tbuckley/cabot-search huggingface dataset:
Issues Raised on Availability Of Breast Cancer Materials For Research
Authors: Linda F. Anderson
Journal: JNCI Journal of the National Cancer Institute (1994)

Journal Article Issues Raised on Availability Of Breast Cancer Materials For Research Get access Linda F. Anderson Linda F. Anderson Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 21, 2 November 1994, Pages 1580–1582, https://doi.org/10.1093/jnci/86.21.1580 Published: 02 November 1994
AB0137 Positive effects of anti-melanocyte stimulating hormone in murine pristane-induced lupus
Authors: T. V. Peixoto, S. B. Mello, D. A. Botte, S. Carrasco, M. B. Vendraminni, C. Goldenstein-Schainberg
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Alfa-melanocyte stimulating hormone (α-MSH) has a variety of biological functions including reduction of skin delayed-type hypersensitivity, blockage of leukocyte migration, downregulation of pro-inflammatory pathways and inhibition of experimental disease models development including rheumatoid arthritis and inflammatory bowel disease. Nevertheless the anti-inflammatory and immunomodulatory effects of α-MSH on pristane-induced lupus remain unknown. <h3>Objectives</h3> To evaluate the effect of a commercial α-MSH analogue (NDP α-MSH)in improving clinical and serological aspects of murine lupus. <h3>Methods</h3> Thirty-five BALB/c mice were injected with a single intraperitoneal (IP) dose of 0.5ml pristane for lupus-like model induction and 5 age/gender matched control mice were given saline. Pristane-induced lupus animals received daily IP saline (n=5) or treatments with 3.1mg/kg/d chloroquine (n=10), 1.25mg/kg/d NDP α-MSH (n=10) or 2.5mg/kg/d NDP α-MSH (n=10). Clinical and laboratorial lupus-like parameters were examined before and 180 days after induction, when all animals were sacrificed. Sera ANA was analyzed by IF using Hep2 cells. Mann-Whitney and Fisher test were performed for statistical analysis and P&lt;0,05 considered significant. <h3>Results</h3> All lupus-like animals presented large amounts of lipogranulomas in peritoneal cavity, and developed arthritis in both hind legs in contrast to all controls. Of note, lupus animals treated with both doses of α-MSH had important less amounts and smaller lipogranulomas, by visual observation. Mean arthritis score in 5 untreated mice, 9 animals treated with chloroquine and 8 with α-MSH 2.5mg/kg/d was 5.2, 3.33 and 3.1 respectively. Remarkably, mean arthritis score of animals treated with α-MSH 1.25 mg/kg/d was 1.6, significantly lower than untreated mice (1.6 vs 5.2, P=0.0291). Sera ANAs were negative in all 40 animals before pristane lupus injection and 180 days after induction remained negative in normal mice but became positive in all 5 (100%) untreated lupus animals, 7 (77%), 4 (50%) and 3 (35%) of lupus models treated with chloroquine, α-MSH 2.5mg/kg/d and α-MSH 1.25mg/kg/d (100% vs 35%, P=0,0256), respectively. Three animals died before the end of the experiment, by day 150: 1 treated with chloroquine and 2 with higher doses of α-MSH. <h3>Conclusions</h3> Improvement of clinical and serological parameters promoted by NDP α-MSH in experimental model of pristane-induced lupus, may suggest a potential role for this drug in human SLE. <h3>Disclosure of Interest</h3> None Declared
Abstract 1579: Establishment of transgenic medaka as a stable tumor model for <i>in vivo</i> screening of anticancer drugs.
Authors: Yuriko Matsuzaki, Haru Hosokai, Yukiyo Mizuguchi, Atsushi Shimizu, Hideyuki Saya
Journal: Cancer Research (2013)

Abstract The development of anticancer drugs would be facilitated by the availability of an in vivo screening system based on a multicellular organism. We intended to construct an animal model which can be stable and easily detected tumors without autopsy for chemical screening and assessment. In this study, the medaka which is a small egg-laying freshwater fish native to East Asia was applied. The medaka has proved suitable for toxicology and carcinogenesis in the past studies. Furthermore most of molecular technology is available to the medaka and the size of the medaka genome (∼800 Mb) is about half that of the zebrafish genome. To construct a tumor model using transgenic medaka fish, a promoter sequence suitable for the tissue specific tumorigenesis was selected. There are some genes having specific expression in melanocyte. Melanocyte specific expression of oncogenes may induce progression to melanoma. Therefore we selected a promoter sequence encoding Tyrosinase, one of the melanocyte specific genes. The recombinant plasmids for microinjection are consisting of the medaka tyrosinase promoter and human oncogenes (cMyc, BRAF mutant V600E and HRAS mutant G12V). One cell stage embryos were applied for microinjection. We obtained three stable transgenic individuals derived from one cMyc and two BRAF mutant (BRAF600E) injected F0, but none from HRAS mutant (HRAS12V). The transgenic (Tg)-cMyc and the Tg-BRAF600E produced tumor in internal organs with more than 50 % of all fish, but in eyes or skins (outer detectable organs) with less than 10 %. The Tg-HRAS12V animals died before achieving adulthood. We therefore developed a conditional gene expression system in which HRAS12V is expressed in response to the induction of Cre recombinase by heat treatment, given that the Cre gene was placed under the control of a medaka heat shock promoter. One of the stable transgenic lines developed abnormal pigment cell proliferation in the eyes and epidermis with 100% penetrance by 6 months postfertilization. Sorafenib, an inhibitor of RAS signaling, was administered to the transgenic fish and was found both to reduce the extent of melanophore proliferation and to improve survival. This Tg-HRAS12V medaka established here thus represents a promising in vivo system with which to screen potential anticancer drugs that target RAS signaling, and this system can readily be adapted for the screening of agents that target other oncogenes. Citation Format: Yuriko Matsuzaki, Haru Hosokai, Yukiyo Mizuguchi, Atsushi Shimizu, Hideyuki Saya. Establishment of transgenic medaka as a stable tumor model for in vivo screening of anticancer drugs. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1579. doi:10.1158/1538-7445.AM2013-1579
Estimated Glomerular Filtration Rate is Associated with Both Arterial Stiffness and N Terminal Pro-brain Natriuretic Peptide in Newly Diagnosed Hypertensive Patients
Authors: Mustafa Gür, Durmuş Yıldıray Şahin, Hakan Uçar, Osman Kuloğlu, Ali Kıvrak, Taner Şeker, Caner Türkoğlu, Betül Özaltun, Onur Kaypaklı, Zafer Elbasan, Halil İbrahim Tanboğa, Murat Çaylı
Journal: Journal of the American College of Cardiology (2013)
Fungal Infection from Sweeping in the Wrong Place
Authors: Tommy Hing Cheung Tang, Owen Tak Yin Tsang
Journal: New England Journal of Medicine (2011)

A 43-year-old man presented with fever, malaise, a nonproductive cough, and skin lesions near the left eyelid and eyebrow (Panel A) and left antecubital fossa (Panel B). The symptoms had developed during the course of several weeks. The patient underwent a biopsy of the facial lesion. Histopathological analysis of the biopsy specimen revealed changes characteristic of coccidioidal infection, including granulomatous inflammation and spherules containing endospores (Panel C, arrow; hematoxylin and eosin). Antibodies to coccidioides species were present in his serum. Although the patient had no history of travel to an area where coccidioidomycosis is endemic, he worked as a driver . . .
Abstract A19: Enhanced leptin receptor expression identifies an aggressive subset of Middle Eastern papillary thyroid cancer
Authors: Khawla S. Al-Kuraya, Prashant Bavi, Abdul K. Siraj, Shahab Uddin
Journal: Cancer Research (2009)

Abstract The putative role of leptin (Ob) and its receptor (Ob-R) in the pathogenesis of various primary human malignancies has been investigated in recent studies. However, the role of leptin and leptin receptor (Ob-R) in papillary thyroid cancer (PTC) has not yet been evaluated. In this study we investigated role of Ob-R in a large tissue microarray cohort of PTC followed by in vitro studies using a panel of PTC cell lines. Ob-R overexpression was seen in 80% PTCs and was significantly associated with poor disease free survival (p=0.0235). PTCs that overexpressed Ob-R showed a aggressive phenotype characterized by older age, extrathyroid extension, larger tumor size, nodal metastasis, advanced stage and tall cell variant histological subtype (p=0.0005, p=0.0006, p=0.0398, p= 0.0004, p=0.0111 and p=0.0003 respectively). Further PTCs with overexpression of Ob-R showed a significant direct association with overexpression of leptin (p=0.0004), XIAP (p&amp;lt;0.0001) and BCL-XL (p&amp;lt;0.0001). In vitro analysis showed that leptin stimulated cell proliferation and inhibited apoptosis via activation of phosphatidylinisitol 3-kinase (PI3K)/AKT signalling pathway. Inhibition of PI3K activity by LY294002, a specific inhibitor of PI3K kinase abrogated leptin-mediated PI3K/AKT signalling. Gene silencing of Ob-R with Ob-R siRNA in PTC cells resulted in down regulation of phospho-AKT, Bcl-XL and XIAP expression suggesting that leptin mediated pathogenesis of PTC occur via involvement of these downstream targets. Altogether these data suggest that leptin plays a critical role in PTC pathogenesis through PI3K/AKT pathway via Ob-R and is a potential prognostic marker associated with an aggressive phenotype and poor disease free survival. Citation Information: Cancer Res 2009;69(23 Suppl):A19.
Strategies to Circumvent Testosterone Surge and Disease Flare in Advanced Prostate Cancer: Emerging Treatment Paradigms
Authors: Venkata K. Pokuri, Houman Nourkeyhani, Bodie Betsy, Laurie Herbst, Marcus Sikorski, Edward Spangenthal, Andrew Fabiano, Saby George
Journal: Journal of the National Comprehensive Cancer Network (2015)

The testosterone surge and disease flare is a feared complication from initiation of gonadotropin-releasing hormone (GnRH) agonist treatment in advanced prostate adenocarcinoma. It is a common practice to start an average 7-day pretreatment regimen with an antiandrogen agent before initiating GnRH agonist therapy, to circumvent disease flare from testosterone surge. However, this might not be the best strategy and can be harmful, especially in patients at high risk of imminent organ damage from minimal testosterone surge. Surgical castration is a simple and cost-effective method that should be considered in these scenarios. But most patients refuse this procedure because of the permanent and psychologic impact of surgery. Novel GnRH antagonists, such as degarelix, and cytochrome P450 17 (CYP17) enzyme inhibitors, such as ketoconazole, achieve castrate-equivalent serum testosterone levels much faster than traditional GnRH agonists without the need for coadministration of antiandrogens. This article reports on 3 cases of impending oncologic emergencies in advanced prostate adenocarcinoma treated promptly with degarelix and ketoconazole without any disease flare related to testosterone surge. In the setting of symptomatic hormone-naïve metastatic prostate cancer, the authors suggest clinical trials using abiraterone, orteronel, and other newer agents that target the CYP17 axis (eg, ketoconazole) for fine-tuning the emergent medical castration methods and avoiding the dangers from the flare phenomenon.
Mitochondrial Inheritance in a Mitochondrially Mediated Disease
Authors: Joseph Egger, John Wilson
Journal: New England Journal of Medicine (1983)

Mendelian inheritance involves the transmission to successive generations of DNA contained in genes in the nucleus, but DNA is also contained in mitochondria, where it is believed to be responsible for the encoding of certain mitochondrial enzymes. Since nearly all mitochondrial DNA is maternally transmitted, one might expect a nonmendelian pattern of inheritance in mitochondrial cytopathy, a syndrome in which there are abnormalities in mitochondrial structure and deficiencies in a variety of mitochondrial enzymes. We studied the pedigrees of 6 affected families whose members we had examined personally and of 24 families described in the literature. In 27 families, exclusively maternal transmission occurred; in 3 there was also paternal transmission in one generation. Altogether, 51 mothers but only 3 fathers had transmitted the condition. These results are consistent with mitochondrial transmission of mitochondrial cytopathy; the inheritance and enzyme defects of mitochondrial cytopathy can be considered in the light of recent evidence that subunits of respiratory-enzyme complexes are encoded solely by mitochondrial DNA. The occasional paternal transmission may be explained if certain enzyme subunits that are encoded by nuclear DNA are affected.
Abstract 3907: Discovery and characterization of AZ285 as a potent and selective inhibitor of CK2 kinase
Authors: James E. Dowling, Marat Alimzhanov, Larry Bao, Patrick Brassil, Emma L. Cooke, Christopher R. Denz, Zhong-Ying Liu, Qing Ye, Paul D. Lyne
Journal: Cancer Research (2012)

Abstract Casein Kinase 2 (CK2) is a highly conserved and ubiquitously expressed serine/threonine kinase that regulates several key oncogenic signaling pathways, including PI3K/AKT, and NFkB and Wnt, and whose targeted overexpression in transgenic animal models results in neoplastic growth. Herein we describe the identification of AZ285, a potent pyrazolo[1,5-a]pyrimidine-derived inhibitor of CK2 with a high degree of kinase selectivity. AZ285 depletes levels of the CK2 substrates pAKTS129 and PTENS370 and induces apoptosis in cells in a concentration-dependent manner. Optimization of early leads was aided in part by cell wash-out experiments and X-ray cocrystallography with huCK2a and resulted in an agent with physical properties and DMPK characteristics suitable for evaluation in disease model studies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3907. doi:1538-7445.AM2012-3907
The Health Services since the War: Volume II. Government and Health Care: British National Health Service 1958-1979, by Charles Webster
Authors: G. Macpherson
Journal: BMJ (1997)

Charles Webster / Stationery Office, £85, pp 988 / ISBN 0 11 630963 6

Maldistribution of resources, capital investment an urgent priority, poor administrative integration, and discontents about pay. Just another year in the life of the National Health Service. Not, however, 1997 but 1958, the year at which Charles Webster starts the second volume of his official history of the NHS.

The author takes readers to 1979, a landmark year that saw widespread turbulence among NHS and other public sector staff, a disappointing royal commission review of the NHS, and the launch of the Thatcherite political revolution. Among the vast catalogue of complex events he covers are the first dramatic change in the service's structure–the 1974 reorganisation–as well as the root and branch reform of the social services and four royal commissions: on doctors' and dentists' pay, mental illness, medical education, and the NHS itself.

Though 1979 proved to be the start of a long march to a market driven NHS, in that year the service was still recognisable as the one launched by Aneurin Bevan 31 years earlier. As Webster rightly observes, with direct taxation still the prime funding source and patients still benefiting from care free at the point of delivery, the health service remained unarguably a national one. But it still had deep seated organisational weaknesses, rooted in its mixed local government, voluntary hospital, …
Abstract LB-400: Conventional and anti-microbial pesticide exposures and increased risk of lung cancer in Mexican Americans
Authors: Michelle K McHugh, Sumesh Kachroo, Mei Liu, Anthony M. D'Amelio, Qiong Dong, Anthony Greisinger, Waun Ki Hong, Margaret R. Spitz, Carol J. Etzel
Journal: Cancer Research (2010)

Abstract Objective: We investigated demographic factors, environmental and occupational exposures, and medical and family cancer histories in a population of Mexican-American lung cancer cases and controls from the Houston Metropolitan area. Methods: Data were collected as a part of a multi-racial/ethnic on-going lung cancer case-control study. Cases included 212 Mexican American lung cancer cases. Controls (n=328) were recruited from Houston's largest multispecialty group practice and frequency matched to the cases by age (±5 years), sex and ethnicity. Odds ratios and 95% confidence intervals were calculated using logistic regression analysis. Environmental and occupational factors were analyzed individually; however pesticides were analyzed as: 1) any exposure to conventional or antimicrobial pesticides; 2) exposure to conventional pesticides only; and 3) exposure to antimicrobial pesticides only. Results: We detected elevated risks of lung cancer associated with asbestos, wood dust, fibers, SVF, benzene, toluene/xylene, dry cleaning fluids, vehicle exhaust, glues and plastics; however only pesticide exposure was statistically significant. We found both conventional and anti-microbial pesticide exposures were associated with an increased risk of lung cancer in Mexican Americans (conventional pesticides and antimicrobial pesticides combined: OR=1.80, 95%CI 1.13-2.86; conventional pesticides: OR=2.05, 95% CI 1.23-2.39; and anti-microbial pesticides: OR=2.48, 95% CI 1.46-4.21). Conclusions: Although we found over a two-fold increased risk of lung cancer among Mexican Americans for conventional and anti-microbial pesticides, we were not able to identify individual pesticides. Our findings are descriptive in nature and we believe are a necessary and important preliminary step in identifying factors that are specifically associated with lung cancer risk among this minority subgroup. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-400.
Familial visceral myopathy diagnosed by exome sequencing of a patient with chronic intestinal pseudo-obstruction
Authors: Øystein Holla, Gunter Bock, Øyvind Busk, Björn Isfoss
Journal: Endoscopy (2014)

A 55-year-old woman with a history of bowel dysmotility presented with abdominal distension and peritonitis. Family history included premature deaths with intestinal symptomatology, suggesting autosomal dominant inheritance. Computed tomography showed a distended small bowel. Symptoms were alleviated by enterocutaneous stomas. Initial ileal biopsy suggested neuropathy; however, exome sequencing revealed an Arg148Ser mutation in the enteric smooth muscle actin gamma 2 (ACTG2) gene. Histological reassessment showed abnormal muscularis propria and smooth muscle actin, with the same findings in sibling, confirming familial visceral myopathy. Thus, noninvasive genomic analysis can provide early and specific diagnosis of familial visceral myopathy, which may help to avoid inappropriate surgery.
Erratum: Corrigendum: Germline RECQL mutations are associated with breast cancer susceptibility
Authors: Cezary Cybulski, Jian Carrot-Zhang, Wojciech Kluźniak, Barbara Rivera, Aniruddh Kashyap, Dominika Wokołorczyk, Sylvie Giroux, Javad Nadaf, Nancy Hamel, Shiyu Zhang, Tomasz Huzarski, Jacek Gronwald, Tomasz Byrski, Marek Szwiec, Anna Jakubowska, Helena Rudnicka, Marcin Lener, Bartłomiej Masojć, Patrica N Tonin, Francois Rousseau, Bohdan Górski, Tadeusz Dębniak, Jacek Majewski, Jan Lubiński, William D Foulkes, Steven A Narod, Mohammad R Akbari
Journal: Nature Genetics (2016)
New Technique To Diagnose Eye Cancer Being Tested
Authors: K. Smigel
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article New Technique To Diagnose Eye Cancer Being Tested Get access Kara Smigel Kara Smigel Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 2, 18 January 1989, Pages 94–95, https://doi.org/10.1093/jnci/81.2.94 Published: 18 January 1989
STATIN USE AT TIME OF RESPIRATORY VIRAL INFECTION IN PATIENTS WITH PRIOR HISTORY OF CARDIOVASCULAR DISEASE AND RISK OF SUBSEQUENT CARDIOVASCULAR EVENTS
Authors: Stacey Knight, Russell R. Miller III, Tami Bair, Benjamin Horne, Bert K. Lopansri, Jeffrey Anderson, J. Muhlestein, John Carlquist
Journal: Journal of the American College of Cardiology (2015)
Doctor Judas; a Portrayal of the Opium Habit.
Journal: JAMA (1895)

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Early detection of pancreatic cancer in patients with intraductal papillary mucinous neoplasms: the pivotal role of endoscopic ultrasound
Authors: Julio Iglesias-Garcia, J. Domínguez-Muñoz
Journal: Endoscopy (2013)

Pancreatic cancer is the fifth leading cause of cancer death in Western countries, and the second highest cause of cancer death among gastrointestinal tumors, with more than 250 000 deaths per year worldwide. With a death rate that nearly equals its incidence, pancreatic cancer is considered to be one of the malignant tumors with the poorest survival [1] [2]. The only group of patients with pancreatic cancer who have an acceptable prognosis are those with potentially resectable lesions [3] [4] [5] [6]. In this context, there is significant interest in the screening and early detection of pancreatic cancer.