tbuckley/cabot-search huggingface dataset:
MYD88, CD79B, and CD79A Gene Mutations in CD5-Positive Diffuse Large B-Cell Lymphoma
Authors: Toshifumi Takeuchi, Motoko Yamaguchi, Kyoko Kobayashi, Kana Miyazaki, Hiroshi Imai, Ryoichi Ono, Isao Tawara, Tetsuya Nosaka, Kyosuke Tanaka, Naoyuki Katayama
Journal: Blood (2016)
Erratum: Moxifloxacin-containing regimen greatly reduces time to culture conversion in murine tuberculosis (American Journal of Respiratory and Critical Care Medicine (2004) 169 (421-426))
Authors: Jacques H. Grosset, E. L. Nuermberger, T. Yoshimatsu, S. Tyasgi, R. J. O'Brien, A. N. Vernon, R. E. Chaisson, W. R. Bishai
Journal: American Journal of Respiratory and Critical Care Medicine (2005)
Clinical evaluation of hepatitis B core-related antigen monitoring during peginterferon alfa treatment for HBeAg-negative chronic hepatitis B
Authors: M.J. van Campenhout, G.W. van Oord, V. Rijckborst, W.P. Brouwer, P. Ferenci, F. Tabak, M. Akdogan, B. Pinarbasi, K. Simon, M. Raptopoulou-Gigi, R.J. de Knegt, A. Boonstra, H.L. Janssen, B.E. Hansen
Journal: Journal of Hepatology (2017)
Functional promoter SNPs in TGFβ1 and the susceptibility to childhood leukemia
Authors: Jasmine Healy, Helene Belanger, Mathieu Lariviere, Damian Labuda, Daniel Sinnett
Journal: Cancer Research (2007)

AACR Annual Meeting-- Apr 14-18, 2007; Los Angeles, CA

390 

Transforming growth factor β1 (TGFβ1) controls proliferation, differentiation, and other cellular processes in a number of cell types. Not surprisingly, pathological deregulation of the TGFβ pathway has been implicated in the development of several major disease groups, including cancers. In keeping with this paradigm, we proposed that sequence variation in the promoter region of TGFβ1 could potentially lead to abnormal expression and variation in gene dosage, thereby predisposing carriers of such susceptibility variants to disease. Here we screened the proximal promoter region of TGFβ1 for single nucleotide polymorphisms (pSNPs) and performed in silico analysis and in vitro functional assays in conjunction with genetic association studies, in order to assess the functional impact of regulatory polymorphisms in TGFβ1 on the development of leukemia in children. Using denaturing high performance liquid chromatography we identified 4 pSNPs that were common in Europeans and that all lead to either a predicted gain and/or loss of putative transcription factor binding sites. When tested for differential binding by electrophoretic mobility shift assays, two of these pSNPs, -1886A>G and -1550DelAGG, showed differential allelic DNA-protein binding in at least one of the cell lines tested. From these common pSNPs we were able to construct 8 promoter haplotypes and following subcloning into a gene reporter system, we demonstrated that the two major promoter haplotypes significantly influenced transcriptional activity in an allele-specific manner. Moreover, a case-control study conducted in 258 acute lymphoblastic leukemia (ALL) patients and 277 healthy controls combined with a family-based analysis using 147 parental trios, all of European descent, was used to evaluate single site genotypic as well as multilocus haplotypic associations. Interestingly, the family-based association test revealed that the TGFβ1 low-expressing promoter haplotype was associated with an increased risk of ALL and was shown to be significantly over-transmitted to affected offspring ( P = 0.032). Although the biological significance of these observations remains to be elucidated, these findings suggest that the expected variability of TGFβ1 expression levels due to regulatory polymorphisms could indeed influence the risk of childhood leukemia and contribute to carcinogenesis.
Baseline serum ferritin is an independent predictive factor of mortality in patients with chronic hepatitis C after long term follow-up
Authors: C. Jezequel, Z.B. Ali, C. Pronier, A. Rabot, I. Renard, L. Legros, T. Uguen, E. Bardou-Jacquet, C.L. Lan, R. Moirand, P. Houssel-Debry, C. Michelet, V. Thibault, D. Guyader
Journal: Journal of Hepatology (2017)
A Prospective Study of the Impact of Current Poverty, History of Poverty, and Exiting Poverty on Accumulation of Disease Damage in Systemic Lupus Erythematosus
Authors: Edward Yelin, Laura Trupin, Jinoos Yazdany
Journal: Arthritis & Rheumatology (2017)

Objective To estimate the effect of current poverty, number of years in poverty, and exiting poverty on disease damage accumulation in systemic lupus erythematosus (SLE). Methods For this study, 783 patients with SLE were followed up from 2003 to 2015 through annual structured interviews. Respondents were categorized in each year by whether they had a household income of ≤125% of the US federal poverty level. Linear and logistic regression analyses were used to assess the impact of poverty in 2009, number of years in poverty between 2003 and 2009, and permanent exits from poverty as of 2009 on the extent of disease damage (according to the Brief Index of Lupus Damage [BILD] score) or accumulation of a clinically meaningful increase in disease damage (defined as a minimum 2‐point increase in the BILD damage score) by 2015. Results After adjustment for sociodemographic features, health care characteristics, and health behaviors, poverty in 2009 was associated with an increased level of accumulated disease damage in 2015 (mean difference in BILD damage score between poor and non‐poor 0.62 points, 95% confidence interval [95% CI] 0.25–0.98) and increased odds of a clinically important increase in damage (odds ratio [OR] 1.67, 95% CI 0.98–2.85). Being poor in every year between 2003 and 2009 was associated with greater damage (mean change in BILD score 2.45, 95% CI 1.88–3.01) than being poor for one‐half or more of those years (mean change in BILD score 1.45, 95% CI 0.97–1.93), for fewer than one‐half of those years (mean change in BILD score 1.49, 95% CI 1.10–1.88), or for none of those years (mean change in BILD score 1.34, 95% CI 1.20–1.49). Those exiting poverty permanently had similar increases in disease damage (mean change in BILD score 1.30, 95% CI 0.90–1.69) as those who were never in poverty (mean change in BILD score 1.36, 95% CI 1.23–1.50) but much less damage than those who remained in poverty (mean change in BILD score 1.98, 95% CI 1.59–2.38). Conclusion The effects of current poverty, “dose” of poverty, and exiting poverty suggest that poverty plays a critical role in the accumulation of damage in patients with SLE.
Prospective prevalence study of adult NAFLD/NASH utilizing multi-modality imaging compared with liver bopsy
Authors: S.A. Harrison, K.K. Roberts, A.H. Paredes, C. Lisanti, R. Schwope, K.M. Cebe, J.M.A. Whitehead, V. Paradis, P. Bedossa, J.K. Aden
Journal: Journal of Hepatology (2017)
Abstract B44: Emerging targets from Cancer Dependency Map v0.1
Authors: Francisca Vazquez, Aviad Tsherniak, Barbara Weir, Phil Montgomery, Glenn Cowley, Stanley Gill, Gregory Kryukov, Sasha Pantel, Will Harrington, Mike Burger, Robin Meyers, Levi Ali, Amy Goodale, Yenarae Lee, Levi Garraway, Jesse Boehm, David Root, Todd Golub, William Hahn
Journal: Clinical Cancer Research (2017)

Abstract Precision Cancer Medicine requires the identification of vulnerabilities linked to genetic features of tumors. Recent studies utilizing highly annotated small molecule collections to assess dependencies across hundreds of genomically annotated cell lines have demonstrated the potential for such large-scale preclinical “Dependency Map” projects. We have undertaken a complementary approach using genetic perturbation tools (RNAi and CRISPR-Cas9 based loss-of-function viability screens), to systematically catalog preferential genetic dependencies and markers that predict response. These efforts are providing a foundation for the discovery of novel targets poised for early therapeutic discovery projects together with patient populations that may be enriched for responders to such therapies. Here, we present results from our initial Cancer Dependency Map consisting of RNAi loss-of-function screens across 503 cell lines, including both solid and hematopoietic tumors. We discovered 43 genes whose mutation or copy number creates a cancer dependency (oncogene addiction) including a novel dependency on the small GTPase, GNAI2 in Diffuse large B-cell Lymphoma. We discovered 142 genes in which elevated levels of expression create a dependency (gene addiction), a group of genes highly enriched for master regulator transcription factors such as SOX10, SPDEF, PAX8 and HNF1B. We discovered 474 genes for which hemizygous copy number creates a dependency (CYCLOPS genes), a group of genes highly enriched for members of macromolecular protein complexes including the spliceosome and proteasome. Finally, we discovered 171 genes that become a dependency when a redundant functional paralog is lost in cancer cells (redundant essentials). We demonstrate the mechanistic basis behind one such redundant essential dependency relationship in which promoter methylation of the UBB ubiquitin gene eliminates a compensatory mechanism leading to a novel vulnerability on the suppression of the UBC ubiquitin gene. These observations begin to provide an initial census, categorization and prioritization of robust cancer dependencies and support the potential impact for expanding early efforts to develop dependency maps of cancer. Citation Format: Francisca Vazquez, Aviad Tsherniak, Barbara Weir, Phil Montgomery, Glenn Cowley, Stanley Gill, Gregory Kryukov, Sasha Pantel, Will Harrington, Mike Burger, Robin Meyers, Levi Ali, Amy Goodale, Yenarae Lee, Levi Garraway, Jesse Boehm, David Root, Todd Golub, William Hahn. Emerging targets from Cancer Dependency Map v0.1. [abstract]. In: Proceedings of the AACR Precision Medicine Series: Targeting the Vulnerabilities of Cancer; May 16-19, 2016; Miami, FL. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(1_Suppl):Abstract nr B44.
Physical activity, weight change and endometrial cancer risk: The multiethnic cohort
Authors: Sung-Shim Park, Marc Goodman, Laurence Kolonel, Malcolm Pike, Brian Henderson, Veronica Setiawan
Journal: Cancer Research (2008)

AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA

3073 

Obesity, adult weight gain, and physical inactivity are known or suspected risk factors for endometrial cancer. We examined the associations of these related factors with endometrial cancer risk among 37,884 postmenopausal African-American, Japanese-American, Latina, Native-Hawaiian, and White women recruited to the prospective Multiethnic Cohort Study from 1993 to 1996 who had natural menopause and complete risk factor data. During an average of 8.2 years of follow-up, 311 cases of invasive endometrial cancers were identified among these women. Information on physical activity, weight at age 21, and weight at time of recruitment was obtained from the baseline questionnaire. In our analysis, “change in weight” was defined as the percentage weight change from the age of 21 years to the time of recruitment; and total physical activity was analyzed as metabolic equivalents of energy expenditure (METs) per day based on participants’ responses to various physical activity questions. Hazard rate ratios (RRs) and 95% confidence intervals (CIs) for endometrial cancer incidence associated with each risk factor were estimated using log-linear (Cox) proportional hazard models stratified by age at and year of recruitment, race/ethnicity, and study area, and adjusted for potential confounders. No association between physical activity and endometrial cancer risk was observed; the RR was 0.97 (95% CI: 0.65, 1.48) among women in the highest compared with the lowest quartile of physical activity (≥1.764 METs/day versus ≤1.418 METs/day). However, adult weight gain was associated with an increased risk (P trend <0.001) of malignancy. Women in the highest quartile of weight change (≥35% weight gained from the age of 21 years) had a RR of 3.52 (95% CI: 2.13, 5.83) compared to women in the lowest quartile (< 8.5% weight gain or any percentage weight loss). In conclusion, a 35% adult weight gain increased the risk of endometrial cancer by 3.5 fold among postmenopausal women in the Multiethnic Cohort Study.
The Quick SOFA, a simple bedside score, identifies hospitalized cirrhotic patients with poor outcomes
Authors: J.-P. Cervoni, D. Weil, C. Bureau, F. Oberti, R. Anty, A. Louvet, A. Plessier, M. Rudler, A. Heurgué-Berlot, I. Rosa, N. Talbodec, T. Dao, V. Ozenne, E. Muel, C. Richou, C. Vanlemmens, G. Piton, P. Saas, V.D. Martino, T. Thévenot
Journal: Journal of Hepatology (2017)
EDP-305, a novel and highly potent farnesoid X receptor agonist, improves liver steatosis, ballooning and non-alcoholic fatty liver disease (NAFLD) activity score (NAS) in a diet-induced murine model of non-alcoholic steatohepatitis
Authors: L.-J. Jiang, M. Chau, Y. Li, F. Briand, T. Sulpice, Y.S. Or
Journal: Journal of Hepatology (2017)
Abstract IA02: Regulation of growth by the mTOR pathway
Authors: David M. Sabatini
Journal: Cancer Research (2017)

Abstract mTOR is the target of the immunosuppressive and anti-cancer drug rapamycin and the central component of a nutrient- and hormone-sensitive signaling pathway that regulates cell growth and proliferation. We now appreciate that this pathway becomes deregulated in many human cancers and has key roles in the control of metabolism, cell and organ size, and aging. We have identified two distinct mTOR-containing proteins complexes, one of which regulates growth through S6K and another that regulates cell survival and metabolism through Akt. These complexes, called mTORC1 and mTORC2, define both rapamycin-sensitive and insensitive branches of the mTOR pathway. Over the last few years we have focused on how nutrients, particularly amino acids, regulate mTORC1. We have identified a complex signaling pathway that relays amino acid availability to mTORC1 through the heterodimeric Rag GTPases. We recently discovered several of the amino acid sensors for the pathway. I will discuss new results from our lab on the regulation and functions of mTORC1. Citation Format: David M. Sabatini. Regulation of growth by the mTOR pathway. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr IA02.
Subgroup analysis of adenocarcinoma patients refractory to first-line chemotherapy from REVEL: A randomized phase III study of docetaxel with ramucirumab or placebo for second-line treatment of stage IV non–small cell lung cancer (NSCLC)
Authors: M. Reck, L. Paz-Ares, D. Moro-Sibilot, F.A. Shepherd, F. Cappuzzo, K.B. Winfree, E. Alexandris, A. Sashegyi, R. Varea, M. Pérol
Journal: Annals of Oncology (2017)
Early changes in perfusion-computed tomography scan parameters as a marker of improved outcomes in patients with hepatocellular carcinoma treated with Sorafenib
Authors: S. Okolicsanyi, D. Ippolito, G. Querques, G. Bonato, V. Pontecorvi, R. Corso, P. Invernizzi, M. Strazzabosco
Journal: Journal of Hepatology (2017)
Risk of acute myocardial infarction with NSAIDs in real world use: bayesian meta-analysis of individual patient data
Authors: Michèle Bally, Nandini Dendukuri, Benjamin Rich, Lyne Nadeau, Arja Helin-Salmivaara, Edeltraut Garbe, James M Brophy
Journal: BMJ (2017)

<b>Objective</b>&nbsp;To characterise the determinants, time course, and risks of acute myocardial infarction associated with use of oral non-steroidal anti-inflammatory drugs (NSAIDs). <b>Design</b>&nbsp;Systematic review followed by a one stage bayesian individual patient data meta-analysis. <b>Data sources</b>&nbsp;Studies from Canadian and European healthcare databases. <b>Review methods</b>&nbsp;Eligible studies were sourced from computerised drug prescription or medical databases, conducted in the general or an elderly population, documented acute myocardial infarction as specific outcome, studied selective cyclo-oxygenase-2 inhibitors (including rofecoxib) and traditional NSAIDs, compared risk of acute myocardial infarction in NSAID users with non-users, allowed for time dependent analyses, and minimised effects of confounding and misclassification bias. <b>Exposure and outcomes</b>&nbsp;Drug exposure was modelled as an indicator variable incorporating the specific NSAID, its recency, duration of use, and dose. The outcome measures were the summary adjusted odds ratios of first acute myocardial infarction after study entry for each category of NSAID use at index date (date of acute myocardial infarction for cases, matched date for controls) versus non-use in the preceding year and the posterior probability of acute myocardial infarction. <b>Results</b>&nbsp;A cohort of 446 763 individuals including 61 460 with acute myocardial infarction was acquired. Taking any dose of NSAIDs for one week, one month, or more than a month was associated with an increased risk of myocardial infarction. With use for one to seven days the probability of increased myocardial infarction risk (posterior probability of odds ratio &gt;1.0) was 92% for celecoxib, 97% for ibuprofen, and 99% for diclofenac, naproxen, and rofecoxib. The corresponding odds ratios (95% credible intervals) were 1.24 (0.91 to 1.82) for celecoxib, 1.48 (1.00 to 2.26) for ibuprofen, 1.50 (1.06 to 2.04) for diclofenac, 1.53 (1.07 to 2.33) for naproxen, and 1.58 (1.07 to 2.17) for rofecoxib. Greater risk of myocardial infarction was documented for higher dose of NSAIDs. With use for longer than one month, risks did not appear to exceed those associated with shorter durations. <b>Conclusions</b>&nbsp;All NSAIDs, including naproxen, were found to be associated with an increased risk of acute myocardial infarction. Risk of myocardial infarction with celecoxib was comparable to that of traditional NSAIDS and was lower than for rofecoxib. Risk was greatest during the first month of NSAID use and with higher doses.
Phenome-wide scanning identifies multiple diseases and disease severity phenotypes associated with HLA variants
Authors: Jason H. Karnes, Lisa Bastarache, Christian M. Shaffer, Silvana Gaudieri, Yaomin Xu, Andrew M. Glazer, Jonathan D. Mosley, Shilin Zhao, Soumya Raychaudhuri, Simon Mallal, Zhan Ye, John G. Mayer, Murray H. Brilliant, Scott J. Hebbring, Dan M. Roden, Elizabeth J. Phillips, Joshua C. Denny
Journal: Science Translational Medicine (2017)

Although many phenotypes have been associated with variants in human leukocyte antigen (HLA) genes, the full phenotypic impact of HLA variants across all diseases is unknown. We imputed HLA genomic variation from two populations of 28,839 and 8431 European ancestry individuals and tested association of HLA variation with 1368 phenotypes. A total of 104 four-digit and 92 two-digit HLA allele phenotype associations were significant in both discovery and replication cohorts, the strongest being
Provision of Long-Term Monitoring and Late Effects Services Following Hematopoietic Cell Transplantation (HCT): A Survey of European Programs By the Complications and Quality of Life Working Party of the EBMT
Authors: Nina Salooja, Steffie van der Werf, Maura Faraci, Angela Hamblin, Anja van Biezen, Grzegorz W. Basak, Rafael F. Duarte
Journal: Blood (2016)
The risk of hepatitis B virus reactivation is considerably high during sorafenib therapy in patients with advanced hepatocellular carcinoma
Authors: S.J. Suh, H.J. Yim, J.H. Seo, Y.S. Lee, J.J. Hyun, Y.K. Jung, J.H. Kim, Y.S. Seo, J.E. Yeon, K.S. Byun, S.H. Um
Journal: Journal of Hepatology (2017)
Current and Binge Drinking Among High School Students — United States, 1991–2015
Authors: Marissa B. Esser, Heather Clayton, Zewditu Demissie, Dafna Kanny, Robert D. Brewer
Journal: MMWR Morbidity and Mortality Weekly Report (2017)

Excessive drinking accounted for approximately 4,300 deaths each year among persons aged <21 years during 2006-2010,* and underage drinking cost the United States $24.3 billion in 2010 (1). CDC analyzed data from the national Youth Risk Behavior Survey (YRBS) for the years 1991-2015 to examine trends in drinking by U.S. high school students, and from the 2015 YRBS to assess the usual source of alcohol consumed† and binge drinking intensity (i.e., the average number of drinks consumed per binge drinking occasion).§ During 1991-2007, the prevalence of current drinking¶ among high school students declined significantly, from 50.8% (1991) to 44.7% (2007), and then significantly declined to 32.8% in 2015. The prevalence of binge drinking** increased from 31.3% in 1991 to 31.5% in 1999, and then significantly declined to 17.7% in 2015. Most high school students who drank were binge drinkers (57.8%), and 43.8% of binge drinkers consumed eight or more drinks in a row. Despite progress, current drinking and binge drinking are common among high school students, and many students who binge drink do so at high intensity (i.e., eight or more drinks in a row). Widespread use of evidence-based strategies for preventing excessive drinking (e.g., increasing alcohol taxes, regulating alcohol outlet density, and having commercial host liability laws) could help reduce underage drinking and related harms.††.
Genotype 3 infection in DAA era: reports of a real life Northern Italy network for viral hepatitis after 2 years by the start
Authors: L. Pasulo, A. Aghemo, M. Puoti, L. Belli, G. Filice, P.D. Poggio, P. Grossi, A. Ciaccio, M. Colpani, M. Colombo, S. Fagiuoli
Journal: Journal of Hepatology (2017)
A Critical Analysis of the Current Knowledge of Surgical Anatomy Related to Optimization of Cancer Control and Preservation of Continence and Erection in Candidates for Radical Prostatectomy
Authors: Jochen Walz, Arthur L. Burnett, Anthony J. Costello, James A. Eastham, Markus Graefen, Bertrand Guillonneau, Mani Menon, Francesco Montorsi, Robert P. Myers, Bernardo Rocco, Arnauld Villers
Journal: European Urology (2009)
Sociodemographic and patient disparities in use of first-line chemotherapy (CT) in older adult patients (pts) with advanced non-small cell lung cancer (AdvNSCLC): Analysis of Surveillance, Epidemiology, and End Results (SEER)-Medicare data.
Authors: Josephine Louella Feliciano, Lisa Gardner, Martin J. Edelman, Amy J. Davidoff
Journal: Journal of Clinical Oncology (2012)

6131 Background: Clinical trials have demonstrated that CT improves survival and quality of life in pts with AdvNSCLC. Our prior studies suggest that only 26% of older pts diagnosed with AdvNSCLC received CT through 2002. In this study, we examined more recent patterns, and the effect of socio-demographics, race, and age on receipt of CT in older pts with AdvNSCLC. Methods: Medicare pts diagnosed with AdvNSCLC from 2001-2005 were identified in SEER registries. Medicare enrollment data provided demographic information (age, race, sex, marital status), augmented with census tract level data on median household income. Comorbid conditions at baseline were identified by ICD9-CM diagnoses on claims. Receipt of 1st line CT was identified based on agent-specific procedure codes in claims. Logistic regression examined predictors of 1st line CT. Results: Of 31,341 pts with Adv NSCLC, 34% received 1st line CT. As reflected in the table, poor predicted PS (PredPS), multiple medical comorbidities, and black race were associated with lower likelihood of CT receipt. Being female, married, having higher income, and being diagnosed at a later year were associated with a higher likelihood of receiving CT. Conclusions: Even when controlling for factors such as PS, our results suggest the presence of age, race, and socio-economic disparities in the receipt of 1st line CT for older patients with AdvNSCLC. [Table: see text]
Pharmacokinetics and safety of glecaprevir/pibrentasvir in adults with chronic genotype 1–6 hepatitis C virus infection and compensated cirrhosis: an integrated analysis
Authors: E. Gane, F. Poordad, J. Valdes, C.-W. Lin, W. Liu, A. Asatryan, S. Wang, C. Stedman, S. Greenbloom, T. Nguyen, M. Elkhashab, M.-A. Wörns, A. Tran, J.-P. Mulkay, Y. Yu, A. Porcalla, F. Mensa
Journal: Journal of Hepatology (2017)