bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A05: Menopausal vasomotor symptoms and mammographic density in the Study of Women's Health Across the Nation
Authors: Hart Vicki , Sturgeon Susan , Reich Nicholas , Sievert Lynnette Leidy , Crawford Sybil , Gold Ellen , Habel Laurel , Reeves Katherine W. 
Published: October 2015

Abstract
Background: Declines in endogenous estrogen during menopause have been linked to the onset of menopausal vasomotor symptoms (VMS) and to reduced breast cancer risk. Percent mammographic density (PMD) is viewed as a marker for breast cancer susceptibility. Establishing a relationship between VMS and PMD may justify future prospective investigations of VMS and breast cancer risk.
Methods: We investigated this association in the Study of Women's Health Across the Nation (SWAN) Mammgraphic Density Substudy (N=833). Women were pre- or perimenopausal at enrollment and followed through menopause. VMS were assessed at annual SWAN visits. PMD was ascertained from routine screening mammograms. A linear mixed effects model was used to evaluate the longitudinal association between VMS and PMD.
Results: Women contributed a total of 4,748 mammograms (2-10 per woman) over a median 5.4 years. We observed no overall association between VMS and PMD. When stratified by menopausal status, VMS was associated with lower PMD among perimenopausal women (β = -1.29%, 95%CI -2.58, -0.001) and those with unknown menopausal status due to hormone use during the study period (β = -3.62%, 95%CI -7.17, -0.07). VMS was not associated with absolute dense area in any analyses. Among women who transitioned to postmenopausal, VMS was not associated with change in PMD across the menopausal transition.
Conclusion: Although our findings do not suggest a strong association between VMS and PMD, we observed a significant effect among perimenopausal women and those using hormones during menopause.. Further prospective studies are needed to establish a relationship between VMS and breast cancer risk, and to ascertain the extent to which this relationship may be mediated by PMD.
Citation Format: Vicki Hart, Susan Sturgeon, Nicholas Reich, Lynnette Leidy Sievert, Sybil Crawford, Ellen Gold, Laurel Habel, Katherine W. Reeves. Menopausal vasomotor symptoms and mammographic density in the Study of Women's Health Across the Nation. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr A05.
Abstract A34: Association of nut consumption and lung cancer risk in a large population-based case-control study
Authors: Lam Tram Kim , Consonni Dario , Pesatori Angela , Bertazzi Pier Alberto , Landi Maria Teresa 
Published: October 2015

Abstract
Background: Increased nut consumption has been associated with a reduced risk of major chronic diseases, including type 2 diabetes mellitus, gallstone disease, and colon cancer. However, the association between nut consumption and lung cancer risk is unclear.
Methods: We investigated the association of nut consumption (walnuts, hazelnuts, almonds, or peanuts) with lung cancer risk in the Environment And Genetics in Lung cancer Etiology (EAGLE), a population-based case-control study. Primary lung cancer cases (n= 2101) were enrolled within the Lombardy region of Italy and matched (on gender, residence, and age) to randomly selected controls (n = 2120). Diet was assessed in 1903 cases and 2073 controls. Multivariable odds ratios (ORs) and 95% confidence intervals (CIs) for sex-specific quintiles of intake were calculated using unconditional logistic regression, adjusted for putative confounders including smoking.
Results: Nut consumption was negatively associated with lung cancer risk (ORQ5-VS-Q1 = 0.72; 95% CI: 0.56-0.92; p-trend =0.014); the association did not change marginally after additional adjustment for consumption of fruits and vegetables (ORQ5-VS-Q1 = 0.74, 95% CI = 0.58-0.95, p-trend = 0.028).
Conclusion: In summary, dietary nut consumption was associated with reduced risk of lung cancer in EAGLE.
Citation Format: Tram Kim Lam, Dario Consonni, Angela Pesatori, Pier Alberto Bertazzi, Maria Teresa Landi. Association of nut consumption and lung cancer risk in a large population-based case-control study. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr A34.
Abstract A40: Multiple locations on 8q24 and 6p21-22 and rare variants associated with gastric cancer susceptibility in a Korean population
Authors: Kim Jeongseon , Park Boyoung , Lee Jeonghee , Cho Young Ae , Woo Hae Dong , Jeong Seung Hwa , Choi Il Ju , Kim Young Woo , Kim Young Woo , Kim Young Woo 
Published: October 2015

Abstract
To efficiently identify genetic susceptibility variants for gastric cancer, including rare coding variants, we performed an exome chip-based array study in 329 gastric cancer cases and 683 controls. We found that a linkage disequilibrium (LD) block containing 2 significant variants in PSCA gene increased the risk and two blocks that included 15 suggested variants including TRIM31, TRIM 40, TRIM 10, and TRIM26 regions, and included one suggested variant and OR2H2 gene showed protective associations with gastric cancer susceptibility. In addition, the PLEC region (rs200893203), FBLN2 region (rs201192415), and EPHA2 region (rs3754334) were associated with increased susceptibility (allele-specific odds ratios (OR)=12.65, 95% confidence interval (CI)=2.82–56.69, P=2.0×10-5; OR=7.40, 95% CI=2.43 – 22.58, P=3.8×10-5; OR=6.49, 95% CI=2.34–18.01, P=4.1×10-5, respectively). Among them, rs200893203 and rs201192415 were classified as rare variants with a minor allele frequency &lt; 1%. 8q24 and 6p21-22 regions where aggregate LD blocks and suggested variations were possible susceptibility regions for gastric cancer and warrant further investigation.
Citation Format: Jeongseon Kim, Boyoung Park, Jeonghee Lee, Young Ae Cho, Hae Dong Woo, Seung Hwa Jeong, Il Ju Choi, Young Woo Kim, Young Woo Kim, Young Woo Kim. Multiple locations on 8q24 and 6p21-22 and rare variants associated with gastric cancer susceptibility in a Korean population. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr A40.
Abstract B18: Thrombospondin-1 regulates carcinogenesis in an in vivo model of colorectal cancer
Authors: Pantoja David R. Soto , Torres Maria E. , Sipes J. Michael , Morris Nicole , Roberts David D. , Emenaker Nancy J. 
Published: October 2015

Abstract
According to the National Cancer Institute more than 140,000 people will be diagnosed in the United States with colorectal cancer this year alone. The adenomatus polyposis coli (APC) gene is frequently mutated in colorectal cancer, the APC-min mouse correspondingly is a widely used model for the study of this type of cancer. Studies indictate that the matricellular protein Thrombospondin 1 (TSP1) is lost during progression of colon cancer. To study the role of TSP1 in this disease we generated APC-min and TSP-/- APC-min mice. Our data indicates that expression of TSP1 in the APC-min mouse prevents the development of adenomas in the large intestine in mice fed a low fat diet. On the other hand lack of TSP1 increases tumor multiplicity in these mice, and up-regulates Ki67 in intestinal tissue. Moreover TSP-/- APC-min mice show 50% reduction in survival when compared to TSP+/+APC-min mice alone. Here we show that ADD1/SREBP1 a key transcription factor linking changes in nutritional status of certain genes that regulate systemic energy metabolism is upregulated only in the TSP null APC min/+ animals indicating and association with increased tumor aggressiveness. Together this data indicates that TSP1 regulates progression of colon carcinogenesis and define molecular targets of TSP1 in the prevention of colorectal cancer.
Citation Format: David R. Soto Pantoja, Maria E. Torres, J. Michael Sipes, Nicole Morris, David D. Roberts, Nancy J. Emenaker. Thrombospondin-1 regulates carcinogenesis in an in vivo model of colorectal cancer. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr B18.
Abstract B19: Malfunction and mutation of airway stem/progenitor cells in preneoplastic bronchial dysplasia
Authors: Ghosh Moumit , Nakachi Ichiro , Keith Robert L. , Merrick Daniel T. , Franklin Wilbur A. , Miller York E. 
Published: October 2015

Abstract
Squamous cell lung cancer (SCC) is the second leading cause of lung cancer death in the US with a 5-year survival rate of 16.8%. Since most SCC is diagnosed at a late stage, chemoprevention or early detection could improve survival. SCC develops through a series of histological alterations including dysplasia and carcinoma in situ. Previous studies have identified genetic changes in epithelial progenitor cells in dysplastic lesions. The goal of this project is to establish a correlation between specific genetic changes in epithelial progenitors and their function. A tissue stem cell is a progenitor cell that is capable of long-term self-renewal as well as differentiation to all the cell-types that make up a specific tissue and therefore is multipotential. Because the normal function of a progenitor cell is to repair and regenerate a native epithelium after injury, histologic changes in dysplasia led us hypothesize that “normal function of airway progenitors is altered in dysplasia”. To address this hypothesis we purified and established clonal cultures of basal progenitors from normal, moderate and severely dysplastic biopsies and compared their self-renewal and differentiation abilities. These analyses revealed that the self-renewal capacity of progenitor cells decreased as dysplasia grade increased. The progenitors from normal biopsies differentiated to all three cell-types (basal, secretory or mucin-secreting and ciliated) of the airways. In contrast, progenitors from dysplasia generated increased numbers of basal cells (p&lt;0.05) and lacked secretory (p&lt;0.001) and ciliated cells (p&lt;0.001), suggesting that multipotential differentiation is impaired in dysplasia. Genetic analyses of dysplastic lesions and cultured dysplastic progenitors (n=4, histology grade ≥ 5.5) identified several mutations (p53, Notch 1, 2 and 3, FBXW7, and FGFR1) that have been previously reported in SCC. Thus, we demonstrate that we are able to culture airway stem/progenitor cells that recapitulate both the phenotypic and mutational characteristics of the lesions from which they originate. We propose that understanding the effect of these mutations in altered progenitor function will help to devise prevention as well as early detection strategies.
Citation Format: Moumit Ghosh, Ichiro Nakachi, Robert L. Keith, Daniel T. Merrick, Wilbur A. Franklin, York E. Miller. Malfunction and mutation of airway stem/progenitor cells in preneoplastic bronchial dysplasia. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr B19.
Abstract B27: RIP1 maintains DNA integrity and cell proliferation by regulating PGC-1α-mediated mitochondrial oxidative phosphorylation and glycolysis
Authors: Chen Wenshu , Wang Qiong , Bai Lang , Chen Weijie , Wang Xia , Tellez Carmen S. , Leng Shuguang , Padilla Mabel T. , Nyunoya Toru , Belinsky Steven A. , Lin Yong 
Published: October 2015

Abstract
In the presence of ample oxygen, cancer cells prefer glycolysis to mitochondrial respiration for energy supply. This metabolic alteration, known as the Warburg effect or aerobic glycolysis, has been shown to contribute to cancer cell proliferation. However, how this glucose metabolism pathway is precisely regulated remains elusive. Receptor-interacting protein 1 (RIP1) is an important cellular signaling molecule that plays a pivotal role in the regulation of cell death, survival and proliferation. However, the role of RIP1 in cell metabolism is unclear. To investigate the function of RIP1 in lung cancer cell proliferation, we established stable RIP1 knockdown lung cancer cell lines using lentivius-mediated shRNA expression. RIP1 knockdown inhibited the proliferation of lung cancer cells, which was associated with DNA damage-induced p53 activation. Compared with control cells, the RIP1 knockdown cells had higher glucose consumption and lactate production, indicating a higher glycolytic rate. The increased glycolysis lowered the cellular level of nicotinamide adenine dinucleotide (NAD+), a cofactor essential for DNA damage repair. By microarray profiling and promoter reporter assays, we determined that RIP1 positively regulates the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), a key factor involved in the regulation of mitochondrial function. The downregulation of PGC-1α reduced the expression of components of electron transfer chain that impaired oxidative phosphorylation, which underlays the increased glycolysis in RIP1 knockdown cells. Moreover, RIP1 knockdown cells were more sensitive to both DNA damage anticancer agents and glycolysis inhibitors. Our data suggest that while aerobic glycolysis within a certain range favors cancer cell proliferation, excessive glycolysis may cause cytostasis. Thus, maintenance of glycolysis by RIP1 is critical to cancer cell energy homeostasis and DNA integrity, which may be exploited for anticancer therapy.
Citation Format: Wenshu Chen, Qiong Wang, Lang Bai, Weijie Chen, Xia Wang, Carmen S. Tellez, Shuguang Leng, Mabel T. Padilla, Toru Nyunoya, Steven A. Belinsky, Yong Lin. RIP1 maintains DNA integrity and cell proliferation by regulating PGC-1α-mediated mitochondrial oxidative phosphorylation and glycolysis. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr B27.
Abstract CN05-02: Exploiting aspirin's mechanism of action for combination chemoprevention
Authors: Chan Andrew T. 
Published: October 2015

Abstract
In human populations, aspirin has emerged as the agent with the most consistently observed chemopreventive effect on cancer, particularly of the colorectum. Remarkably consistent data demonstrating aspirin's efficacy have accumulated from prospective studies and randomized controlled trials conducted for the prevention of polyp recurrence, hereditary colorectal cancer, cardiovascular disease, and overall cancer. In addition, there are now convincing data supporting an association between aspirin use and lower risk of metastases and improved survival among colorectal cancer patients. This substantial evidence base has stimulated interest in the molecular underpinnings of aspirin's mode of action. Although a complete understanding of aspirin's anti-cancer mechanism remains elusive, several interrelated biological pathways have been uncovered which appear to, at least in part, mediate aspirin's effect on both tumor initiation and progression. These include fundamental pathways of prostaglandin synthesis and Wnt signaling, offering additional molecular targets for chemopreventive intervention that may enhance aspirin's effectiveness and/or reduce its associated toxicities. In this presentation, we will provide an update on investigation into the mechanistic basis of the effect of aspirin on cancer with a focus on potential molecularly-targeted strategies for combinatorial chemoprevention.
Citation Format: Andrew T. Chan. Exploiting aspirin's mechanism of action for combination chemoprevention. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr CN05-02.
Abstract CN08-01: Air pollution and cancer: Implications of IARC's causal classification
Authors: Samet Jonathan M. 
Published: October 2015

Abstract
This presentation will identify the main lessons learned from the extensive analysis and discussion of the carcinogenicity of outdoor air and describe potential areas for future research. The IARC classification of “outdoor air pollution” and “particulate matter air pollution” as carcinogenic to humans are based on a broad research foundation, but nonetheless there are important gaps to be addressed. For example, research is needed to understand more specifically the components of the air pollution mixture that drive cancer risk, in part to develop useful indicators for control and tracking. Further information is needed on potential determinants of susceptibility to lung cancer caused by air pollution and on the combined effect of smoking and air pollution. Most importantly, this presentation will also cover the implications of the IARC evaluation for public health, including regulatory, societal, and personal actions that, collectively, could improve global public health. Outdoor air pollution now constitutes a cause of cancer to which most people are exposed, and understanding of underlying mechanisms implies that there is no threshold below which there is no risk. Risk assessment will likely play a critical role in considering air quality standards to protect the public from the cancer risk posed by outdoor air pollution.
Citation Format: Jonathan M. Samet. Air pollution and cancer: Implications of IARC's causal classification. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr CN08-01.
Abstract CN12-03: Epigenetic targets of sulforaphane and epigallocatechin gallate in cancer prevention
Authors: Tollefsbol Trygve , Li Yuanyuan 
Published: October 2015

Abstract
Interest in cancer epigenetics has arisen from the fact that epigenetic processes affect many aspects of tumor formation and progression. The reversibility of epigenetic changes that may arise in early tumorigenesis is an important aspect of their potential in approaches for cancer prevention. Many of the components of the human diet have bioactive effects that lead to reversal of epigenetic aberrations in cancer. We have found that both (-)-epigallocatechin-3-gallate (EGCG) from green tea and sulforaphane (SFN) from cruciferous vegetables are able to down-regulate telomerase in breast cancer cells. This occurs through epigenetic modifications of the promoter region of hTERT, the gene that encodes the catalytic subunit of telomerase. Since telomerase promotes tumor formation and is active in about 90% of cancers, this epigenetic inhibition of its catalytic subunit gene may have considerable potential in breast cancer prevention. Our studies also indicate that these bioactive dietary compounds are able to convert estrogen-receptor (ER)-negative breast cancer cells to ER-positive breast cancer cells and to prevent the formation of highly lethal ER-negative breast cancer. This occurs through epigenetic modifications of the ERalpha gene in response to EGCG and SFN. These findings have significance in that ER-positive cells are amenable to breast cancer prevention or therapy with compounds such as tamoxifen while ER-negative cells confer few preventive or treatment options for patients. Moreover, our studies have also indicated that EGCG and SFN have additive or synergistic epigenetic effects on cancer prevention and that the oral administration of green tea polyphenols and SFN-rich broccoli sprouts inhibits the formation of breast cancer in mice. These results are important because the combination of these dietary products may have potential in lowering their efficacious consumption and increase their utility for breast cancer prevention in humans.
Citation Format: Trygve Tollefsbol, Yuanyuan Li. Epigenetic targets of sulforaphane and epigallocatechin gallate in cancer prevention. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr CN12-03.
Abstract PL01-01: Meet your microbiome: An introduction to the who, what, and how of mixed microbial communities
Authors: Hollister Emily B. 
Published: October 2015

Abstract
The human microbiome is comprised of the bacteria, archaea, fungi, protists, and viruses that live in and on our bodies. It is estimated that the microbial cells that comprise your individual microbiome outnumber your own cells by a factor of 10 and that their collective gene content outnumbers your own by a factor of 100. Although scientists and physicians have appreciated the diversity of our “fellow travelers” for decades, our ability to count, study, and categorize our microbes was long limited by the challenges associated with their culture in the laboratory. The utilization of high-throughput sequencing platforms, development of new and improved bioinformatics resources, and the introduction of other ‘omics technologies have shed new light on the composition and function of the human microbiome. The NIH-sponsored Human Microbiome Project characterized the microbial communities of hundreds of healthy individuals in an attempt to define the “healthy” microbiome at various sites throughout the body, and other projects have examined the human microbiome under varying states of disease and health. Microbiome and metagenomic studies have revealed that microbes may contribute to metabolic disorders, inflammatory bowel disease, heart disease, and cancer; and emerging evidence from mouse models suggests a strong link between gut microbiome composition and brain development and behavior. Microbiome and metagenomic studies have also demonstrated that our microbiota may confer protective or beneficial effects, and the depletion or loss of these “good” microbes may leave us susceptible to disease or infection. This talk will introduce the concept of the human microbiome, discuss the techniques that are used to characterize the structure and function of mixed microbial communities, and highlight recent findings from the literature.
Citation Format: Emily B. Hollister. Meet your microbiome: An introduction to the who, what, and how of mixed microbial communities. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PL01-01.