This abstract was not presented at the meeting.
Citation Format: Don Weldon, Yuko Williams, Victor Koong, Alex Ko. Elucidating heterogeneity within cancer cell populations using single cell RNA detection. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1977. doi:10.1158/1538-7445.AM2015-1977
Abstract 1987: Molecular characterization of the breast cancer-associated antigen NY-BR-1
Authors: Bitzer Julia , Kosaloglu Zeynep , Halama Niels , Ziegelmeier Claudia , Lerchl Tina , Spille Anna , Pudenz Maria , Koellensperger Eva , Eichmueller Stefan , Osen Wolfram , Schneeweiss Andreas , Marmé Frederik , Zoernig Inka , Jaeger Dirk 
Published: August 2015

Abstract
Breast cancer is one of the most common malignancies with increasing incidence every year and a leading cause of death among women. Although early stage breast cancer can be effectively treated, there are limited numbers of treatment options available for patients with advanced and metastatic disease.
The breast cancer associated antigen NY-BR-1 was identified by a serological screening strategy (SEREX). NY-BR-1 is expressed in the majority (&gt;70%) of breast tumors as well as metastases, in normal breast tissue, in testis, and occasionally in prostate tissue. NY-BR-1 was confirmed as an immunogenic antigen as we could detect NY-BR-1 specific spontaneous humoral and cellular immune responses in several breast cancer patients.
However, biological function, regulatory mechanisms, and interaction partners of NY-BR-1 are still unknown. Therefore, we combined integrative functional analysis (genomics, transcriptomics and epigenetics) and experiments to unravel the transcriptional regulation of NY-BR-1 and to detect its function within the mammary gland.
As numerous binding sites for nuclear hormone receptors (e.g. Estrogen Receptor alpha, Progesterone receptor and Glucocorticoid receptor) and CpG islands were predicted within the promoter sequence of NY-BR-1, primary-tissues from breast reductions or tumor cells obtained from pleural effusions were treated with different hormones (Estradiol, Dexamethasone, Progesterone, Retinoic acid, Vitamin D) or with the HDAC inhibitors Valproic acid, Trichostatin A and the demethylating agent 5´Aza-Deoxycytidine in order to analyze the transcriptional regulation of NY-BR-1.
Additionally, we analyzed the methylation status at various sites within the promoter region of NY-BR-1 using EpiTyper MassARRAY technology and publicly available resources such as the TCGA database. Here, we present preliminary results of our analysis and evaluate their implication for further investigation of NY-BR-1.
Citation Format: Julia Bitzer, Zeynep Kosaloglu, Niels Halama, Claudia Ziegelmeier, Tina Lerchl, Anna Spille, Maria Pudenz, Eva Koellensperger, Stefan Eichmueller, Wolfram Osen, Andreas Schneeweiss, Frederik Marmé, Inka Zoernig, Dirk Jaeger. Molecular characterization of the breast cancer-associated antigen NY-BR-1. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1987. doi:10.1158/1538-7445.AM2015-1987