tbuckley/cabot-search huggingface dataset:
Immunophenotypic clustering of B-Cell chronic lymphocytic leukemia (B-CLL) reveals a good prognosis disease subset characterized by the coordinated over-expression of CD62L, CD54, CD49c, CD25 And CD55
Authors: V. Gattei, M. Degan, S. Russo, R. Bomben, M. Dal Bo, M. Rupolo, F. Buccisano, G. Del Poeta, P. Sonego, A. Zucchetto
Journal: Journal of Clinical Oncology (2004)

6567 Background: Studies of B-CLL gene expression profiling revealed a phenotype mainly related to experienced B cells, although only a B-CLL subset has IgVH gene mutations. Methods: We investigated in flow cytometry the expression of a panel (36 markers) of cell-adhesion molecules, integrins, complement activity regulators, myeloid, T and B antigens in 123 well-characterized B-CLLs (94 with survivals, 109 with IgVH mutations). Data analyses was made by applying unsupervised (hierarchical and non-hierarchical) clustering algorithms, and the nearest-centroid method as class predictor. Results: Hierarchical clustering identified at least three subgroups, one of them (62 cases), over-expressing CD62L, CD54, CD49c, CD55 and CD25, with a significantly longer survival (p=0.00031). We applied, therefore, a non-hierarchical K-Means clustering algorithm by requiring to divide cases into three subgroups. The following phenotypic profiles were found: i) group I (51 cases): low/negative expression of CD38, CD49d, CD29, CD49e; high expression of CD62L, CD54, CD49c, CD25 and CD55; ii) group II (36 cases): high expression of CD38, CD49d, CD29, CD49e; low/negative expression of CD62L, CD54, CD49c, CD25 and CD55; iii) group III (36 cases) low/negative expression of both the above groups of markers. Other molecules were either negative (CD49a, b, f, CD26, CD70, CD103, FMC7) or expressed by all samples (SmIg, CD20, CD79a, CD24, CD19, CD5, CD52, CD27, CD23, CD43, CD59). According to survival data, B-CLL patients belonging to group I were all alive for the duration of follow-up (p=0.0001). Class predictor methods identified the coordinated above-average expression of CD62L, CD54, CD49c, CD25 and CD55 as the signature for group I cases. Group I B-CLLs were characterized by a high number of mutated IgVH cases (30/38 vs. 40/71, p<0.05) and of cases with IgVH mutations consistent with antigen-driven selection (26/38 vs. 27/71, p<0.01). Conclusions: We propose the use of CD62L, CD54, CD49c, CD25 and CD55 as additional prognosticators for identify good prognosis B-CLL. No significant financial relationships to disclose.
Dose-Dependent Fate of Vinyl Chloride and Its Possible Relationship to Oncogenicity in Rats
Authors: P. G. Watanabe, P. J. Gehring
Journal: Environmental Health Perspectives (1976)

Studies on the fate of 14C-labeled vinyl chloride (VC) following oral administration and inhalation exposure in rats demonstrated that the disposition of VC in the body is a function of the dose. More importantly, from the data available, it appears that a correlation exists between doses of VC which cause tumors and those that saturate metabolic or detoxifying pathways. Additional studies characterized the depression of liver non-protein sulfhydryl content (primarily GSH) with the duration and concentration of exposure to VC. The results of these investigations indicate that statistical projections utilizing data collected from rats exposed to high doses of VC are invalid for predicting the hazard of low level exposure, because such projections violate a priori assumption that the dynamics governing the fate of VC in the body are unaltered.
Failure of isoniazid to cure localized BCG infection
Authors: B. Lorber
Journal: JAMA (1977)

INFECTIOUS complications of BCG vaccination and immunotherapy have been rare, even in immunosuppressed patients who have responded readily to two to four months of isoniazid therapy.<sup>1,2</sup>We report a case in which accidental BCG inoculation led to a localized hand infection that failed to respond to three months of isoniazid therapy. <h3>Report of a Case</h3> On Sept 10, 1975, a physician engaged in laboratory research accidentally inoculated the dorsum of her right index finger over the distal interphalangeal joint with BCG diluted in saline. It is estimated that she received a maximum of 12 × 10<sup>7</sup>colonyforming units. Over the next two days the finger became painful and swollen, and two weeks later an ulcerative lesion developed at the injection site. A smear of the lesion showed acid-fast bacilli, and cultures grew an organism subsequently identified as BCG. After three months of isoniazid treatment (300 mg/day), there was
Drug-Induced Pulmonary Fibrosis
Authors: Ian Y. R. Adamson
Journal: Environmental Health Perspectives (1984)

The lung is a primary target of cell injury in patients receiving cytotoxic drugs, and in many cases the reaction is severe enough to produce diffuse pulmonary fibrosis. Although many different agents may damage the lung, the patterns of cellular injury and repair are relatively constant. Using bleomycin toxicity as an example, it has been shown that, after IV injection, the selective site of lung injury is the vascular endothelium; this is followed by the accumulation of interstitial edema and later by necrosis of Type I epithelial cells. In normal repair, rapid proliferation of Type II cells, followed by differentiation to Type I, restores the epithelial surface without fibrosis. However, after bleomycin, Type II cell proliferation is frequently followed by abnormal differentiation to a metaplastic form of epithelium. Fibroblast proliferation accompanies this abnormal epithelial response which is related either to selective retention of bleomycin by epithelial cells or to the toxic effects of administering more drug at the time of Type II cell division. It is concluded that diffuse interstitial fibrosis results from prolonged disturbance of the normal epithelial-mesenchymal interrelationships at the alveolar wall. Disruption of the fibroblastic control system by extensive epithelial necrosis or by delayed or inappropriate repair may be the key factor in instigating fibroblast proliferation and subsequent deposition of collagen. This mechanism may account for the development of diffuse fibrosis or fibrosing alveolitis in response to a variety of pulmonary toxins.
Erratum to: DNA methylome profiling of human tissues identifies global and tissue-specific methylation patterns
Authors: Kaie Lokk, Vijayachitra Modhukur, Balaji Rajashekar, Kaspar Märtens, Reedik Mägi, Raivo Kolde, Marina Koltšina, Torbjörn K. Nilsson, Jaak Vilo, Andres Salumets, Neeme Tönisson
Journal: Genome biology (2016)
The Liverpool Statement 2005: Priorities for the European Union/United States Spiral Computed Tomography Collaborative Group
Authors: J K. Field, R A. Smith, S W. Duffy, C D. Berg, R van Klaveren, C I. Henschke, D Carbone, P E. Postmus, E Paci, F R. Hirsch, J L. Mulshine
Journal: Journal of Thoracic Oncology (2006)
Side effects of glucocorticoid treatment. Experience of the Optic Neuritis Treatment Trial
Authors: G. A. Chrousos
Journal: JAMA (1993)

<h3>Objective.</h3> —To determine the incidence of side effects from short-term glucocorticoid therapy prescribed for treatment of optic neuritis in the Optic Neuritis Treatment Trial. <h3>Design.</h3> —Randomized, placebo-controlled, multicenter clinical trial. <h3>Setting.</h3> —Fifteen university- or hospital-based centers throughout the United States. <h3>Patients.</h3> —A total of 457 patients between the ages of 18 and 46 years with acute demyelinative optic neuritis were studied. <h3>Interventions.</h3> —(1) Intravenous methylprednisolone (250 mg every 6 hours) for 3 days while hospitalized followed by oral prednisone (1 mg/kg per day) for 11 days; (2) oral prednisone (1 mg/kg per day) for 14 days; and (3) oral placebo for 14 days. Each regimen was followed by a short taper. <h3>Results.</h3> —Only two patients experienced major side effects, psychotic depression in one and acute pancreatitis in the other. Both of these patients were from the intravenous methylprednisolone group and both of the side effects resolved without sequelae. Patients in both groups receiving active drugs more often reported sleep disturbances, mood change, stomach upset, and facial flushing and gained more weight during the treatment period than patients in the placebo group (<i>P</i>&lt;.001 for each comparison). <h3>Conclusions.</h3> —Although minor side effects are common, short-term glucocorticoid therapy in young, healthy adults is relatively safe. Because of the infrequency of serious side effects, outpatient administration of high-dose intravenous glucocorticoids may be feasible. (<i>JAMA</i>. 1993;269:2110-2112)
A Doctor Studies Crime
Journal: JAMA (1934)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Gamma, Not Beta, Radiation
Journal: JAMA (1969)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
LETTER FROM NEW YORK.
Authors: None P. B. P.
Journal: JAMA (1889)

(FROM OUR OWN CORRESPONDENT.) Meeting of the New York County Medical Association—A Paper on Diphtheria by Dr. J. Lewis Smith—Its Etiology—Mode of Propagation—The Specific Cause received chiefly by Inhalation with the Air—Capability of being Communicated from Man to Animals and the Reverse—Means of Prevention by different Modes of Disinfection, etc. At the last meeting of the New York County Medical Association Dr. J. Lewis Smith read a paper on<i>The Cause, Mode of Propagation, and Prevention of Diphtheria</i>. Stating that, although the belief that this disease is of microbic origin is constantly being strengthened by the investigations made in regard to it, it is still a matter of doubt what microbe (or possibly microbes), is the causal agent, he first gave an admirable<i>résumé</i>of the bacteriology of the subject, as developed by various observers during the last twenty years. It was, he said, the conclusions of Drs. Curtis and
Notes on New Names
Journal: JAMA (1964)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Contact urticaria and airway obstruction from carbonless copy paper
Authors: J. G. Marks
Journal: JAMA (1984)

A 27-year-old woman experienced pruritus, eye and throat irritation, hoarseness, shortness of breath, and fatigue within half an hour of exposure to carbonless copy paper. On two separate occasions, she was purposely challenged in a controlled-blinded fashion with portions of the carbonless copy paper. This resulted on both occasions in contact urticaria of the hand that held the paper and changes in pulmonary function flow-volume loops characteristic of upper airway obstruction. To determine if alterations in prostaglandin (PG) metabolism might explain these findings, plasma PGF<sub>2α</sub>and thromboxane B<sub>2</sub>(both capable of causing these symptoms) were measured before and during the second exposure period. Both PGF<sub>2α</sub>and thromboxane B<sub>2</sub>increased substantially. We conclude that the cutaneous and respiratory symptoms induced by carbonless copy paper were probably related to PG release. (<i>JAMA</i>1984;252:1038-1040)
Circulation Research, New York
Journal: JAMA (1966)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Analysis of angiogenesis biomarkers for ramucirumab (RAM) efficacy in patients with metastatic colorectal cancer (mCRC) from RAISE, a global, randomized, double-blind, Phase 3 study
Authors: J. Tabernero, R.R. Hozak, T. Yoshino, A.L. Cohn, R. Obermannova, G. Bodoky, R. Garcia-Carbonero, T-E. Ciuleanu, D.C. Portnoy, K. Muro, H. Ouyang, S. Melemed, D. Ferry, F. Nasroulah, E. Van Cutsem
Journal: Annals of Oncology (2017)
Human Exposure to Urban Air Pollution
Authors: Carl-Elis Bostrom, Jacob Almen, Bengt Steen, Roger Westerholm
Journal: Environmental Health Perspectives (1994)

This study deals with some methods of making human exposure estimates, aimed at describing the human exposure for selected air pollutants in Sweden that are suspected carcinogens.Nitrogen oxides (NOX) have been chosen as an indicator substance for estimating the concentration of the urban plume.Earlier investigations have shown that the traffic in Swedish cities contributes around 85% to the measured NOx concentrations, and that most of the mutagenicity in urban air originates from traffic.The first section of this paper describes measurements in Stockholm of some unregulated light hydrocarbons, such as ethene, ethyne, propane, propene, butane, and isobutane.In addition, measurements of some volatile aro- matic hydrocarbons are presented.Simultaneous measurements of carbon monoxide (CO) were made.The ratios between CO and the individual specific compounds were determined by linear regression analysis.By analysis of relationships between CO and NO X, NO concentrations can be used as a tracer to describe the exposure for these specific compounds.NOX are considered to be a better tracer than CO, because NOX or NO2 values exist for many places over a long time, while CO is measured mostly in streets with high concentrations.At low concentrations, instruments that measure normal CO levels give no detectable signals.Through use of atmospheric dispersion models and models that describe how people live and work in urban areas it has been possible to describe the average exposure to NOx in cities of different sizes.The exposure to NOx for people liv- ing in the countryside has also been estimated.In this way, it has been possible to calculate the average exposure dose for NOX for the Swedish population.This figure is 23 pg/mi3.By use of the relationships between NOX and specific compounds the average dose has been calculated for the following compounds: polyaromatic compounds (PAH); ethene, propene, and butadiene; benzene, toluene, and xylene; formaldehyde and actaldehyde; nickel, chromium (VI), arsenic, and cadmium; asbestos; and silicon.
National Diabetes Awareness Month—November 1997
Journal: JAMA (1997)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 5505: MyD88-dependent signaling decreases the anti-tumor efficacy of epidermal growth factor receptor inhibition in head and neck cancer cells
Authors: Andrean L. Simons-Burnett, Adam T. Koch, Laurie Love-Homan, Aditya Stanam
Journal: Cancer Research (2015)

Abstract Epidermal growth factor receptor (EGFR) is upregulated in the majority of head and neck squamous cell carcinomas (HNSCC). However many HNSCC patients respond poorly to EGFR inhibitors (EGFRIs) despite tumor expression of EGFR. Gene expression analysis of erlotinib-treated HNSCC cell lines revealed an upregulation of genes involved in MyD88-dependent interleukin-6 (IL-6) expression compared to their respective vehicle treated cell lines. We therefore proposed that MyD88-dependent signaling may reduce the anti-tumor efficacy of the EGFR inhibitor erlotinib in HNSCC. Erlotinib significantly upregulated IL-6 secretion which we have previously reported to result in reduced drug efficacy and drug resistance (Fletcher et al, 2013). Suppression of MyD88 expression significantly blocked erlotinib-induced IL-6 secretion in vitro and increased the anti-tumor activity of erlotinib in vivo. There was little to no evidence of toll-like receptor (TLR) or interleukin-18 receptor (IL-18R) involvement in erlotinib-induced IL-6 secretion. However, suppression of the interleukin-1 receptor (IL-1R) signaling through pharmacologic and genetic methods significantly reduced erlotinib-induced IL-6 production and increased HNSCC cell sensitivity to erlotinib in vitro. A time-dependent increase of IL-1 alpha (IL-1α) but not IL-1 beta (IL-1β) was observed in response to erlotinib treatment and IL-1α blockade significantly increased the anti-tumor activity of erlotinib and the EGFR antibody inhibitor cetuximab in vivo. Pre-treatment with a pan-caspase inhibitor but not a caspase-1 inhibitor reduced erlotinib-induced IL-1α secretion suggesting that IL-1α was released due to cell death. Human HNSCC tumors showed higher IL-1α mRNA levels compared to matched normal tissue, and IL-1α was found to be negatively correlated with survival in HNSCC patients. Overall, the IL-1α/IL-1R/MYD88/IL-6 pathway may be responsible for the reduced anti-tumor efficacy of erlotinib and other EGFRIs; and blockade of the MyD88-dependent signaling may improve the efficacy of EGFRIs in the treatment of HNSCC. Citation Format: Andrean L. Simons-Burnett, Adam T. Koch, Laurie Love-Homan, Aditya Stanam. MyD88-dependent signaling decreases the anti-tumor efficacy of epidermal growth factor receptor inhibition in head and neck cancer cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 5505. doi:10.1158/1538-7445.AM2015-5505
Industrial bladder cancer
Authors: R W Glashan
Journal: BMJ (1982)

Industrial bladder cancer SIR,-In a leading article on industrial bladder cancer (27 February, p 614) Robin Glashan claims that evidence from a study by Vineis et al purports to show that engineering workers using lubricating oil are at risk.'The paper by Vineis gives the results of a study into the incidence of larynx, bladder, and infantile tumours occurring among residents of towns in the province of Turin in the period 1965-9 and is in Italian.A careful reading of the paper, and the English abstract, reveals no reference to lubricating oil, greases, or lubricant in any form.I feel it is important to put this correction on record as there is no evidence either from this article or elsewhere that workers using lubricant oils are at any special risk of bladder cancer.
Rab27a controls HIV-1 assembly by regulating plasma membrane levels of phosphatidylinositol 4,5-bisphosphate
Authors: P. Pereyra Gerber, M. Cabrini, C. Jancic, L. Paoletti, C. Banchio, C. von Bilderling, L. Sigaut, L. Pietrasanta, G. Duette, E Freed, G. de Saint Basile, C. Ferreira Moita, L. Ferreira Moita, S. Amigorena, P. Benaroch, J. Geffner, Matias Ostrowski
Journal: The Journal of Experimental Medicine (2015)