tbuckley/cabot-search huggingface dataset:
Impact of smoking cessation on global gene expression in bronchial epithelium of chronic smokers
Authors: Li Zhang, Jack Lee, Hongli Tang, You-Hong Fan, Lianchun Xiao, Hening Ren, Jonathan Kurie, Rodolfo C. Morice, Waun K. Hong, Li Mao
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

880 

Quit smoking is believed to reduce the risk of developing lung cancer. But little is known on the molecular level about the impact of smoking cessation. We compared global gene expression profiles in bronchial epithelial cells taken from current smokers (>20 pack years) with that from former smokers (>20 pack years history but ceased smoking for least 12 months). Affymetrix HG-U133A microarrays were used to measure gene expression profiles in 20 bronchial brush samples obtained from 15 individuals including 10 current smokers and 5 former smokers who participated in an ongoing chemoprevention clinical trial. All individuals had available baseline bronchial brush samples and 5 individuals in the placebo treatment group had also samples obtained after 3 months. Among ∼16,000 unique genes analyzed, we identified a list of ∼80 genes differentially expressed in the bronchial epithelium between the current and former smokers with the estimated 15% false discovery rate. To validate the list, we used real-time reverse transcription-polymerase chain reaction to measure gene expression of 5 selected genes and obtained very good concordance with the microarray results. To further determine the reliability of our data and to identify critical genes important in smoking induced carcinogenesis, we cross validated our microarray data with the microarray data recently reported by Spira et al (Proc Natl Acad Sci 101:10143-8, 2004), where gene expression profiles of bronchial epithelium from 34 current smokers and 18 former smokers were analyzed. Despite significant biases are expected between our study and that of Spira et al due to differences in sample preparation, individual genetic variation of the study cohorts, age, sex and criteria of smoking status, we found a rather remarkable concordance between the list of differentially expressed genes from our data and that of Spira et al.’s study (R = 0.85, correlation with differential expression between current smoker vs. former smokers). When Log fold-change >0.3 was used for expression change in both datasets with P <0.01 in our dataset, we identified 12 unique genes consisting 11 up-regulated genes in current smokers involving in carcinogen detoxification as well as oncogenic process and only one down-regulated gene (hypothetical protein [FLJ10134][1]). Our study demonstrates first time that the global gene expression analysis is highly reliable and if perform properly may be used for a meta-analysis of data generated from different groups. We have also identified a panel of genes that are induced by active smoking and may play critical role in both carcinogen detoxification and carcinogenesis. (Supported in part by NCI PO1 CA91844 and DOD DAMD17-01-1-0689)

 [1]: /lookup/external-ref?link_type=GENPEPT&access_num=FLJ10134&atom=%2Fcanres%2F65%2F9_Supplement%2F207.1.atom
Ambient PM <sub>2.5</sub> , O <sub>3</sub> , and NO <sub>2</sub> Exposures and Associations with Mortality over 16 Years of Follow-Up in the Canadian Census Health and Environment Cohort (CanCHEC)
Authors: Dan L. Crouse, Paul A. Peters, Perry Hystad, Jeffrey R. Brook, Aaron van Donkelaar, Randall V. Martin, Paul J. Villeneuve, Michael Jerrett, Mark S. Goldberg, C. Arden Pope, Michael Brauer, Robert D. Brook, Alain Robichaud, Richard Menard, Richard T. Burnett
Journal: Environmental Health Perspectives (2015)

BackgroundFew studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up.ObjectiveWe investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 μm; PM2.5), ozone (O3), and nitrogen dioxide (NO2) in a national cohort of about 2.5 million Canadians.MethodsWe assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects’ residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 μg/m3 for PM2.5, 9.5 ppb for O3, and 8.1 ppb for NO2.ResultsPM2.5, O3, and NO2 were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM2.5 alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM2.5 and O3, but increased associations with NO2.ConclusionsIn this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM2.5, O3, and NO2.CitationCrouse DL, Peters PA, Hystad P, Brook JR, van Donkelaar A, Martin RV, Villeneuve PJ, Jerrett M, Goldberg MS, Pope CA III, Brauer M, Brook RD, Robichaud A, Menard R, Burnett RT. 2015. Ambient PM2.5, O3, and NO2 exposures and associations with mortality over 16 years of follow-up in the Canadian Census Health and Environment Cohort (CanCHEC). Environ Health Perspect 123:1180–1186; http://dx.doi.org/10.1289/ehp.1409276
A new three dimensional biomimetic hydrogel to deliver factors secreted by human mesenchymal stem cells in spinal cord injury
Authors: Ilaria Caron, Filippo Rossi, Simonetta Papa, Rossella Aloe, Marika Sculco, Emanuele Mauri, Alessandro Sacchetti, Eugenio Erba, Nicolò Panini, Valentina Parazzi, Mario Barilani, Gianluigi Forloni, Giuseppe Perale, Lorenza Lazzari, Pietro Veglianese
Journal: Biomaterials (2015)
Implication of discoidin domain receptors in the activation of hepatic stellate cells during liver metastasis
Authors: Iker Badiola, Beatriz Arteta, Iratxe Basaldua, Vidal-Vanaclocha Fernando, Olaso Elvira
Journal: Cancer Research (2007)

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

2457 

Discoidin Domain Receptors DDR1 and DDR2 are two novel tyrosine kinase receptors whose ligands are collagens. DDR1 is expressed by cells of epithelial origin while DDR2 is expressed by activated myofibroblasts of the healing tissue. In the metastasized liver, tumor-activated stellate cells of myofibroblastic phenotype are recruited into the stromal areas of developing micrometastases and release tumor cell proliferation- and migration-stimulating factors. The aim of our study was to elucidate the role of DDRs in tumor-activated stellate cells during liver metastasis. Immunohistochemical analysis of human livers metastasized by colon carcinoma demonstrated co-expression of DDR1, DDR2 and the myofibroblast marker alpha-smoth muscle actin in the stromal cells, but not in cancer cells. In vitro, freshly isolated human hepatic stellate cells cultured in the presence of media conditioned by human colon carcinoma cells showed enhanced DDR1, DDR2 and alpha smooth actin expression at both RNA and protein level, compared to cells cultured in basal media. Production of experimental liver metastases by intrasplenic injection of MC38 colon carcinoma cells in syngenic C57Bl/6J mice generated a higher density of micrometastases in livers from DDR2-KO mice than in wild type ones. Co-localization of desmin and alpha-smooth muscle actin was also 3-fold higher in livers from DDR2-KO mice than in the wild type, indicating a higher rate of tumor-associated activated stellate cells. The supernatant from primary cultures of DDR2-KO mouse stellate cells exposed to MC38 tumor-conditioned media exerted a 2-fold higher MMP2 activity than wild type ones. Finally, MC38 cell proliferation, migration and adhesion to collagen was maximal when cultured in the presence of supernatants from DDR2-KO stellate cells where used. Real time quantitative RT-PCR analysis showed a 10-fold higher expression of DDR1 mRNA in DDR2-KO hepatic stellate cells compared to wild type ones. To evaluate a possible compensatory effect of DDR1 when DDR2 is lacked, primary cultures of DDR2-KO mouse-derived hepatic stellate cells where transfected with a vector encoding a DDR1-RNA interference RNA. As a result, diminished proliferative, adhesive and migratory rates were observed, compared to cells treated with a control vector encoding an irrelevant RNA. These results demonstrate for the first time a direct role of DDR receptors in stromal hepatic stellate cell functional behavior during liver metastasis.
Stomatitis, Cutaneous Bullae, and Renal Failure
Authors: Connie Tran, Elizabeth Wilder, John R. Griffin
Journal: JAMA (2015)

A 64-year-old African American woman presented with crusted scalp plaques, erosive stomatitis, and multiple bullae, erosions, and hyperpigmented patches on her trunk and extremities. Her serum creatinine level was 7.1 mg/dL; a complete blood cell count was unremarkable. What would you do next?
The prevalence and distribution of major depression in a national community sample: the National Comorbidity Survey
Authors: D G Blazer, R C Kessler, K A McGonagle, M S Swartz
Journal: American Journal of Psychiatry (1994)

Major depression is a frequent and disabling psychiatric disorder in the United States. This report examines the prevalence and risk factor profile of both pure and comorbid major depression according to data from the National Comorbidity Survey.To estimate the prevalence of psychiatric comorbidity in the United States, a national sample of 8,098 persons 15-54 years of age from the 48 conterminous states was surveyed with a modified version of the Composite International Diagnostic Interview.From the survey data the prevalence of current (30-day) major depression was estimated to be 4.9%, with a relatively higher prevalence in females, young adults, and persons with less than a college education. The prevalence estimate for lifetime major depression was 17.1%, with a similar demographic distribution. Both 30-day and lifetime prevalence estimates were higher than estimates from the earlier Epidemiologic Catchment Area study. When pure major depression was compared with major depression co-occurring with other psychiatric disorders, the risk factor profiles exhibited clear differences.These findings suggest a greater burden of major depression in community-dwelling persons than has been estimated from previous community samples. The risk factor profile showed significant differences between persons with pure and combined major depression.
International Registry of Abnormal Karyotypes
Authors: Digamber S. BORGAONKAR
Journal: JAMA (1975)

<h3>To the Editor.—</h3> We have established an International Registry of Abnormal Karyotypes. For inclusion of data in the Registry we would need information on the person reporting on the case, the chromosomal variation or abnormality in as much detail<sup>1</sup>as possible as to the region and band of the chromosome, and the case number of the laboratory. The latter is to avoid duplication of the data in multiple publications and to facilitate further communications. The Registry has been "computerized." It is possible to obtain readily information on any abnormality and to sort data with respect to the chromosome, or type of abnormality, or the locale of the reporting laboratory. It is planned to have computer printouts of the Registry about two or three times a year, and they will be available at cost. The Registry has been established to simplify such projects as storage of data that otherwise lie
Effects of angiotensin II on endothelial cell growth
Authors: M Montón, M A Castilla, M V Alvarez Arroyo, D Tan, F R González-Pacheco, A López Farré, S Casado, C Caramelo
Journal: Journal of the American Society of Nephrology (1998)

Angiotensin II (AngII) is a main mediator in the regulation of vascular tone. Although its effects on vascular smooth muscle cells are well known, data on its role on endothelial biology are still insufficient. The present study examined the effect of endogenous and exogenous AngII on bovine aortic endothelial cells possessing both AT-1 and AT-2 receptors. A DNA synthesis-promoting effect of AT-2 blockade by PD123319 (10(-9) to 10(-7) M) was demonstrated. This effect was transduced through an AT-1-mediated pathway, as shown by using the AT-1 antagonist, losartan. In addition, an AT-1-mediated effect of AngII was demonstrated on bovine aortic endothelial cell proliferation, which occurred despite the absence of AngII-induced Ca2+ transients. In summary, the present study disclosed relevant characteristics of the effect of AngII on endothelial cell growth that have potential pathophysiologic projections, particularly for the use of selective AngII blocking agents.
Multimodality Therapy in Mesothelioma: an Epidemiological and Effectiveness Analysis
Authors: M.A. Damiano, A.K. Patané, M. Chacon, R. Chacon, V. Vilchez, A. Rosales, A. Falco, C. Poleri, M. Rosenberg, C. Martin
Journal: Annals of Oncology (2012)
Influence of stromal elements on resident T cell migration in human and murine tumors analyzed by real-time imaging
Authors: Elisa Peranzoni, Houcine Bougherara, Audrey Mansuet-Lupo, Vincent Feuillet, Julia Weiss, Fabienne Reigner, Diane Damotte, Marco Alifano, Marie-Aude Le Frere-Belda, Fabrice Lécuru, Emmanuel Donnadieu
Journal: Journal for ImmunoTherapy of Cancer (2015)

Meeting abstracts It is well established that T cells are crucial for the anti-tumor response, through the production of cytokines, direct cytotoxicity, and the activation of other “killer” cells of the innate arm. In order to perform their antitumor activities, T cells need to adequately
Exercise for osteoarthritis of the knee: a Cochrane systematic review
Authors: Marlene Fransen, Sara McConnell, Alison R Harmer, Martin Van der Esch, Milena Simic, Kim L Bennell
Journal: British Journal of Sports Medicine (2015)

Objective To determine whether land-based therapeutic exercise is beneficial for people with knee osteoarthritis (OA) in terms of reduced joint pain or improved physical function and quality of life. Methods Five electronic databases were searched, up until May 2013. Randomised clinical trials comparing some form of land-based therapeutic exercise with a non-exercise control were selected. Three teams of two review authors independently extracted data and assessed risk of bias for each study. Standardised mean differences immediately after treatment and 2–6 months after cessation of formal treatment were separately pooled using a random effects model. Results In total, 54 studies were identified. Overall, 19 (35%) studies reported adequate random sequence generation, allocation concealment and adequately accounted for incomplete outcome data. However, research results may be vulnerable to selection, attrition and detection bias. Pooled results from 44 trials indicated that exercise significantly reduced pain (12 points/100; 95% CI 10 to 15) and improved physical function (10 points/100; 95% CI 8 to 13) to a moderate degree immediately after treatment, while evidence from 13 studies revealed that exercise significantly improved quality of life immediately after treatment with small effect (4 points/100; 95% CI 2 to 5). In addition, 12 studies provided 2-month to 6-month post-treatment sustainability data which showed significantly reduced knee pain (6 points/100; 95% CI 3 to 9) and 10 studies which showed improved physical function (3 points/100; 95% CI 1 to 5). Conclusions Among people with knee osteoarthritis, land-based therapeutic exercise provides short-term benefit that is sustained for at least 2–6 months after cessation of formal treatment.
The rabbit alpha-like globin gene cluster is polymorphic both in the sizes of BamHI fragments and in the numbers of duplicated sets of genes.
Authors: J F Cheng, R C Hardison
Journal: Molecular Biology and Evolution (1988)

The alpha-like globin gene cluster in rabbits contains embryonic zeta-globin genes, an adult alpha-globin gene, and theta-globin genes of undetermined function. The basic arrangement of genes, deduced from analysis of cloned DNA fragments, is 5'-zeta 0-zeta 1-alpha 1-theta 1-zeta 2-zeta 3-theta 2-3'. However, the pattern of restriction fragments containing zeta- and theta-globin genes varies among individual rabbits. Analysis of BamHI fragments of genomic DNA from 24 New Zealand white rabbits revealed eight different patterns of fragments containing zeta-globin genes. The large BamHI fragments containing genes zeta 0 and zeta 1 are polymorphic in length, whereas a 1.9-kb fragment containing the zeta 2 gene and the 3.5-kb fragment containing the zeta 3 gene do not vary in size. In contrast to this constancy in the size of the restriction fragments, the copy number of the zeta 2 and zeta 3 genes does vary among different rabbits. No length polymorphism was detected in the BamHI fragments containing the theta-globin genes, but again the copy number varies for restriction fragments containing the theta 2 gene. The alpha 1- and theta 1-globin genes are located in a nonpolymorphic 7.2-kb BamHI fragment. The combined data from hybridization with both zeta and theta probes shows that the BamHI cleavage pattern does not vary within the region 5'-alpha 1-theta 1-zeta 2-zeta 3-theta 2-3', but the pattern genomic blot-hybridization patterns for the progeny of parental rabbits with different zeta-globin gene patterns shows that the polymorphic patterns are inherited in a Mendelian fashion. Two different haplotypes have been mapped based on the genomic blot-hybridization data. The variation in the alpha-like globin gene cluster in the rabbit population results both from differences in the copy number of the duplication block containing the zeta-zeta-theta gene set and from the presence or absence of polymorphic BamHI sites.
Situation of hantavirus infections and haemorrhagic fever with renal syndrome in European countries as of December 2006
Authors: P Heyman, A Vaheri
Journal: Eurosurveillance (2008)

Hantavirus infections are widely distributed in Europe with the exception of the far north and the Mediterranean regions. The underlying causes of varying epidemiological patterns differ among regions: in western and central Europe epidemics of haemorrhagic fever with renal syndrome (HFRS) caused by hantavirus infections follow mast years with increased seed production by oak and beech trees followed by increased rodent reproduction. In the northern regions, hantavirus infections and HFRS epidemics occur in three to four year cycles and are thought to be driven by prey - predator interactions. Hantavirus infections and HFRS seem to be on the increase in Europe, partly because of better diagnostics, partly perhaps due to environmental changes. Unfortunately, hantavirus infections are still heavily under-diagnosed in many European countries. Here we report the results of a survey conducted in 2007 amongst the member laboratories of the European Network for diagnostics of Imported Viral Diseases (ENIVD).
Role of Immunotherapy for Renal Cell Cancer in 2011
Authors: Saby George, Roberto Pili, Michael A. Carducci, Jenny J. Kim
Journal: Journal of the National Comprehensive Cancer Network (2011)

High-dose interleukin-2 (IL-2) and interferon were the most commonly administered therapies before the recent introduction of targeted agents, including vascular endothelial growth factor and mammalian target of rapamycin pathway inhibitors. Although the new agents result in a progression-free survival benefit, high-dose IL-2 remains the only agent with proven efficacy in producing durable complete and partial responses in patients with metastatic renal cell carcinoma (RCC). Furthermore, although the use of single-agent interferon has decreased significantly since the introduction of targeted therapy, it remains in the frontline setting in combination with bevacizumab as a result of 2 large phase III trials. Lastly, improved understanding of immune regulation has led to the advancement of targeted immunotherapy using immune checkpoint inhibitors that have shown promising activity and are moving forward in clinical development. This article focuses on the current status of immunotherapy in the management of metastatic RCC.
Postchemoradiotherapy Pathologic Stage Classified by the American Joint Committee on the Cancer Staging System Predicts Prognosis of Patients with Locally Advanced Esophageal Squamous Cell Carcinoma
Authors: Jhe-Cyuan Guo, Ta-Chen Huang, Chia-Chi Lin, Min-Shu Hsieh, Chin-Hao Chang, Pei-Ming Huang, Jang-Ming Lee, Feng-Ming Hsu, Jason Chia-Hsien Cheng, Hsiu-Po Wang, Kun-Huei Yeh, Ann-Lii Cheng, Chih-Hung Hsu
Journal: Journal of Thoracic Oncology (2015)
Serum Immunoregulatory Proteins as Predictors of Overall Survival of Metastatic Melanoma Patients Treated with Ipilimumab
Authors: Yoshinobu Koguchi, Helena M. Hoen, Shelly A. Bambina, Michael D. Rynning, Richard K. Fuerstenberg, Brendan D. Curti, Walter J. Urba, Christina Milburn, Frances Rena Bahjat, Alan J. Korman, Keith S. Bahjat
Journal: Cancer Research (2015)

Abstract Treatment with ipilimumab improves overall survival (OS) in patients with metastatic melanoma. Because ipilimumab targets T lymphocytes and not the tumor itself, efficacy may be uniquely sensitive to immunomodulatory factors present at the time of treatment. We analyzed serum from patients with metastatic melanoma (247 of 273, 90.4%) randomly assigned to receive ipilimumab or gp100 peptide vaccine. We quantified candidate biomarkers at baseline and assessed the association of each using multivariate analyses. Results were confirmed in an independent cohort of similar patients (48 of 52, 92.3%) treated with ipilimumab. After controlling for baseline covariates, elevated chemokine (C-X-C motif) ligand 11 (CXCL11) and soluble MHC class I polypeptide–related chain A (sMICA) were associated with poor OS in ipilimumab-treated patients [log10 CXCL11: HR, 1.88; 95% confidence interval (CI), 1.14–3.12; P = 0.014; and log10 sMICA quadratic effect P = 0.066; sMICA (≥ 247 vs. 247): HR, 1.75; 95% CI, 1.02–3.01]. Multivariate analysis of an independent ipilimumab-treated cohort confirmed the association between log10 CXCL11 and OS (HR, 3.18; 95% CI, 1.13–8.95; P = 0.029), whereas sMICA was less strongly associated with OS [log10 sMICA quadratic effect P = 0.16; sMICA (≥247 vs. 247): HR, 1.48; 95% CI, 0.67–3.27]. High baseline CXCL11 and sMICA were associated with poor OS in patients with metastatic melanoma after ipilimumab treatment but not vaccine treatment. Thus, pretreatment CXCL11 and sMICA may represent predictors of survival benefit after ipilimumab treatment as well as therapeutic targets. Cancer Res; 75(23); 5084–92. ©2015 AACR.