bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract LB-155: Effects of alcohol consumption, cigarette smoking, betel quid chewing in upper digestive disease: A large cross-sectional study in Taiwan and meta-analysis
Authors: Chuang Yun-Shiuan , Wu Meng-Chieh , Lin Pi-i , Yu Fang-Run , Wang Yao-Kuang , Wu Deng-Chyang , Wu I-Chen , Wu Ming-Tsang 
Published: July 2017

Abstract
Alcohol drinking and cigarette smoking are well-known risk factors of upper digestive diseases, especially esophageal cancer. In Taiwan, betel quid chewing is another common risk factor. This study investigated the association between use of these three substances and upper digestive diseases. We collected data from 9,275 patients (&gt;20 years) receiving esophagogastroduodenoscopy at four hospitals starting in 2008. Multiple imputation was used to handle missing questionnaire data and polynomial regressions were used to analyze the association between risk factors and clinical stage in the esophagus, stomach and duodenum. A random effects model was used to perform a meta-analysis and arrive at overall odds ratio and 95% confidence intervals. Participants who habitually smoked cigarettes, drank alcohol and chewed betel areca simultaneously had a 16.32-fold risk of esophageal cancer (95% CI =7.13-37.36), 2.93-fold risk of Barrette’s esophagus (95% CI =1.99-4.30), 1.59-fold risk of grade A-B erosive esophagitis (95% CI = 1.27-1.98), 1.97-fold risk of gastric ulcer (95% CI =1.50-2.59), 2.10-fold risk of duodenitis (95% CI =1.54-2.87) and 1.27-fold risk of duodenal ulcer (95% CI =1.00-2.69). Using more substances concurrently was associated with a significant trend at higher risk to develop those diseases. Meta-analysis also revealed the use of three substances came with a high risk of esophageal diseases. Our data concluded that cigarette smoking, alcohol drinking and betel quid chewing were associated with upper digestive tract disease. People who habitually used all three substances in Taiwan were at significantly higher risk of developing Barrette’s esophagus and esophageal cancer. This extremely high elevated risk of esophageal cancer alarms the clinical community and proper public health measures must be implemented in the clinical setting when identifying patients with exposure to the three risk factors.
Citation Format: Yun-Shiuan Chuang, Meng-Chieh Wu, Pi-i Lin, Fang-Run Yu, Yao-Kuang Wang, Deng-Chyang Wu, I-Chen Wu, Ming-Tsang Wu. Effects of alcohol consumption, cigarette smoking, betel quid chewing in upper digestive disease: A large cross-sectional study in Taiwan and meta-analysis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-155. doi:10.1158/1538-7445.AM2017-LB-155
Abstract LB-157: Association of aflatoxin and gallbladder cancer in Shanghai
Authors: Koshiol Jill E. , Gao Yu-Tang , Dean Michael , Egner Patricia , Nepal Chirag , Jones Kristine , Wang Bingsheng , Rashid Asif , Lou Wen , Dyke Alison Van , Ferreccio Catterina , Malasky Michael , Shen Ming-Chang , zhu Bin , Andersen Jesper , Hildesheim Allan , Hsing Ann W. , Groopman John 
Published: July 2017

Abstract
Background: Aflatoxin, which is a risk factor for developing hepatocellular carcinoma, may also cause gallbladder cancer (GBC). We hypothesized that GBC patients have higher aflatoxin exposure than gallstone patients.
Methods: We used samples and data from the Shanghai Biliary Tract Cancer Case-control Study conducted from 1997-2001. Of the 267 GBC and 730 gallstone participants with plasma available, 250 GBC patients and 250 controls with gallstones were randomly selected for measurement of aflatoxin B1 (AFB1)-lysine plasma adducts using isotope dilution mass spectrometry. In 54 GBC patients, tumor tissue was examined for the aflatoxin-related R249S TP53 mutation through targeted sequencing.
Results: We calculated age- and sex-adjusted odds ratios (ORs) and 95% confidence intervals (CIs), as well as the population attributable fraction (PAF). AFB1-lysine adduct detection was nearly 3-fold higher in GBC patients (OR, 2.96; 95% CI, 1.90 to 4.61). Among the 85 GBC patients (34%) with detectable AFB1-lysine adduct levels, the median was 4.6 pg/mg, compared to 1.2 pg/mg among the 37 gallstone-patient controls (15%) with detectable levels, and the OR was 9.97(95% CI, 2.73 to 36.44) for quartile 4 versus 1 in GBC compared to gallstone patients. The PAF for cancer related to aflatoxin was 22% (95% CI: 17%-27%). In 54 GBC patients, tumor tissue was examined for the aflatoxin-related R249S TP53 mutation through targeted sequencing, however, all patients were negative for the mutation.
Conclusions: Aflatoxin is significantly associated with GBC, although it does not appear to be correlated with the R249S TP53 mutation in the gallbladder. If aflatoxin is shown to cause GBC, it may have accounted for up to 22% of the gallbladder cancers in Shanghai during the study period and may account for an even higher proportion in high-risk areas. If verified, reducing aflatoxin exposure may reduce GBC incidence.
Citation Format: Jill E. Koshiol, Yu-Tang Gao, Michael Dean, Patricia Egner, Chirag Nepal, Kristine Jones, Bingsheng Wang , Asif Rashid, Wen Lou, Alison Van Dyke, Catterina Ferreccio, Michael Malasky, Ming-Chang Shen, Bin zhu, Jesper Andersen, Allan Hildesheim, Ann W. Hsing, John Groopman. Association of aflatoxin and gallbladder cancer in Shanghai [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-157. doi:10.1158/1538-7445.AM2017-LB-157
Abstract LB-167: A novel metabolite of citrus tangeretin epigenetically inhibits the growth of human prostate cancer cells
Authors: Chao Yen-Hsiang , Su Zheng-Yuan 
Published: July 2017

Abstract
Prostate cancer is the second leading cause of cancer death in men in the United States. Polymethoxyflavonoids (PMFs) such as tangeretin which exclusively exist in citrus fruit peels have been studied to have many bioactivities. In this study, we investigated the inhibitory effect of the metabolites of tangeretin in human prostate cancer LNCaP and PC3 cells. The results showed that PMF1 is a synthetic tangereitin metabolite can significantly inhibits the growth of LNCaP and PC-3 cells (IC50 14.0 and 13.5 µM, respectively) while PMF1 at 15 µM cannot affect the growth of human normal prostate epithelial RWPE-1 cells. The results of the anchorage-independent growth analysis indicated that PMF1 can suppress the colony formation in LNCaP and PC-3 cells as well as LNCaP and PC-3 stem-like cells which were isolated when the parent cells were cultured in the serum-free medium on the ultra-low attached dishes. Furthermore, PMF1 can induce apoptosis in LNCaP cells in which PMF1 increases protein expressions of Bax and Bad and decreases protein expressions of procaspases-3 and Bcl-2. We also found that PMF1 also decreases the protein levels of DNA Methyltransferase 1 and histone deacetylases 1, 2, and 4/5/9. These results suggested that PMF1 might effectively inhibit the growth of human prostate cancer cells as well as prostate cancer stem cells, which provides new insights in the prevention and treatment of prostate cancer.
Citation Format: Yen-Hsiang Chao, Zheng-Yuan Su. A novel metabolite of citrus tangeretin epigenetically inhibits the growth of human prostate cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-167. doi:10.1158/1538-7445.AM2017-LB-167
Abstract LB-172: Chemotherapy impact on the gut microbiota: clinical trial on patients
Authors: Pensec Cindy , Martino Alessandra De , Serres Laure-Anne ,   IMODI consortium, Amouzou Yao , Leuillet Sebastien , campone Mario , Carton Thomas , VACON Françoise LE 
Published: July 2017

Abstract
The French Consortium IMODI (Innovative MODels Initiative) aims to develop predictive preclinical mouse models for new chemotherapeutic treatment discovery, to progress toward personalized medicine. In this consortium, Biofortis Merieux NutriSciences issue is to better understand the relation between gut microbiota and cancer, particularly during chemotherapeutic treatment. Because chemotherapy can lead to disruption in microbiota composition and several side effects, our purpose is to identify and track the impact of chemotherapy treatment on the gut microbiota.
To this aim, we coordinate a clinical study to recruit patients with four types of cancer (breast, ovary, liver and prostate) from 7 clinical centers. Gut microbiota composition is assessed by targeted metagenomic, from patient stool samples, collected before, during and after chemotherapy. The 16S rDNA sequences will be analyzed using an in-house bioinformatic pipeline based on mothur software.
Interestingly, preliminary results from preclinical studies showed that some chemotherapeutic treatments could have an effect on gut microbiota composition associated with weight loss. These results support that microbiota is an important additional parameter for evaluating the efficacy and the toxicity of pharmacological treatments. The clinical study is ongoing to better understand the effect of chemotherapy on the gut microbiota. This approach may lead to beneficial intervention for cancer patients, particularly to minimize side effects and infectious complications.
Note: This abstract was not presented at the meeting.
Citation Format: Cindy Pensec, Alessandra De Martino, Laure-Anne Serres, IMODI consortium, Yao Amouzou, Sebastien Leuillet, Mario campone, Thomas Carton, Françoise LE VACON. Chemotherapy impact on the gut microbiota: clinical trial on patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-172. doi:10.1158/1538-7445.AM2017-LB-172
Abstract LB-176: Extracts of Psidium guajava (guava) and Syzygium samarangense (wax apple) leaves and teas with Nrf2 induction activity protect mouse AML12 hepatocytes from tumor-initiating acetaminophen-induced damage
Authors: Su Zheng-Yuan , Chan Yen-Fan , Chen Pei-Chun , Sung Ping-Hua , Lin Zi-Han 
Published: July 2017

Abstract
The liver is the primary organ responsible for the major detoxifications and metabolic functions in the human body; however, liver carcinogenesis can be triggered by acetaminophen (paracetamol, APAP), a tumor-initiator. Nrf2 is a master regulator to induce the expression of phase II detoxification/antioxidant enzymes. Some of fruit plant leaves in Taiwan have hepatoprotective potential, including Psidium guajava (guava) leaves (GL) and Syzygium samarangense (wax apple) leaves (WAL) as well as the processing guava tea (GT) and wax apple tea (WAT). In this study, we found that water extracts (WE), including GL-WE (250 μg/mL), WAL (250 μg/mL), GT (500 μg/mL), and WAT (500 μg/mL) without cytotoxicity can active Nrf2 pathway at 24 hrs in HepG2-C8 cells which are stably transfected with an antioxidant response element (ARE)-luciferase construct. These extracts also effectively recovered the cell viability of mouse liver AML12 cells with APAP-induced injury when the cells were pretreated with the extracts for 24 hrs and then co-treated with extracts and APAP for another 48 hrs. A better understanding of the mechanisms how these extracts inhibit oxidative stress/inflammation related to APAP-induced liver carcinogenesis in the future would open new avenues of approaches for the prevention of liver cancer in human.
Citation Format: Zheng-Yuan Su, Yen-Fan Chan, Pei-Chun Chen, Ping-Hua Sung, Zi-Han Lin. Extracts of Psidium guajava (guava) and Syzygium samarangense (wax apple) leaves and teas with Nrf2 induction activity protect mouse AML12 hepatocytes from tumor-initiating acetaminophen-induced damage [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-176. doi:10.1158/1538-7445.AM2017-LB-176
Abstract LB-177: Chemopreventive effect of aged citrus peel (Chenpi) extracts against tumor initiator acetaminophen-induced hepatotoxicity through regulating Nrf2 pathway
Authors: Lin Zi-Han , Luo Wan-Tzu , Chan Yen-Fan , Su Zheng-Yuan 
Published: July 2017

Abstract
The liver is a critical organ responsible for the major detoxification and metabolism in the human body. Acetaminophen (APAP) is a widely used analgesic and antipyretic drug, but it has been demonstrated to be a cancer-initiating agent to induce liver cancer. Aged Citrus peel (Chenpi, CP) is a Chinese herb with hepatoprotective potential to be usually used as foods in Taiwan. Three extracts of CP were prepared in this study, including water extract (CP-WE), ethanol extract (CP-EE), and water extraction residue ethanol extract (CP-WREE). Among these extracts, we found CP-WREE (100 μg/mL) can effectively enhance the Nrf2-ARE pathway in HepG2-C8 cell line which is stably transfected ARE-luciferase construct. CP-WREE (50 μg/mL) also exhibit a significant protective effect on the mouse AML12 hepatocytes from APAP-induced damage. We further find that CP-WREE enhances the activity of some glutathione-related enzymes and inhibits lipid peroxidation in AML12 cells. Furthermore, CP-WREE can also increase the expressions of Nrf2 and Nrf2 downstream enzymes while the expressions of some epigenetic modifying enzymes are regulated. Therefore, CP-WREE may have beneficial effects to protect liver carcinogenesis caused by APAP-induced damage through the regulation of Nrf2/antioxidant pathway as well as epigenetic modification.
Citation Format: Zi-Han Lin, Wan-Tzu Luo, Yen-Fan Chan, Zheng-Yuan Su. Chemopreventive effect of aged citrus peel (Chenpi) extracts against tumor initiator acetaminophen-induced hepatotoxicity through regulating Nrf2 pathway [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-177. doi:10.1158/1538-7445.AM2017-LB-177
Abstract LB-191: Combination checkpoint inhibitor therapy: Anti-PD1 and Beta-alethine lead to complete responses of melanoma in a syngeneic mouse model
Authors: Taub Floyd E. , Wright Suzin , Guth Amanda 
Published: July 2017

Abstract
Previously we reported that the combination of anti-PD1 and β-alethine completely stopped cancer growth in a syngeneic mouse melanoma model even under conditions when neither of the drugs had statistically significant effects as a single agent. In order to further examine this dramatic result, we extended the studies, evaluated immune parameters and tested if long-term immunity to re-challenge occurred. Surprisingly, three low doses of anti-PD1, spread over 9 days, were sufficient to allow concurrent and continuing weekly dosing of β-alethine to not only halt tumor growth, but to reverse it. The established melanoma regressed over the subsequent 4-6 weeks. Even more striking was that the short course of anti-PD1, which failed to reduce cancer growth as a single therapy, altered the immune system such that subsequent treatment with β-alethine was effective. β-alethine therapy, beginning eight days after the conclusion of anti-PD1 therapy, when tumors averaged 40 mm2, was sufficient to cause at least stabilization of cancer in all animals and complete response (no palpable tumor on repeated measurements) in the majority of animals. Statistical comparisons of all animals receiving combination therapy (either concurrently or sequentially) with controls resulted in significant differences using ANOVA for tumor size (p=0.005) or X2 tests for tumor presence (p &lt;0.000). No toxicity was noted in treated animals. This is consistent with previous animal and GLP toxicity studies and the completed human Phase I/II trial. The human trial showed that β-alethine, as a single agent, caused no drug-related adverse events and lead shrinkage or stabilization in all patients with lymphoma who were not anergic to recall antigens pre-trial. The final result of re-challenging the mice with the original Cloudman melanoma at a higher dose than the initial cancer inoculation level will be presented.
Citation Format: Floyd E. Taub, Suzin Wright, Amanda Guth. Combination checkpoint inhibitor therapy: Anti-PD1 and Beta-alethine lead to complete responses of melanoma in a syngeneic mouse model [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-191. doi:10.1158/1538-7445.AM2017-LB-191
Abstract LB-202: A novel neoepitope screening platform for generating effective and safe neoantigen-based vaccines and immunotherapeutics in a hepatocellular carcinoma model
Authors: Chao Cheng-chi , Yuan Fengjiao , Liu Geng , Li Guanglei , Li Bo , Lu Lian , Tian Yaomei , Li Dongli , Zhou Bailing , An Ting , Fan Yingzi , Jiang Chongming , Shu Yang , Lin Honggang , Xu Heng , Yang Hanshuo , zhang Rui , Zhang Xueyan , Cheng Zhen , Huang Rong , Dean Michael , Men Ke , Zhang Xiuqing , Yu Chaoheng , Wang Jian , Cheng Shuang , Yang Huanming , Wang Yantai , Hou Yong , Wei Yuquan , Yang Li 
Published: July 2017

Abstract
Immunotherapy has emerged as a novel and promising strategy for cancer treatment, while available markers for immunotherapy have poor effectiveness and safety. The advance of next-generation sequencing (NGS) technology enables us to identify tumor-specific neoantigen which could be more effective and safer for personalized immunotherapy. In this study, we demonstrated a novel workflow for the development of liver cancer personalized vaccine. Xenograft models for liver cancer were built in mice using Hepa1-6 cell lines. Tumor-specific candidate neoantigen were determined by performed whole exome sequencing (WES) and used a comprehensive bioinformatics pipeline integrating multiple factors such as MHCI-binding affinity fold change (FC), variant allele frequencies (VAFs) of somatic mutation, mRNA expression and hydrophobicity of peptides. The results showed that peptide vaccine of Gpr55 neoantigen not only triggered striking neo-antigen specific CD8+ T cell response, but also significantly inhibited the growth of tumors in both prophylactic and therapeutic models. Moreover, our results demonstrated that VAFs and FC were the effective and safety property for immunogenicity. The identified Gpr55 neoantigen was an ideal vaccine for Hepa1-6 induced xenograft models considering the immunogenicity, anti-tumor effect and safety evaluation. It was also possible to identify and develop highly effective personalized cancer vaccine by our workflow within 13 weeks. The results illustrated huge potential of tumor-specific neoantigen as a potent vaccine for clinical tumor therapy and the workflow built in this study could be used to develop more specific, safer, more effective treatments to all types of cancer patients.
Note: This abstract was not presented at the meeting.
Citation Format: Cheng-chi Chao, Fengjiao Yuan, Geng Liu, Guanglei Li, Bo Li, Lian Lu, Yaomei Tian, Dongli Li, Bailing Zhou, Ting An, Yingzi Fan, Chongming Jiang, Yang Shu, Honggang Lin, Heng Xu, Hanshuo Yang, Rui zhang, Xueyan Zhang, Zhen Cheng, Rong Huang, Michael Dean, Ke Men, Xiuqing Zhang, Chaoheng Yu, Jian Wang, Shuang Cheng, Huanming Yang, Yantai Wang, Yong Hou, Yuquan Wei, Li Yang. A novel neoepitope screening platform for generating effective and safe neoantigen-based vaccines and immunotherapeutics in a hepatocellular carcinoma model [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-202. doi:10.1158/1538-7445.AM2017-LB-202
Abstract LB-247: Early detection of gastric cancer using global and gene-specific promoter DNA methylation in endoscopic biopsies
Authors: Pirini Francesca , Noazin Sassan , Arias Martha Jahuira , Rodriguez-Torres Sebastian , Friess Leah , Michailidi Christina , Cok Jaime , Combe Juan , Vargas Goria , Prado William , Soudry Ethan , Perez Jimena , Yudin Tikki , Mancinelli Andrea , Unger Helen , Ili Carmen , Brebi Priscilla , Berg Douglas , Hayashi Masamichi , Sidransky David , Gilman Robert , Guerrero-Preston Rafael E. 
Published: July 2017

Abstract
Clinically useful molecular tools to triage gastric cancer patients are not currently available. We aimed to develop a molecular tool to predict gastric cancer risk in endoscopy-driven biopsies obtained from high-risk gastric cancer clinics in low resource settings. We discovered and validated a DNA methylation biomarker panel in endoscopic samples obtained from 362 patients seen between 2004 and 2009 in three high-risk gastric cancer clinics in Lima, Perú, and validated it in 306 samples from the Cancer Genome Atlas project (“TCGA”). Global, genome wide and gene-specific DNA methylation analyses were used in a Phase I Biomarker Development Trial to identify a continuous biomarker panel that combines a Global DNA Methylation Index (GDMI) and promoter DNA methylation levels of IRF4, ELMO1, CLIP4 and MSC. We observed an inverse association between the GDMI and histological progression to gastric cancer, when comparing gastritis patients without metaplasia (mean= 5.74, 95% CI, 4.97-6.50), gastritis patients with metaplasia (mean= 4.81, 95% CI, 3.77-5.84), and gastric cancer cases (mean=3.38, 95% CI, 2.82-3.94), respectively (p&lt;0.0001). Promoter methylation of IRF4 (p &lt;0.0001), ELMO1 (p &lt;0.0001), CLIP4 (p &lt;0.0001), and MSC (p &lt;0.0001), is also associated with increasing severity from gastritis with no metaplasia to gastritis with metaplasia and gastric cancer. Our findings suggest that promoter methylation of IRF4, ELMO1, CLIP4 and MSC and a GDMI &gt; 4, is a useful molecular tool for gastric cancer risk stratification in endoscopic biopsies.
Citation Format: Francesca Pirini, Sassan Noazin, Martha Jahuira Arias, Sebastian Rodriguez-Torres, Leah Friess, Christina Michailidi, Jaime Cok, Juan Combe, Goria Vargas, William Prado, Ethan Soudry, Jimena Perez, Tikki Yudin, Andrea Mancinelli, Helen Unger, Carmen Ili, Priscilla Brebi, Douglas Berg, Masamichi Hayashi, David Sidransky, Robert Gilman, Rafael E. Guerrero-Preston. Early detection of gastric cancer using global and gene-specific promoter DNA methylation in endoscopic biopsies [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-247. doi:10.1158/1538-7445.AM2017-LB-247