tbuckley/cabot-search huggingface dataset:
Abstract B57: Continuous exposure to epidermal growth factor in ovarian cancer cells causes a persistent increase in N-cadherin expression which then results in multicellular aggregate compaction
Authors: Sabrina L. Samudio-Ruiz, Laurie G. Hudson
Journal: Clinical Cancer Research (2013)

Abstract Ovarian cancer is the leading cause of death arising from gynecological malignancies. Overexpression of the epidermal growth factor receptor (EGFR) or its ligands is associated with poor prognosis. The presence of EGFR activators in patient ascites fluid may lead to constitutive activation of the EGFR and thereby contribute to metastasis and/or resistance to therapy. Acquired chemoresistance following initial chemotherapeutic treatment prevents clinical effectiveness and occurs in a large majority of patients. Thus, our studies evaluated the cellular consequences to prolonged EGF exposure/EGFR activation and how this could contribute to metastasis or chemoresistance. We found that extended exposure to EGF (10 nM, ~40 days) resulted in a change in cell phenotype that was retained even when the EGF ligand was removed for at least 7 days (removal). There was a persistent increase in N-cadherin and vimentin levels in EGF treated and removal cells. This increase in mesenchymal markers in EGF treated cells is associated with a significant increase in multicellular aggregate (MCA) compaction. Furthermore, EGF treated MCAs displayed a significant increase in cell spreading when allowed to adhere to collagen. MCA compaction and enhanced spreading were largely due to elevated N-cadherin levels as we found that knock down of N-cadherin resulted in less compact MCAs and reduced spreading on collagen. MCAs have been shown to be chemoresistant and the compact MCA structure due to prolonged EGF treatment conferred resistance to cisplatin treatment. Our results indicate that prolonged EGFR activation causes a persistent change in mesenchymal marker expression, which regulates MCA compaction and sensitivity to chemotherapeutics. This finding suggests that activators of the EGFR in the tumor environment may drive changes in ovarian cancer cells that contribute to the low patient survival rates. Citation Format: Sabrina L. Samudio-Ruiz, Laurie G. Hudson. Continuous exposure to epidermal growth factor in ovarian cancer cells causes a persistent increase in N-cadherin expression which then results in multicellular aggregate compaction. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: From Concept to Clinic; Sep 18-21, 2013; Miami, FL. Philadelphia (PA): AACR; Clin Cancer Res 2013;19(19 Suppl):Abstract nr B57.
Na+/H+ exchange and regulation of intracellular Ca2+
Authors: M. KARMAZYN, M. P MOFFAT
Journal: Cardiovascular Research (1993)

Journal Article Na+/H+ exchange and regulation of intracellular Ca2+ Get access MORRIS KARMAZYN, MORRIS KARMAZYN Department ot Pharmacology and Toxicology, University of Western Ontano. London, Ontano N6A 5C1. Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar MARGARET P MOFFAT MARGARET P MOFFAT Department ot Pharmacology and Toxicology, University of Western Ontano. London, Ontano N6A 5C1. Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 27, Issue 11, November 1993, Pages 2079–2080, https://doi.org/10.1093/cvr/27.11.2079a Published: 01 November 1993
Fighting Spirit: The Story of Women in the Bristol Breast Cancer Survey
Authors: I. M Peat
Journal: BMJ (1996)

Ed Heather Goodare Scarlet Press, £8.99, pp 168 ISBN 1 85727 033 9

In June 1986, women being treated for breast cancer who were also attending the Bristol Cancer Help Centre for complementary therapies agreed to participate in a research project. The five-year study to compare their quality of life and survival with that of a control group of women receiving orthodox treatment only was funded by cancer research charities.

In September 1990, when interim results from the first two years were published, there was incredulity and alarm—it appeared that those attending …
Intérêt de l'examen du grêle par vidéocapsule chez les patients atteints de spondylarthrite ankylosante (SPA) prenant des anti-inflammatoires non stéroïdiens (AINS) au long cours
Authors: M Ould Hocine, A Chryssostalis, V Abitbol, C Roux, D Lamarque, M Breban, F Prat, S Chaussade
Journal: Endoscopy (2007)

La SPA est un rhumatisme inflammatoire constituant un modèle de prise continue d'AINS au long cours. Chez le rat, la toxicité des AINS sur l'intestin grêle est diminuée par la prise d'Anti Tumor Necrosis Factor alpha (Anti-TNFα).
Treatment of Cytomegalovirus Retinitis with 9-[2-Hydroxy-1-(hydroxymethyl)ethoxymethyl]guanine
Authors: DONNA FELSENSTEIN
Journal: Annals of Internal Medicine (1985)

Cytomegalovirus infections can cause significant morbidity and mortality in immunosuppressed patients, and present antiviral agents have had little efficacy against these infections. We describe the use of an acyclic nucleoside 9-[2-hydroxy-1-(hydroxymethyl)ethoxymethyl]guanine (BW B759U), in the treatment of two patients with cytomegalovirus retinitis. The efficacy of this agent was evident, with healing of retinal lesions and resolution of viremia and viral shedding. BW B759U appears to be similar pharmacokinetically to intravenous acyclovir in terms of half-life, peak serum levels, and renal excretion.
The Effect of Fine-Needle Aspiration Biopsy on the Thyroid Scan
Authors: DONALD L. GORDON, ROBERT WAGNER, GARY L. DILLEHAY, NANDA KHEDKAR, CHARLES J. MARTINEZ, WILLIAM BAYER, MARION H. BROOKS
Journal: Clinical Nuclear Medicine (1993)

Fine-needle aspiration biopsy (FNAB) is the most sensitive and specific procedure in diagnosing benign from malignant thyroid nodular disease. The effects of a FNAB on the thyroid scan, however, have never been studied. This assumes importance because a hot nodule on scan has been advocated as useful to differentiate certain benign from malignant follicular neoplasms. Thyroid scans were performed before and after FNAB on 11 patients with nodular thyroid disease and an area of normal or increased uptake either in the nodule or in a contralateral enlarged lobe to determine if the biopsy changed the pattern of isotope uptake. For this study, biopsies were done in the area of normal or increased uptake. In two patients, there was a reduction in isotope concentration in three nodules after FNAB, whereas no change was demonstrable in nine other patients. Review of the literature revealed a number of prior reports of hemorrhage, necrosis, or infarction of thyroid nodules after FNAB. Based on these data and the demonstration of a change in scan pattern in a patient following FNAB, it is concluded that FNAB may decrease the isotope uptake in thyroid nodules; therefore, the concept of clinical judgments being based on the scan pattern after FNAB should be reevaluated.
ATTENUATED VASOCONSTRICTOR RESPONSES TO CORONARY ARTERIAL ASPIRATE FROM PATIENTS WITH PACLITAXEL ELUTING STENT VERSUS BARE METAL STENT IMPLANTATION FOR SAPHENOUS VEIN AORTO-CORONARY BYPASS STENOSIS
Authors: Petra Kleinbongard, Dirk Böse, Thomas Konorza, Florian Steinhilber, Stefan Möhlenkamp, Holger Eggebrecht, Theodor Baars, Hubertus Degen, Michael Haude, Bodo Levkau, Raimund Erbel, Gerd Heusch
Journal: Journal of the American College of Cardiology (2011)
Surgery for combined type small cell lung carcinoma
Authors: R Hage, J R J Elbers, A B. de la Riviere, J M M van den Bosch
Journal: Thorax (1998)

<h3>BACKGROUND</h3> Combined type small cell lung cancer (SCLC) has been reported to occur in, at most, 1% of all cases of SCLC. These tumours consist of SCLC with a component of squamous cell carcinoma and/or adenocarcinoma. The survival of patients with combined and pure SCLC after surgical resection was assessed. <h3>METHODS</h3> From 1977 to 1994 2115 patients with bronchogenic carcinoma underwent pulmonary resection. From this group 26 patients (1.2%) were diagnosed as having combined SCLC and 74 patients (3.5%) as having pure SCLC. <h3>RESULTS</h3> From the 26 patients with combined SCLC (mean age 66.4 years) three were classified as pT1N0M0, eight as pT2N0M0, four as postoperative stage II, and 11 as postoperative stage III. Histological examination showed a component of squamous cell carcinoma in 21 patients. There were 18 (69%) lobectomies, seven (27%) pneumonectomies, and one (4%) segmentectomy. In all patients surgery was thought to be curative. Overall hospital mortality was 4% (n = 1). Cumulative five year survival was 31% for all hospital survivors with combined SCLC postoperative stage I, 50% for those with pT1N0M0, and 25% for those with pT2N0M0 disease. No patients with postoperative stage II and III disease survived for five years. In the 74 patients with pure SCLC hospital mortality was 3% (n = 2); cumulative five year survival was 39% in patients with postoperative stage I disease, 46% for those with pT1N0M0 and 35% for those with pT2N0M0. When compared with pure SCLC, no significant differences in five year survival were evident in patients with postoperative stage I disease. <h3>CONCLUSIONS</h3> Surgical resection in patients with combined SCLC postoperative stage I yields a cumulative five year survival of 31% while for those with stage II and III disease there were no survivors at five years. In patients with stage I combined or pure SCLC surgery can offer a long term disease free interval or may even be curative.
Hazards of an Alternative Medicine Device in a Patient with a Pacemaker
Authors: Marcel Furrer, Barbara Naegeli, Osmund Bertel
Journal: New England Journal of Medicine (2004)

To the Editor: Both patients and health care professionals should be aware of potential pacemaker interactions in the environment, since cardiac pacemakers and defibrillators are sensitive to many kinds of electromagnetic interference. A 52-year-old man with a dual-chamber pacemaker, implanted because of intermittent, symptomatic, high-degree atrioventricular block, presented with short episodes of dizziness and near-fainting. A detailed history revealed that the symptoms occurred exclusively during self-prescribed therapy with a Zapper device. The Zapper, which is available worldwide, is a simple, battery-powered, direct-current–offset pulse generator with square-wave output at a constant frequency of 33.3 kHz ±10 percent. These electronic pulse frequencies . . .
Abstract A16: Role of Hsp90alpha-1, a splice variant of Hsp90alpha, in cancer
Authors: Suman Ghosh, Laura B. Peterson, George Vielhauer, Brian S. J Blagg
Journal: Cancer Research (2013)

Abstract Molecular chaperone complexes, such as heat shock proteins 90 (Hsp90) and its co-chaperones, are essential for folding nascent polypeptides into their biologically active structures and for the refolding of aggregated and denatured proteins that occur upon cellular stress including cancer. Hsp90 exists as four isoforms in humans. Among them, Hsp90alpha is induced under stressful conditions, detected in the cytoplasm, nucleus and is secreted into extracellular space under metastatic conditions. Hsp90alpha is phosphorylated by DNA-PK at the nucleus under apoptotic conditions and localizes at the edge of the nucleus. Intrigued by the fact that Hsp90alpha might play a role in metastasis as well as in stress resistance, the mechanism of action of Hsp90alpha was investigated. Here we report that Hsp90alpha-1, a splice variant of Hsp90alpha, is up-regulated in cancer cells, predominantly associates with co-chaperone Aha1 in-vivo at the filopodia like extrusion of cell. The Hsp90alpha-1/Aha1 complex was partially disrupted by C- terminal inhibitors in-vivo conditions; and Hsp90alpha-1 and Aha1 redistributed to the cytoplasm from the filopodia following the treatment with the C- terminal inhibitors. Gene knock down analysis reveals that several P-Akt pathway and MAP Kinase pathway proteins were Hsp90alpha-1 dependent. P-Akt also co-localized with the Hsp90alpha-1/Aha1 complex at the filopodia region and suggests that Hsp90alpha-1 plays critical role in maturing/folding proteins that are important for establishing and maintaining cell polarity which is perturbed by the C- terminal inhibitors. Under apoptotic conditions the Hsp90alpha-1/Aha1 complex is present in the cytoplasm and nucleus and Hsp90alpha-1 is phosphorylated. Survivin, being a Hsp90alpha-1 dependent client protein, binds with the Hsp90alpha-1/Aha1 complex at normal and apoptotic conditions confirms that Survivin play dual role in mediating metastases as well as an Inhibitor of Apoptotic Protein (IAP). Citation Format: Suman Ghosh, Laura B. Peterson, George Vielhauer, Brian S. J Blagg. Role of Hsp90alpha-1, a splice variant of Hsp90alpha, in cancer. [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr A16.
Mutation analysis and characterization of alternative splice variants of the Wilson disease gene ATP7B
Authors: Lei Wan, Chang-Hai Tsai, Chin-Moo Hsu, Chin-Chang Huang, Chih-Chao Yang, Chiu-Chu Liao, Chin-Ching Wu, Yu-An Hsu, Cheng-Chun Lee, Su-Ching Liu, Wei-De Lin, Fuu-Jen Tsai
Journal: Hepatology (2010)

Wilson disease is a copper metabolism disorder caused by mutations in ATP7B, a copper-transporting adenosine triphosphatase. A molecular diagnosis was performed on 135 patients with Wilson disease in Taiwan. We identified 36 different mutations, eight of which were novel: five missense mutations (Ser986Phe, Ile1348Asn, Gly1355Asp, Met1392Lys, and Ala1445Pro), one deletion (2810delT) in the coding region, and two nucleotide substitutions (−133A→C and −215A→T) in the promoter region. These mutations were not observed in 100 control subjects and reduced the activity of the mutated protein by at least 50% when compared with wild-type ATP7B. In addition to exon 8, our data indicate another mutation hotspot in exon 12 where 9.62% of all mutations occurred. An alternative splice variant of ATP7B lacking exon 12 was observed in one patient who had a homozygous 2810delT mutation and very mild clinical symptoms. Clinical examination and functional characterization of alternative splice variants of ATP7B lacking exon 12 showed that they retained 80% of their biological activity. The 2810delT mutation increased the expression of these variants, which may have explained the mild symptoms in the patient with the 2810delT mutation. We also discovered that treating liver cancer cells with a Na+/H+ exchanger inhibitor, 5-( N -ethyl - N -isopropyl)-amiloride, significantly enhanced the expression of the alternative splice variant of ATP7B lacking exon 12. Conclusion: This study suggests a novel therapeutic strategy for patients with mutations in exon 12. (Hepatology 2010;52:1662-1670)
Rapid Diagnosis and Treatment of TIAs Help Reduce Recurrent Stroke Risk
Authors: Mike Mitka
Journal: JAMA (2007)

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
Sorafenib Inhibits the Imatinib-Resistant <i>KIT</i> <i>T670I</i> Gatekeeper Mutation in Gastrointestinal Stromal Tumor
Authors: Tianhua Guo, Narasimhan P. Agaram, Grace C. Wong, Glory Hom, David D'Adamo, Robert G. Maki, Gary K. Schwartz, Darren Veach, Bayard D. Clarkson, Samuel Singer, Ronald P. DeMatteo, Peter Besmer, Cristina R. Antonescu
Journal: Clinical Cancer Research (2007)

Abstract Purpose: Resistance is commonly acquired in patients with metastatic gastrointestinal stromal tumor who are treated with imatinib mesylate, often due to the development of secondary mutations in the KIT kinase domain. We sought to investigate the efficacy of second-line tyrosine kinase inhibitors, such as sorafenib, dasatinib, and nilotinib, against the commonly observed imatinib-resistant KIT mutations (KITV654A, KITT670I, KITD820Y, and KITN822K) expressed in the Ba/F3 cellular system. Experimental Design: In vitro drug screening of stable Ba/F3 KIT mutants recapitulating the genotype of imatinib-resistant patients harboring primary and secondary KIT mutations was investigated. Comparison was made to imatinib-sensitive Ba/F3 KIT mutant cells as well as Ba/F3 cells expressing only secondary KIT mutations. The efficacy of drug treatment was evaluated by proliferation and apoptosis assays, in addition to biochemical inhibition of KIT activation. Results: Sorafenib was potent against all imatinib-resistant Ba/F3 KIT double mutants tested, including the gatekeeper secondary mutation KITWK557-8del/T670I, which was resistant to other kinase inhibitors. Although all three drugs tested decreased cell proliferation and inhibited KIT activation against exon 13 (KITV560del/V654A) and exon 17 (KITV559D/D820Y) double mutants, nilotinib did so at lower concentrations. Conclusions: Our results emphasize the need for tailored salvage therapy in imatinib-refractory gastrointestinal stromal tumors according to individual molecular mechanisms of resistance. The Ba/F3 KITWK557-8del/T670I cells were sensitive only to sorafenib inhibition, whereas nilotinib was more potent on imatinib-resistant KITV560del/V654A and KITV559D/D820Y mutant cells than dasatinib and sorafenib.
Interaction of dietary cholesterol and triglycerides in the regulation of hepatic low density lipoprotein transport in the hamster.
Authors: D K Spady, J M Dietschy
Journal: Journal of Clinical Investigation (1988)

These studies report the effects of dietary cholesterol and triglyceride on rates of receptor-dependent and receptor-independent LDL transport in the liver of the hamster. In animals fed diets enriched with 0.1, 0.25, or 1% cholesterol for 1 mo, receptor-dependent LDL transport in the liver was suppressed by 43, 63, and 77%, respectively, and there were reciprocal changes in plasma LDL-cholesterol concentrations. In addition, dietary triglycerides modified the effect of dietary cholesterol on hepatic LDL transport and plasma LDL concentrations so that at each level of cholesterol intake, polyunsaturated triglycerides diminished and saturated triglycerides accentuated the effect of dietary cholesterol. When animals were raised from weaning on diets containing small amounts of cholesterol, the decline in receptor-dependent LDL transport was nearly abolished by the addition of polyunsaturated or monounsaturated triglycerides, but was markedly augmented by the addition of saturated lipids. When animals raised on diets containing cholesterol and saturated triglycerides were returned to the low cholesterol, low triglyceride control diet, hepatic receptor-dependent LDL transport and plasma LDL-cholesterol concentrations returned essentially to normal within 2 wk. Neither receptor-independent LDL transport nor the receptor-dependent uptake of asialofetuin was significantly altered by dietary cholesterol or triglyceride suggesting that the effect of these lipids on hepatic LDL receptor activity was specific and not due to a generalized alteration in the physiochemical properties of hepatic membranes. These studies demonstrate the important role of saturated triglycerides in augmenting the effect of cholesterol in suppressing hepatic LDL receptor activity and elevating LDL-cholesterol levels.
A seroepidemiological study of cytomegalovirus and Epstein-Barr virus in rheumatoid arthritis and sicca syndrome.
Authors: P J Venables, M G Ross, P J Charles, R D Melsom, P D Griffiths, R N Maini
Journal: Annals of the Rheumatic Diseases (1985)

Antibodies to cytomegalovirus (CMV) and Epstein-Barr virus capsid antigen (EBVCA) were examined in 41 patients with rheumatoid arthritis (RA), 26 patients with primary sicca syndrome, and 26 healthy subjects of similar age and sex. IgG antibody titres to EBVCA and CMV were similar in all three groups, apart from a trivial increase of antibodies to EBVCA in RA. False positive IgM anti-CMV antibodies detected in serum from one patient with sicca syndrome and 20 patients with RA were shown to be due to rheumatoid factors. These data did not support recent suggestions that patients with these diseases showed exaggerated immunological responses to either virus and emphasised the need to incorporate adequate laboratory and disease controls when seroepidemiological studies are performed on sera containing rheumatoid factors and autoantibodies.
Hyperplastic Polyposis Coli Syndrome and Colorectal Carcinoma
Authors: C. Rubio, S. Stemme, E. Jaramillo, A. Lindblom
Journal: Endoscopy (2006)

Background: Patients with hyperplastic polyposis coli syndrome (HPCS) have a propensity to develop colorectal carcinoma (CRC). Patients and Methods: Details were retrieved from the files of patients attending our hospital between 1988 and 2004 who fulfilled the World Health Organization criteria for HPCS. Results: Over a period of 16 years, 10 cases of HPCS were identified at our hospital (0.625 cases/year or one case every 1.6 years). A mean of 40.3 hyperplastic polyps per patient were found (range 6 - 159). Other colorectal lesions were found as follows: two patients each had one mixed polyp; there were 15 serrated adenomas in eight patients; and there were 30 tubular, tubulovillous, or villous adenomas in eight patients. Among the 10 patients with HPCS, seven developed a CRC. Of the four villous adenomas, three were associated with a CRC, but only one of the 15 serrated adenomas was associated with a CRC. The pathway of cancer evolution in HPCS patients remains unresolved. Conclusions: Similarly to our results, a review of the literature indicates a high incidence of CRCs in HPCS patients. These patients are at a high risk of developing a CRC and should therefore receive regular colonoscopic surveillance.
SUDDEN AND TEMPORARY MENTAL ABERRATION—UNCONSCIOUS AUTOMATISM— TEMPORARY IRRESPONSIBLE STATES.
Authors: SAMUEL AYRES
Journal: JAMA (1902)

The problems in psychology are numerous and fascinating, and many are yet unsolved. A man may be able to carry on a considerable conversation to-day, during which he betrays only slight peculiarities, perhaps only some exaggeration in speech; or, unless he is watched closely, he may not appear out of the ordinary; to-morrow he declares he has no recollection of the conversation. But what a loophole this hiatus may offer to one dissatisfied with his contract, or to one on the wrong side of the market who wishes to repudiate the order to his broker of the previous day, or to the one who wants to curse or annihilate his enemy! It is a fact, though, that there are certain individuals who at times perform certain automatic acts, or say certain things, or are seized with sudden delusions or hallucinations, who, after a period of a few minutes, or a
TIME TRENDS IN CARDIOVASCULAR DRUG TREATMENT AND CARDIOVASCULAR EVENTS IN PATIENTS WITH ACUTE HEART FAILURE
Authors: Olav R. De Peuter, Gregory Y. Lip, Olaf H. Klungel, Patrick C. Souverein, Deirdre Lane, Harry R. Büller, Anthonius De Boer, Pieter W. Kamphuisen
Journal: Journal of the American College of Cardiology (2010)