bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 5288: Perception of barriers and facilitators to hepatitis B virus screening, vaccination, and treatment care among Asian American physicians
Authors: Estrella Patricia , Yeh Ming Chin , Tan Yin , Fang Carolyn Y. , Golub Sarit A. , Ma Grace X. 
Published: July 2017

Abstract
Objective: To examine practices and factors affecting Hepatitis B Virus (HBV) screening, vaccination, and treatment among Asian-American physicians in New York City.
Methods: Members of the Chinese American Independent Practice Association (CAIPA) will be recruited to participate in a comprehensive survey, developed based on prior research, to assess physicians’ practice in HBV screening, vaccination and treatment. This study will also examinebarriers/facilitators toward HBV prevention and treatment in knowledge, familiarity or awareness of guidelines, perception, attitude/behaviors, self-efficacy, motivation, patient factors, cultural, and environmental factors. A bivariate analysis and multivariate regressions will be conducted to evaluate factors that predict study outcomes.
Results: We hypothesize that Asian American physicians are more likely to screen for HBV, but are experiencing many barriers unique to the Asian American physicians that are leading them improperly perceive certain patients not at risk for HBV infection. Furthermore, we anticipate finding significant key barriers and facilitators among Asian American physicians for HBV screening and vaccination and treatment towards Asian patients. Preliminary findings will be presented at the conference.
Conclusions & Implications: Asian/Pacific Islanders (APIs) are disproportionally affected by chronic hepatitis B. Therefore, identifying chronically infected persons and linking them to care is crucial. As a result of the reverence of the doctors, a cultural norm prevalence within the Asian community, physicians are uniquely positioned to improve HBV screening and vaccination rates and if necessary, recommend linkage to care. This study will fill in an important gap in creating a culturally-relevant, physician-focused intervention to improve HBV care and reduce the burden of HBV infection within the Asian community.
Citation Format: Patricia Estrella, Ming Chin Yeh, Yin Tan, Carolyn Y. Fang, Sarit A. Golub, Grace X. Ma. Perception of barriers and facilitators to hepatitis B virus screening, vaccination, and treatment care among Asian American physicians [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 5288. doi:10.1158/1538-7445.AM2017-5288
Abstract 5289: Assessment of environmental influences, behavioral risk factors and genetic differences among a cohort of 819 African American community members
Authors: Bucci Jacquelyn , Yeh Ming Chin , Navder Khursheed , Erblich Joel , Blackman Elizabeth , Ma Grace X. , Ragin Camille 
Published: July 2017

Abstract
Objectives: This study was designed to address genetic, environmental and lifestyle risk factors for cancer in populations of African Ancestry. We have established a non-cancer control registry which involves the collection of epidemiological, lifestyle, culture and cancer prevention behaviors (such as cancer screening and diet, etc).
Methods: Data was coded and analyzed using Stata from initial study surveys.
Results: At analysis, the cohort consisted of 819 participants. The cohort was 65.9% female, ages 18-89 (23.5% within 50-59 age group), 35.9% college graduates, and 17.4% with income level $20,000-$25,000. Two-thirds of the cohort had BMI greater than 25, indicating overweight or obese. When stratified by country of birth, participants born in the US & Territories were more likely to be current smokers (23.3%) and have higher rates of environmental exposure to smoking than any other region of birth analyzed. Participants from US & Territories had the highest access to health care (85.9%). Pap smears were the only screening test with statistically significant difference between the regions, with US & Territories having the highest rates of screening (p &lt; 0.001).
Conclusions & Implications: Overall, the cohort and its data provide researchers with a resource to further investigate health disparities in cancer as well as other chronic diseases and tailor culturally relevant education materials to help decrease the rates of cancer in this vulnerable population.
Citation Format: Jacquelyn Bucci, Ming Chin Yeh, Khursheed Navder, Joel Erblich, Elizabeth Blackman, Grace X. Ma, Camille Ragin. Assessment of environmental influences, behavioral risk factors and genetic differences among a cohort of 819 African American community members [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 5289. doi:10.1158/1538-7445.AM2017-5289
Abstract 530: The role of EGFR in c-fos-dependent osteosarcoma formation
Authors: Linder Markus , Glitzner Elisabeth , Srivatsa Sriram , Shahrouzi Parastoo , Bakiri Latifa , Dumanic Monika , Mitterhauser Markus , Wagner Erwin F. , Sibilia Maria 
Published: July 2017

Abstract
The Epidermal Growth Factor Receptor (EGFR) is overexpressed or mutated in human carcinomas and glioblastomas, which are tumors of epithelial and glial origin, respectively. Some publications indicated that EGFR overexpression could occur in human osteosarcomas (OS). Using EGFR knockout mice (Egfr-/-), we have recently shown that EGFR plays a role in bone development and osteoblast function, raising the possibility that EGFR is also involved in OS formation. Here we show that Egfrf/f Runx2-Cre mice (EgfrΔOb), lacking the EGFR in osteo-chondroprogenitor cells, develop an increased zone of hypertrophic chondrocytes in long bones and decreased bone formation. When bred to c-fos transgenic mice (H2-c-fosLTR) that develop osteosarcomas with 100% penetrance, EgfrΔOb mice show reduced tumor incidence and burden. At the molecular level, tumors from EgfrΔOb mice exhibit decreased expression levels of c-Fos and Cyclin D1. In vitro experiments in primary bone tumor cells further show that EGFR inhibition leads to reduced proliferation and increased apoptosis. Importantly, Egfr and c-Fos also play an important role in human OS, as co-expression of both proteins in tumor sections correlated with significantly reduced survival in patients suffering from primary OS. Taken together our data suggest an essential role of EGFR signaling during both development and progression of c-Fos-dependent OS and newly identified molecular targets currently under investigation will be presented.
Citation Format: Markus Linder, Elisabeth Glitzner, Sriram Srivatsa, Parastoo Shahrouzi, Latifa Bakiri, Monika Dumanic, Markus Mitterhauser, Erwin F. Wagner, Maria Sibilia. The role of EGFR in c-fos-dependent osteosarcoma formation [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 530. doi:10.1158/1538-7445.AM2017-530
Abstract 5301: Cancer causation: rethinking the role of analogy
Authors: Weed Douglas L. 
Published: July 2017

Abstract
Introduction. Fifty years has passed since the publication of Austin Bradford Hill’s classic paper on causal inference. Much has changed in the biomedical and public health sciences regarding cancer causation during that half century, but Hill’s considerations (often called “criteria”) remain durable. That said, there is a curious phenomenon involving Hill’s seminal work that has escaped the attention of the scientific community. His consideration of analogy—the last on his list just after experimentation—has all but disappeared. The purpose of this paper is to rethink and resurrect analogy as an important consideration in causal inference in environmental epidemiology.
Methods. Given that this is a conceptual—non-quantitative—project, the methods used are the informal logic of scientific thinking, methods of systematic reviews, and judgment.
Results. In contemporary epidemiology, analogy is either completely ignored (e.g. in many textbooks), equated with biologic plausibility or coherence, or aligned with the scientist’s imagination. None of these examples, however, capture Hill’s description of analogy which emphasizes the contrast of two bodies of evidence. Coupled with developments in the methods of systematic assessments of evidence—including but not limited to meta-analysis—analogy can be restructured as a key component of causal inference. For theoretical support see similar methods in biomedical ethics and artificial intelligence. Practical examples will be discussed.
Conclusions. Analogical reasoning—an updated version of analogy—can emerge assuming the following developments: (1) a collection—a library—of known cases of causal inference (i.e. bodies of evidence involving established causal relationships), including, for example, the assessments of the International Agency for Research on Cancer (IARC) and the National Toxicology Program (NTP), (2) a systematic process for describing the key features of a causal relationship creating paradigm cases, and (3) an objective comparison of a “new” body of evidence for a putative causal relationship with a relevant paradigm case.
Citation Format: Douglas L. Weed. Cancer causation: rethinking the role of analogy [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 5301. doi:10.1158/1538-7445.AM2017-5301
Abstract 5306: p16INH4a status helps predict clinical outcome of dysplasia in the oral cavity irrespective of HPV status
Authors: Lubpairee Tarinee , Prigge Elena , Doeberitz Magnus von Knebel , Reuschenbach Miriam , Zhang Lewei , Rosin Miriam P. 
Published: July 2017

Abstract
Objectives: p16INK4a is a key gatekeeper for multiple biological processes that are associated with protection from cancer, including cell cycle control and senescence. Elevated expression of this gene is strongly correlated with biological activity of HPV infection and cancer development in uterine cervix and tonsil. Although HPV DNA has been found in a small portion of oral cavity cancers and dysplasia, the relevance of its presence to cancer development at this site is unclear, as is the significance of an expression change in p16INK4a as a predictor of HPV status, tissue behavior and outcome.
Methods: Formalin-fixed, paraffin-embedded biopsies from 164 patients with mild, moderate and severe oral dysplasia in the “Oral Cancer Prediction Longitudinal study” (OCPL), British Columbia, Canada, were analyzed for HPV DNA using a semi-quantitative viral load Luminex technology. Expression of p16INK4a was assessed and categorized into 3 staining patterns (diffuse, focal, and negative).
Results: HPV DNA was found in 13 (8%) lesions, 7 had HPV-16 infection and 1 HPV-18. Of the 164 samples, diffuse p16INK4a expression was present in 18%, focal in 56% and no p16 staining in 23% of samples. There was no significant correlation between HPV DNA-positivity and p16INK4a staining. Different p16 staining patterns showed significantly different progression rates (P &lt; 0.0001): progression occurred in 1/92 (1.1%) focally stained, 1/29 (3.5%) diffusely stained and 10/43 (23.3%) with no staining.
Conclusion: HPV DNA-positivity occurs in a small proportion of oral dysplasia but is poorly associated with p16INK4a expression. Future assessment of these samples for HR-HPV oncogene transcripts will provide information on its biological activity. The low likelihood of progression of p16INK4a focally stained lesions suggests a value of this marker in identification of low-risk cases.
Acknowledgements: Supported by Else Kröner-Fresenius-Stiftung Foundation, Germany
Citation Format: Tarinee Lubpairee, Elena Prigge, Magnus von Knebel Doeberitz, Miriam Reuschenbach, Lewei Zhang, Miriam P. Rosin. p16INH4a status helps predict clinical outcome of dysplasia in the oral cavity irrespective of HPV status [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 5306. doi:10.1158/1538-7445.AM2017-5306
Abstract 5307: Analysis of volatile organic compounds for the diagnosis of lung cancer
Authors: Inoue Takuya , Takagi Hironori , Owada Yuki , Watanabe Yuzuru , Fukuhara Mitsuro , Yamaura Takumi , Muto Satoshi , Okabe Naoyuki , Matsumura Yuki , Hasegawa Takeo , Manami Takeda , Sato Atsushi , Suzuki Hiroyuki 
Published: July 2017

Abstract
Background: Lung cancer is the leading cause of cancer-related deaths in the world. The prognosis of lung cancer depends on disease detection at an early stage. Recently, effectiveness of lung cancer screening by using low dose computed tomography scanning have been showing. However, it still has problems such as cost of screening and radiation exposure. Thus, less invasive and cost beneficial lung cancer screening procedure would be needed. In this context, several study to understand the efficacy of molecules from expiration of patients as a lung cancer screening were showing, but it was still controversial. In this study, we investigated to determine whether volatile organic compounds (VOC) from patients could be used for the detection for lung cancer by using novel small and unique absorbent material named MonoTrap .
Method: The subjects’ gas was collected from skin and exhaled breath in a MonoTrap (GL sciences), and the VOCs were analyzed by gas chromatography/ mass spectrometry (GC/MS). First of all, we preliminary analyzed for both sample from skin and exhaled breath for 12 patients and 11 healthy volunteers to clarify which samples were more sensitive to diagnose lung cancer. Subsequently, each VOC was determined in detail for 7 healthy individuals and 4 lung cancer patients and these values were statistically analyzed.
Results: By preliminary study, characteristics of VOC derived from skin were significantly correlated with cancer condition as compared with healthy volunteer by using comprehensive multivariate analysis. Therefore, we performed further quantitative analysis by targeting unique individual molecules derived from skin. In VOCs from skin, Mann-Whitney U test showed that 4-hydroxy-4-methyl-2-pentanone, hexadecane, and acetamide were significantly higher in lung cancer patients (p=0.036, p=0.006, p=0.036, respectively).
Conclusion: In this study, we found that 3 kinds of VOCs could be a potential diagnostic biomarkers of lung cancer. Further prospective study is now planning to validate these data using large number samples.
Citation Format: Takuya Inoue, Hironori Takagi, Yuki Owada, Yuzuru Watanabe, Mitsuro Fukuhara, Takumi Yamaura, Satoshi Muto, Naoyuki Okabe, Yuki Matsumura, Takeo Hasegawa, Takeda Manami, Atsushi Sato, Hiroyuki Suzuki. Analysis of volatile organic compounds for the diagnosis of lung cancer [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 5307. doi:10.1158/1538-7445.AM2017-5307
Abstract 5314: Long-term folate intake and prostate cancer risk in the health professionals follow-up study
Authors: Hamieh Nadine M. , Batista Julie L. , Markt Sarah C. , Downer Mary K. , Mucci Lorelei A. , Stampfer Meir J. , Giovannucci Edward L. , Wilson Kathryn M. 
Published: July 2017

Abstract
Background: Randomized trials of supplemental folate and observational studies of circulating folate support a positive association with prostate cancer risk. However, epidemiological studies of dietary and synthetic folate intake are conflicting. Given mandatory folic acid fortification of grains in the US beginning in 1998, evaluation of long-term folate intake from natural and synthetic sources in relation to prostate cancer risk is warranted.
Methods: We examined the association between folate intake and prostate cancer risk among 47,884 men in the Health Professionals Follow-up Study who were free from diagnosed cancer at baseline in 1986. Total, natural (from food sources), and synthetic (from supplements/fortification) folate intake was assessed every 4 years using a validated food frequency questionnaire, and categorized as the cumulative average and lagged (0-4, 4-8, 8-12, and 12-16 years in the past) intakes. Cox proportional hazards regression was used to calculate multivariable hazard ratios (HRs) and 95% confidence intervals (CI).
Results: We identified 6,186 incident prostate cancer cases from 1986-2012, including 1,078 with lethal disease (distant metastasis or death). Mean total folate intake was 481 µg/day in 1986 and increased to 671 µg/day by 2010. The proportion of men meeting the recommended intake of 400 µg/day increased from 47% in 1986 to 74% after fortification began in 1998. Folate intake was positively correlated with physical activity, multivitamin use, and PSA testing, and inversely correlated with smoking. Total folate intake averaged over time was not significantly associated with total prostate cancer risk: HR≥800 vs. 400-599=1.03 (95% CI: 0.95-1.13, p-trend=0.76). Neither natural nor synthetic folate intake was associated with risk of total prostate cancer. No associations were observed between total, natural, or synthetic folate intake and risk of lethal, advanced stage, or high-grade disease.
Conclusions: Our findings do not support strong associations between intakes of total, natural, or synthetic folate and prostate cancer risk. We found no indication that folate intake of ≥800 µg/day (twice the recommended level) increases prostate cancer risk.
Citation Format: Nadine M. Hamieh, Julie L. Batista, Sarah C. Markt, Mary K. Downer, Lorelei A. Mucci, Meir J. Stampfer, Edward L. Giovannucci, Kathryn M. Wilson. Long-term folate intake and prostate cancer risk in the health professionals follow-up study [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 5314. doi:10.1158/1538-7445.AM2017-5314
Abstract 5320: Folate and other nutrients related to one-carbon metabolism and risk of melanoma
Authors: Dhana Ashar , Yen Hsi , Li Tricia , Holmes Michelle , Qureshi Abrar , Cho Eunyoung 
Published: July 2017

Abstract
Background: Nutrients involved in one-carbon metabolism - folate, vitamins B6 and B12, methionine, choline, and betaine - have been associated with multiple cancer sites. However, no study has assessed the association between these nutrients and risk of melanoma. Thus, the aim of this study was to evaluate the association between intake of these nutrients and melanoma risk within two prospective cohorts: the Nurses’ Health Study (NHS) and Health Professionals Follow-up Study (HPFS).
Methods: The cohorts included a total of 81,685 women in the NHS (1984 to 2010) and 49,617 men in the HPFS (1986 to 2010). We assessed nutrient intakes using a semi-quantitative food frequency questionnaire every 2 to 4 years. Total nutrient intake included both dietary and supplemental intake. Dietary intake included intake from food only. Study physicians reviewed medical and pathological records to confirm self-reported cases of invasive melanoma. We used Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) and then pooled the HRs for both cohorts using a random effects model.
Results: Over 24 to 26 years of follow-up, we documented 1,321 cases (641 men and 680 women) of invasive melanoma. Higher intake of folate from food only, but not total folate, was associated with increased risk of melanoma. The pooled multivariable HRs for the top versus bottom quintiles were 1.17 (95 % CI: 0.98-1.41; P for trend = 0.17) for total folate and 1.37 (95 % CI: 1.13-1.65; P for trend = 0.001) for folate from food only. The association was statistically significant in men, but not in women. Higher intake of vitamins B6 and B12, choline, betaine, and methionine was not associated with risk of melanoma.
Conclusion: We found some evidence that folate from food only, but not total folate, was associated with a modest increased risk of melanoma - a finding that warrants further investigation. Conversely, our findings suggest that other nutrients involved in one-carbon metabolism do not play an important role in the etiology of melanoma.
Citation Format: Ashar Dhana, Hsi Yen, Tricia Li, Michelle Holmes, Abrar Qureshi, Eunyoung Cho. Folate and other nutrients related to one-carbon metabolism and risk of melanoma [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 5320. doi:10.1158/1538-7445.AM2017-5320
Abstract 5328: RNF12 inhibits the proliferation of hepatocellular carcinoma through c-Myc and p21
Authors: Nie Meng , Huang Yongsheng , Wang Lin 
Published: July 2017

Abstract
Purpose: RNF12/RLIM, a RING E3 ubiquitin ligase, plays an important role in the epigenetic regulation of sex-specific nurturing tissues in female mice. Recently, a few studies demonstrated a correlation between RNF12 and the proliferation of multiple cancers. The role of RNF12 in hepatocellular carcinoma is incompletely understood. The purpose of this study is to investigate the effect of RNF12 on the proliferation of human hepatocellular carcinoma cells. RNF12 is also known to interact with a number of nuclear proteins, including CLIM, HDAC2, and Smad4. We also explored whether c-Myc and p21, an oncogene and tumor suppressor essential to liver tumorigenesis, were affected by RNF12.
Methods: Immunohistochemistry of RNF12 and c-Myc was performed on surgically dissected human hepatocellular carcinoma tissues. The soft-agar cloning, flow cytometry and Transwell invasion assays were carried out to investigate the role of RNF12 in SK-Hep1 cell proliferation, cell cycle and invasiveness. Real-time quantitative PCR and Western blotting were used to examine the mRNA and protein levels of RNF12 and related proteins in SK-Hep1 cells.
Results: We found that the level of RNF12 was lower in hepatocellular carcinoma, compared with the surrounding non-cancerous tissues, while the c-Myc expression was higher. Using a SK-Hep1 cell line stably expressing RNF12, we showed that RNF12 over-expression inhibited cell proliferation and induced cell cycle arrest at G1 phase. Furthermore, we showed that RNF12 over-expression decreased the level of oncoprotein c-Myc, while not much affecting its mRNA level. Co-immunoprecipitation demonstrated that RNF12 and c-Myc associated with each other, suggesting a direct protein-protein interaction. RNF12 over-expression also markedly increased the mRNA and protein levels of p21, a tumor suppressor and the downstream target of p53, c-Myc and many other cancer-related regulators. Consistently, silencing of RNF12 reduced p21 mRNA and protein levels and increased c-Myc protein.
Conclusion: Our study demonstrated reduced expression of RNF12 in hepatocellular carcinoma, and RNF12 over-expression inhibited the proliferation and cell cycle progression of SK-Hep1 cells. Mechanistically, RNF12 may directly regulate the level of c-Myc, similarly as other transcription factors such as CLIM and Smad4. The mechanisms underlying the increased expression of p21 is being investigated. Taken together, RNF12 may serve as a tumor suppressor in hepatocellular carcinoma, partly through oncoprotein c-Myc and tumor suppressor p21.
Note: This abstract was not presented at the meeting.
Citation Format: Meng Nie, Yongsheng Huang, Lin Wang. RNF12 inhibits the proliferation of hepatocellular carcinoma through c-Myc and p21 [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 5328. doi:10.1158/1538-7445.AM2017-5328