tbuckley/cabot-search huggingface dataset:
Diet and Gastric Cancer: Nutrition Survey in a High-Risk Area&lt;xref ref-type="fn" rid="fn2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn3"&gt;3&lt;/xref&gt;
Authors: P Correa, C Cuello, L F Fajardo, W Haenszel, O Bolaños, B de Ramírez
Journal: JNCI Journal of the National Cancer Institute (1983)

A nutrition survey was done in four Colombian villages situated in the rural area of Nariño, previously identified as exhibiting different levels of risk for gastric cancer and its precursor lesions. The survey was based on personal visits by trained interviewers to a random sample of families in each village. The major findings of the survey reflected a higher consumption of fava beans in villages with high indices of gastric cancer risk and a higher consumption of fresh fruits and vegetables in villages where such indices were lower. Excessive salt intake and lower potassium intake in villages with a high risk of gastric cancer were suggested, but further work is required to test this preliminary observation. A generally low intake of animal proteins and a high intake of cereals in Nariño did not discriminate between villages at different levels of risk to gastric cancer and its precursors.
Carbon monoxide reverses established pulmonary hypertension
Authors: Brian S. Zuckerbraun, Beek Yoke Chin, Barbara Wegiel, Timothy R. Billiar, Eva Czsimadia, Jayashree Rao, Larissa Shimoda, Emeka Ifedigbo, Shin Kanno, Leo E. Otterbein
Journal: The Journal of Experimental Medicine (2006)

Pulmonary arterial hypertension (PAH) is an incurable disease characterized by a progressive increase in pulmonary vascular resistance leading to right heart failure. Carbon monoxide (CO) has emerged as a potently protective, homeostatic molecule that prevents the development of vascular disorders when administered prophylactically. The data presented in this paper demonstrate that CO can also act as a therapeutic (i.e., where exposure to CO is initiated after pathology is established). In three rodent models of PAH, a 1 hour/day exposure to CO reverses established PAH and right ventricular hypertrophy, restoring right ventricular and pulmonary arterial pressures, as well as the pulmonary vascular architecture, to near normal. The ability of CO to reverse PAH requires functional endothelial nitric oxide synthase (eNOS/NOS3) and NO generation, as indicated by the inability of CO to reverse chronic hypoxia-induced PAH in eNOS-deficient (nos3−/−) mice versus wild-type mice. The restorative function of CO was associated with a simultaneous increase in apoptosis and decrease in cellular proliferation of vascular smooth muscle cells, which was regulated in part by the endothelial cells in the hypertrophied vessels. In conclusion, these data demonstrate that CO reverses established PAH dependent on NO generation supporting the use of CO clinically to treat pulmonary hypertension.
Foretinib Is Effective Therapy for Metastatic Sonic Hedgehog Medulloblastoma
Authors: Claudia C. Faria, Brian J. Golbourn, Adrian M. Dubuc, Marc Remke, Roberto J. Diaz, Sameer Agnihotri, Amanda Luck, Nesrin Sabha, Samantha Olsen, Xiaochong Wu, Livia Garzia, Vijay Ramaswamy, Stephen C. Mack, Xin Wang, Michael Leadley, Denis Reynaud, Leonardo Ermini, Martin Post, Paul A. Northcott, Stefan M. Pfister, Sidney E. Croul, Marcel Kool, Andrey Korshunov, Christian A. Smith, Michael D. Taylor, James T. Rutka
Journal: Cancer Research (2014)

Medulloblastoma is the most common malignant pediatric brain tumor, with metastases present at diagnosis conferring a poor prognosis. Mechanisms of dissemination are poorly understood and metastatic lesions are genetically divergent from the matched primary tumor. Effective and less toxic therapies that target both compartments have yet to be identified. Here, we report that the analysis of several large nonoverlapping cohorts of patients with medulloblastoma reveals MET kinase as a marker of sonic hedgehog (SHH)-driven medulloblastoma. Immunohistochemical analysis of phosphorylated, active MET kinase in an independent patient cohort confirmed its correlation with increased tumor relapse and poor survival, suggesting that patients with SHH medulloblastoma may benefit from MET-targeted therapy. In support of this hypothesis, we found that the approved MET inhibitor foretinib could suppress MET activation, decrease tumor cell proliferation, and induce apoptosis in SHH medulloblastomas in vitro and in vivo. Foretinib penetrated the blood-brain barrier and was effective in both the primary and metastatic tumor compartments. In established mouse xenograft or transgenic models of metastatic SHH medulloblastoma, foretinib administration reduced the growth of the primary tumor, decreased the incidence of metastases, and increased host survival. Taken together, our results provide a strong rationale to clinically evaluate foretinib as an effective therapy for patients with SHH-driven medulloblastoma.
Treatment of pancreatic carcinoma by adenoviral mediated gene transfer of vasostatin in mice
Authors: L Li
Journal: Gut (2005)

<b>Background:</b> Tumour growth is angiogenesis dependent and antiangiogenesis therapy may represent a promising therapeutic option. <b>Aims:</b> To evaluate the inhibitory effect of vasostatin gene mediated by a replication deficient recombinant adenovirus (Ad) on human pancreatic cancer in vivo and to investigate the mechanism of action of vasostatin. <b>Methods:</b> Human umbilical vein endothelium derived ECV304 cells were infected with Ad-vasostatin and Ad-lacZ, and compared with phosphate buffered saline (PBS). MTT (3,-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay was used to estimate the proliferation of ECV304 cells; tube formation assay and choriallantoic membrane assay were used to evaluate angiogenesis in vivo and in vitro. Xenografted nude mice with pancreatic cancer were established to observe in vivo tumour growth suppression. Microvessel density revealed by CD31 immunohistochemical staining was measured. <b>Results:</b> Growth and tube formation of ECV304 cells infected with Ad-vasostatin were suppressed significantly compared with cells infected with Ad-lacZ or cells treated with PBS. Neovascularisation in the Ad-vasostatin group was less than that in the PBS and Ad-lacZ groups, based on chorioallantoic membrane results. Volumes of pancreatic tumours in the Ad-vasostatin group were significantly smaller than those in the PBS and Ad-lacZ groups at the end of the treatment period. Microvessel density in the Ad-vasostatin group was significantly lower than that in the Ad-lacZ and PBS groups. <b>Conclusion:</b> The vasostatin gene mediated by adenovirus is efficient for gene therapy for pancreatic carcinoma. Suppression of vasostatin on proliferation of vascular endothelium cells and angiogenesis may account for its effect.
Association With Clinical Outcome of Expression of VLA-4 in Primary Cutaneous Malignant Melanoma as Well as P-selection and E-selectin on Intratumoral Vessels
Authors: D. Schadendorf, J. Heidel, C. Gawlik, L. Suter, B. M. Czarnetzki
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Association With Clinical Outcome of Expression of VLA-4 in Primary Cutaneous Malignant Melanoma as Well as P-selection and E-selectin on Intratumoral Vessels Get access Dirk Schadendorf, Dirk Schadendorf Department of Dermatology, University Hospital Rudolf Virchow, Freie University at BerlinFederal Republic of Germany Dirk Schadendorf, M.D.. Department of Dermatology, University Hospital Rudolf Virchow, FU Berlin, Augustenburger Platz I, 13344 Berlin, Federal Republic of Germany. Search for other works by this author on: Oxford Academic PubMed Google Scholar Jens Heidel, Jens Heidel Department of Dermatology, University Hospital Rudolf Virchow, Freie University at BerlinFederal Republic of Germany Search for other works by this author on: Oxford Academic PubMed Google Scholar Christian Gawlik, Christian Gawlik HÄmatologisch-Onkologische-Praxis-AmbulanzHamburg, Federal Republic of Germany Search for other works by this author on: Oxford Academic PubMed Google Scholar Ludwig Suter, Ludwig Suter Fachklinik HomheideMünster, Federal Republic of Germany Search for other works by this author on: Oxford Academic PubMed Google Scholar Beate M. Czarnetzki Beate M. Czarnetzki Department of Dermatology, University Hospital Rudolf Virchow, Freie University at BerlinFederal Republic of Germany Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 5, 1 March 1995, Pages 366–371, https://doi.org/10.1093/jnci/87.5.366 Published: 01 March 1995 Article history Received: 19 July 1994 Revision received: 23 November 1994 Accepted: 30 November 1994 Published: 01 March 1995
That old familiar feeling: On uniquely identifying the role of perirhinal cortex
Authors: M. J. Eacott
Journal: Behavioral and Brain Sciences (1999)

Perirhinal cortex contributes to judgements about stimulus familiarity, but its role is far greater than this. Impairments on tasks that do not involve familiarity judgements attest to the fact that perirhinal cortex is involved in the greater role of knowing about objects, including, but not limited to, their relative familiarity.
Association of HLA-A3 and HLA-B14 antigens with idiopathic haemochromatosis.
Authors: M Simon, M Bourel, R Fauchet, B Genetet
Journal: Gut (1976)

The frequency of HLA-A3 and HLA-B14 antigens was significantly higher in a series of 51 patients with idiopathic haemochromatosis than in a control group, being respectively 78-4 versus 27-0% and 25-5 versus 3-4%. This finding strongly supports the suggestion that idiopathic haemochromatosis is a genetic disease and suggests that the gene(s) responsible for the disease may be linked to the histocompatibility genes.
Global trends in antiretroviral resistance in treatment-naive individuals with HIV after rollout of antiretroviral treatment in resource-limited settings: a global collaborative study and meta-regression analysis
Authors: Ravindra K Gupta, Michael R Jordan, Binta J Sultan, Andrew Hill, Daniel HJ Davis, John Gregson, Anthony W Sawyer, Raph L Hamers, Nicaise Ndembi, Deenan Pillay, Silvia Bertagnolio
Journal: The Lancet (2012)
Extended Survival of Glioblastoma Patients After Chemoprotective HSC Gene Therapy
Authors: Jennifer E. Adair, Brian C. Beard, Grant D. Trobridge, Tobias Neff, Jason K. Rockhill, Daniel L. Silbergeld, Maciej M. Mrugala, Hans-Peter Kiem
Journal: Science Translational Medicine (2012)

Gene therapy using P140K-modified hematopoietic progenitor cells is chemoprotective, enabling glioblastoma patients to withstand myelotoxic doses of chemotherapy.
A Woman and Her Canary: A Tale of Chlamydiae and Lymphomas
Authors: A. J. M. Ferreri, R. Dolcetti, S. Magnino, C. Doglioni, M. G. Cangi, L. Pecciarini, P. Ghia, A. Dagklis, E. Pasini, N. Vicari, G. P. Dognini, A. G. Resti, M. Ponzoni
Journal: JNCI Journal of the National Cancer Institute (2007)
Nested Case-Control Study of Lung Cancer in the Meat Industry
Authors: E S Johnson
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Nested Case-Control Study of Lung Cancer in the Meat Industry Get access Eric S. Johnson Eric S. Johnson * Correspondence to: Eric S. Jphnson, Ph.D., Epidemiology Branch, National Instituteof Environmental Health Sciences, National Institutes of Health, P.O. Box 12233, Research Tringle Park, NC 27709. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 18, 18 September 1991, Pages 1337–1339, https://doi.org/10.1093/jnci/83.18.1337 Published: 18 September 1991 Article history Received: 10 December 1990 Revision received: 18 June 1991 Accepted: 25 June 1991 Published: 18 September 1991
Modulation of extracellular matrix/adhesion molecule expression by BRG1 is associated with increased melanoma invasiveness
Authors: Srinivas Vinod Saladi, Bridget Keenen, Himangi G Marathe, Huiling Qi, Khew-Voon Chin, Ivana L de la Serna
Journal: Molecular Cancer (2010)

Metastatic melanoma is an aggressive malignancy that is resistant to therapy and has a poor prognosis. The progression of primary melanoma to metastatic disease is a multi-step process that requires dynamic regulation of gene expression through currently uncharacterized epigenetic mechanisms. Epigenetic regulation of gene expression often involves changes in chromatin structure that are catalyzed by chromatin remodeling enzymes. Understanding the mechanisms involved in the regulation of gene expression during metastasis is important for developing an effective strategy to treat metastatic melanoma. SWI/SNF enzymes are multisubunit complexes that contain either BRG1 or BRM as the catalytic subunit. We previously demonstrated that heterogeneous SWI/SNF complexes containing either BRG1 or BRM are epigenetic modulators that regulate important aspects of the melanoma phenotype and are required for melanoma tumorigenicity in vitro.To characterize BRG1 expression during melanoma progression, we assayed expression of BRG1 in patient derived normal skin and in melanoma specimen. BRG1 mRNA levels were significantly higher in stage IV melanomas compared to stage III tumors and to normal skin. To determine the role of BRG1 in regulating the expression of genes involved in melanoma metastasis, we expressed BRG1 in a melanoma cell line that lacks BRG1 expression and examined changes in extracellular matrix and adhesion molecule expression. We found that BRG1 modulated the expression of a subset of extracellular matrix remodeling enzymes and adhesion proteins. Furthermore, BRG1 altered melanoma adhesion to different extracellular matrix components. Expression of BRG1 in melanoma cells that lack BRG1 increased invasive ability while down-regulation of BRG1 inhibited invasive ability in vitro. Activation of metalloproteinase (MMP) 2 expression greatly contributed to the BRG1 induced increase in melanoma invasiveness. We found that BRG1 is recruited to the MMP2 promoter and directly activates expression of this metastasis associated gene.We provide evidence that BRG1 expression increases during melanoma progression. Our study has identified BRG1 target genes that play an important role in melanoma metastasis and we show that BRG1 promotes melanoma invasive ability in vitro. These results suggest that increased BRG1 levels promote the epigenetic changes in gene expression required for melanoma metastasis to proceed.
Clinical Significance of Cellular Distribution of Moesin in Patients with Oral Squamous Cell Carcinoma
Authors: Hiroichi Kobayashi, Junji Sagara, Hiroshi Kurita, Masayo Morifuji, Masamichi Ohishi, Kenji Kurashina, Shun’ichiro Taniguchi
Journal: Clinical Cancer Research (2004)

Moesin is a linking protein of the submembraneous cytoskeleton and plays a key role in the control of cell morphology, adhesion, and motility. The aim of the present study was to elucidate the clinical significance of expression patterns of moesin in patients with oral squamous cell carcinoma (OSCC).Immunohistochemistry for moesin monoclonal antibody was performed on 103 paraffin-embedded specimens from patients with primary OSCC, including 30 patients with locoregional lymph node metastasis, and in the sections from nude mice transplanted with two cell lines derived from a single human tongue cancer (SQUU-A and SQUU-B).Expression patterns of moesin in OSCCs were divided into three groups: membranous pattern; mixed pattern; and cytoplasmic pattern. These expression patterns correlated with tumor size, lymph node metastasis, mode of invasion, differentiation, and lymphocytic infiltration. In about two-thirds of the patients with metastatic lymph node, homogeneous cytoplasmic expression was detected in the metastatic lymph nodes. In addition, SQUU-B with high metastatic potential showed more reduced levels of membrane-bound moesin than SQUU-A with low metastatic potential. A multivariate analysis demonstrated that expression patterns of moesin can be an independent prognostic factor.Our results suggest that moesin expression contributed to discriminating between patients with the potentiality for locoregional lymph node metastasis and those with a better prognosis and might improve the definition of suitable therapy for each.
House Dust Endotoxin and Wheeze in the First Year of Life
Authors: JU-HYEONG PARK, DIANE R. GOLD, DONNA L. SPIEGELMAN, HARRIET A. BURGE, DONALD K. MILTON
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

We examined endotoxin exposure and wheezing episodes during the first year of life in a birth cohort of 499 infants with one or both parents having a history of asthma or allergy. We measured endotoxin in settled dust from the baby's bed, bedroom floor, family room, and kitchen floor within the first 3 mo after birth. The primary outcomes were any wheeze (versus no wheeze), and repeated wheeze (versus one or no report of wheeze). We found a significant univariate association of elevated endotoxin ( ⩾ 100 EU/ mg) in family room dust with increased risk of any wheeze (Relative Risk = 1.29, 95% CI = 1.03–1.62). The association was not confounded by cockroach allergen, lower respiratory illness (croup, bronchitis, bronchiolitis, and pneumonia), smoking during pregnancy, lower birth weight, maternal asthma, presence of dog, and race/ethnicity in a multivariate model; the multivariate relative risk (RR = 1.33) was marginally significant (95% CI: 1.00–1.76, p < 0.05). In a multivariate model, controlling for the above covariates, elevated endotoxin in family room dust was significantly associated with increased risk (RR = 1.56, 95% CI = 1.03–2.38) of repeated wheeze. These results suggest that home endotoxin exposure may independently increase risk of any wheeze and repeated wheeze during the first year of life for children with a familial predisposition to asthma or allergy.
Proposal for a new clinical entity, IgG4-positive multiorgan lymphoproliferative syndrome: analysis of 64 cases of IgG4-related disorders
Authors: Y Masaki, L Dong, N Kurose, K Kitagawa, Y Morikawa, M Yamamoto, H Takahashi, Y Shinomura, K Imai, T Saeki, A Azumi, S Nakada, E Sugiyama, S Matsui, T Origuchi, S Nishiyama, I Nishimori, T Nojima, K Yamada, M Kawano, Y Zen, M Kaneko, K Miyazaki, K Tsubota, K Eguchi, K Tomoda, T Sawaki, T Kawanami, M Tanaka, T Fukushima, S Sugai, H Umehara
Journal: Annals of the Rheumatic Diseases (2008)

<h3>Background:</h3> Mikulicz's disease (MD) has been considered as one manifestation of Sjögren's syndrome (SS). Recently, it has also been considered as an IgG<sub>4</sub>-related disorder. <h3>Objective:</h3> To determine the differences between IgG<sub>4</sub>-related disorders including MD and SS. <h3>Methods:</h3> A study was undertaken to investigate patients with MD and IgG<sub>4</sub>-related disorders registered in Japan and to set up provisional criteria for the new clinical entity IgG<sub>4</sub>-positive multiorgan lymphoproliferative syndrome (IgG<sub>4</sub>+MOLPS). The preliminary diagnostic criteria include raised serum levels of IgG<sub>4</sub> (&gt;135 mg/dl) and infiltration of IgG<sub>4</sub><sup>+</sup> plasma cells in the tissue (IgG<sub>4</sub>+/IgG+ plasma cells &gt;50%) with fibrosis or sclerosis. The clinical features, laboratory data and pathologies of 64 patients with IgG<sub>4</sub>+MOLPS and 31 patients with typical SS were compared. <h3>Results:</h3> The incidence of xerostomia, xerophthalmia and arthralgia, rheumatoid factor and antinuclear, antiSS-A/Ro and antiSS-B/La antibodies was significantly lower in patients with IgG<sub>4</sub>+MOLPS than in those with typical SS. Allergic rhinitis and autoimmune pancreatitis were significantly more frequent and total IgG, IgG<sub>2</sub>, IgG<sub>4</sub> and IgE levels were significantly increased in IgG<sub>4</sub>+MOLPS. Histological specimens from patients with IgG<sub>4</sub>+MOLPS revealed marked IgG<sub>4</sub>+ plasma cell infiltration. Many patients with IgG<sub>4</sub>+MOLPS had lymphocytic follicle formation, but lymphoepithelial lesions were rare. Few IgG<sub>4</sub>+ cells were seen in the tissue of patients with typical SS. Thirty-eight patients with IgG<sub>4</sub>+MOLPS treated with glucocorticoids showed marked clinical improvement. <h3>Conclusion:</h3> Despite similarities in the involved organs, there are considerable clinical and pathological differences between IgG<sub>4</sub>+MOLPS and SS. Based on the clinical features and good response to glucocorticoids, we propose a new clinical entity: IgG<sub>4</sub>+MOLPS.
Evolution of the Vertebrate Gene Regulatory Network Controlled by the Transcriptional Repressor REST
Authors: R. Johnson, J. Samuel, C. K. L. Ng, R. Jauch, L. W. Stanton, I. C. Wood
Journal: Molecular Biology and Evolution (2009)

Specific wiring of gene-regulatory networks is likely to underlie much of the phenotypic difference between species, but the extent of lineage-specific regulatory architecture remains poorly understood. The essential vertebrate transcriptional repressor REST (RE1-Silencing Transcription Factor) targets many neural genes during development of the preimplantation embryo and the central nervous system, through its cognate DNA motif, the RE1 (Repressor Element 1). Here we present a comparative genomic analysis of REST recruitment in multiple species by integrating both sequence and experimental data. We use an accurate, experimentally validated Position-Specific Scoring Matrix method to identify REST binding sites in multiply aligned vertebrate genomes, allowing us to infer the evolutionary origin of each of 1,298 human RE1 elements. We validate these findings using experimental data of REST binding across the whole genomes of human and mouse. We show that one-third of human RE1s are unique to primates: These sites recruit REST in vivo, target neural genes, and are under purifying evolutionary selection. We observe a consistent and significant trend for more ancient RE1s to have higher affinity for REST than lineage-specific sites and to be more proximal to target genes. Our results lead us to propose a model where new transcription factor binding sites are constantly generated throughout the genome; thereafter, refinement of their sequence and location consolidates this remodeling of networks governing neural gene regulation.
Azithromycin has an antiproliferative and autophagic effect on airway smooth muscle cells
Authors: R. Stamatiou, E. Paraskeva, K. Boukas, K. I. Gourgoulianis, P-A. Molyvdas, A. A. Hatziefthimiou
Journal: European Respiratory Journal (2009)

Azithromycin is used in long-term, low-dose treatment of airway diseases where airway wall remodelling is present. Since it improves total score symptom and respiratory function of such patients, we hypothesise that azithromycin's additional clinical benefits are due to an inhibition of airway smooth muscle cell (SMC) proliferation. Rabbit tracheal SMCs were treated with azithromycin (10(-5) to 10(-6) M) in the presence or absence of 10% fetal bovine serum (FBS). The proliferation was estimated using the Cell Titer 96(R) AQ(ueous) One Solution Assay (Promega, Madison, WI, USA). Cell viability was assessed with Trypan blue staining and flow cytometry after 7-aminoactinomycin D (7-AAD) staining. Induction of autophagy was studied by indirect immmunofluorescence and/or Western blotting with antibodies against human smooth muscle alpha-actin, beclin 1, light chain 3 and caspase 3. The involvement of the phosphoinositide 3-kinase pathway was investigated with the inhibitors LY294002 and wortmannin. Incubation with azithromycin for 72 h in the presence of FBS reduced SMC proliferation and viability in a dose-dependent manner. Azithromycin treatment was accompanied by the formation of cytoplasmic vacuoles, characteristic of autophagy. All these effects were reversible after azithromycin removal and prevented by the autophagy inhibitor, 3-methyladenine, or LY294002, but not by wortmannin. In conclusion, azithromycin reduces proliferation and causes autophagy of airway SMCs.