tbuckley/cabot-search huggingface dataset:
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Authors: Thomas B. Cole
Journal: JAMA (2009)

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
Bolus fluorouracil for metastatic colorectal carcinoma?
Authors: J A Ajani
Journal: Journal of Clinical Oncology (1989)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1989.7.9.1366 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 2769332 Bolus fluorouracil for metastatic colorectal carcinoma? J A AjanixJ A AjaniSearch for articles by this author https://doi.org/10.1200/JCO.1989.7.9.1366 PDF "Bolus fluorouracil for metastatic colorectal carcinoma?." Journal of Clinical Oncology, 7(9), pp. 1366–1367© 1989 by American Society of Clinical Oncology
Rituximab Is Highly Effective In The Treatment Of Patients With Autoimmune Blood Cytopenias, Particularly When It Is Followed By a Post-Induction Consolidation / Maintenance Phase
Authors: Argiris Symeonidis, Nikolaos Giannakoulas, Eleni Kapsali, Anna Christoforidou, Zoe Topouzoglou, Polyxeni Lampropoulou, Evangelia Tzouvara, Nikolaos Anagnostopoulos, Dimitris Margaritis, George Vassilopoulos, Evangelos Briasoulis, Alexandra Kouraklis
Journal: Blood (2013)
Next‐generation sequencing in systemic mastocytosis: Derivation of a mutation‐augmented clinical prognostic model for survival
Authors: Animesh Pardanani, Terra Lasho, Yoseph Elala, Emnet Wassie, Christy Finke, Kaaren K. Reichard, Dong Chen, Curtis A. Hanson, Rhett P. Ketterling, Ayalew Tefferi
Journal: American Journal of Hematology (2016)

In routine practice, the World Health Organization classification of systemic mastocytosis (SM) is also the de facto prognostic system; a core value is distinguishing indolent (ISM) from advanced SM (includes aggressive SM [ASM], SM with associated hematological neoplasm [SM-AHN] and mast cell leukemia [MCL]). We sequenced 27 genes in 150 SM patients to identify mutations that could be integrated into a clinical-molecular prognostic model for survival. Forty four patients (29%) had ISM, 25 (17%) ASM, 80 (53%) SM-AHN and 1 (0.7%) MCL; overall KITD816V prevalence was 75%. In 87 patients, 148 non-KIT mutations were detected; the most frequently mutated genes were TET2 (29%), ASXL1 (17%), and CBL (11%), with significantly higher mutation frequency in SM-AHN > ASM > ISM (P < 0.0001). In advanced SM, ASXL1 and RUNX1 mutations were associated with inferior survival. In multivariate analysis, age > 60 years (HR = 2.4), hemoglobin < 10 g/dL or transfusion-dependence (HR = 1.7), platelet count < 150 × 10(9) /L (HR = 3.2), serum albumin < 3.5 g/dL (HR = 2.6), and ASXL1 mutation (HR = 2.3) were associated with inferior survival. A mutation-augmented prognostic scoring system (MAPSS) based on these parameters stratified advanced SM patients into high-, intermediate-, and low-risk groups with median survival of 5, 21 and 86 months, respectively (P < 0.0001). These data should optimize risk-stratification and treatment selection for advanced SM patients. Am. J. Hematol. 91:888-893, 2016. © 2016 Wiley Periodicals, Inc.
Abstract A31: Monitoring the activity of various classes of methylltransferases in vitro using a universal, homogenous and bioluminescent assay
Authors: Said A. Goueli
Journal: Cancer Research (2016)

Abstract Post transcriptional modifications of proteins and nucleic acids are well-recognized to play major role in mediation of extensive and broad range of cellular functions. Such modifications that include phosphorylation, acetylation, methylation, etc. are known to be critical for normal and abnormal cell growth, and thus, the enzymes involved in these reactions have been validated as drug targets resulting in the development of several drugs. Recent biochemical and biological data suggest that the enzymatic activities of several of these enzymes have pathogenic roles in cancer, inflammation, and neurodegenerative diseases. Thus, pharmacological modulation of these enzymes by small molecules will be beneficial in the development of novel therapeutics for multiple unmet medical needs. Of these, methyltransferases are known to alter the epigenome by altering the methylation status of nucleic acids or proteins resulting in changes in cellular phenotypes. Towards this goal of searching for activators/inhibitors of these enzymes for the development of next generation of drugs, screening assays for these modulators are urgently needed. To address these unmet needs, we have developed a novel assay that monitors the activities of these enzymes and their modulation by small molecules. The assay is bioluminescent based, HTS formatted and highly sensitive. The assay is universal since it is based on monitoring the formation of the universal product S-adenosylhomocysteine (SAH), i.e., capable of detecting changes in activity of a broad range of methyltransferases such as DNA, protein, RNA, and small molecules methyltransferases. In addition, the assay has been validated for all classes of protein methyltransferases (Lysine and Arginine), and with different types of substrates (small peptides, large proteins, or even nucleosomes). This enables determining the specificity of these enzymes and their substrate requirements. The assay has high signal to background and low C.V. The assay is robust (Z’ value &amp;gt; 0.7) and has been validated using various plate densities such as 96-, 384, and 1536-well plates. A strong feature of this assay is its utility with broad range of substrates with no limitations on the use of high concentrations of substrates or the composition of the substrates (short vs. long peptides), thus enabling the generation of kinetic data and determining the mechanism of action of various modulators of methyltransferases of interest. Citation Format: Said A. Goueli. Monitoring the activity of various classes of methylltransferases in vitro using a universal, homogenous and bioluminescent assay. [abstract]. In: Proceedings of the Fourth AACR International Conference on Frontiers in Basic Cancer Research; 2015 Oct 23-26; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2016;76(3 Suppl):Abstract nr A31.
Failure of Bile as Abetting Agent for 20-Methylcholanthrene in Induction of Gastric Tumors in Mice&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;
Authors: Claude R. Hitchcock, M. D.
Journal: JNCI Journal of the National Cancer Institute (1951)

Failure of Bile as Abetting Agent for 20-Methylcholanthrene in Induction of Gastric Tumors in Mice2 Claude R. Hitchcock, M. D. Claude R. Hitchcock, M. D. Department of Surgery, University of Minnesota Medical School, Minneapolis, Minn. Search for other works by this author on: Oxford Academic PubMed Google Scholar 3Senior Cancer Research Fellow, U. S. Public Health Service. 4The author expresses his gratitude to Dr. Robert Hebbel, Department of Pathology, University of Minnesota Medical School, for his assistance in reviewing the microscopic material and aiding in the diagnosis of lesions. Author Notes JNCI: Journal of the National Cancer Institute, Volume 12, Issue 2, October 1951, Pages 369–397, https://doi.org/10.1093/jnci/12.2.369 Published: 01 October 1951 Article history Received: 25 May 1951 Published: 01 October 1951
Is adjuvant therapy justified for women with small breast cancers?
Authors: D B Duggan
Journal: Journal of Clinical Oncology (1988)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1988.6.9.1520 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 3418378 Is adjuvant therapy justified for women with small breast cancers? D B DugganxD B DugganSearch for articles by this author https://doi.org/10.1200/JCO.1988.6.9.1520 PDF "Is adjuvant therapy justified for women with small breast cancers?." Journal of Clinical Oncology, 6(9), p. 1520© 1988 by American Society of Clinical Oncology
RNA interference
Authors: Julian Downward
Journal: BMJ (2004)

Over the past decade “RNA interference” has emerged as a natural mechanism for silencing gene expression. This ancient cellular antiviral response can be harnessed to allow specific inhibition of the function of any chosen target genes, including those involved in causing diseases such as cancer, AIDS, and hepatitis. RNA interference is already proving to be an invaluable research tool, allowing much more rapid characterisation of the function of known genes. More importantly, the technology considerably bolsters functional genomics to aid in the identification of novel genes involved in disease processes. But can RNA interference be used as an effective therapeutic strategy? Many people in the biotechnology industry are betting that it can, but first considerable problems relating to delivery to target cells will have to be solved. This problem has proved the undoing of previous wonder technologies such as gene therapy and antisense. This review discusses the promises and pitfalls of RNA interference in research and treatment.

This article is based on a review of the literature on RNA interference and post-transcriptional gene silencing appearing in the PubMed database, along with personal experience of working in this field for the past four years. It also draws on consensus views expressed at several international conferences on RNA interference in 2003.
Abstract P3-06-10: t-Darpp enhances protein kinase A signaling through direct effects on PKA holoenzyme and indirectly influences cell metabolism, proliferation and apoptosis
Authors: G Lenz, D Theile, SE Kane
Journal: Cancer Research (2016)

Abstract Trastuzumab has dramatically improved the adjuvant therapy of Her2-positive breast cancer. However, acquired resistance to trastuzumab frequently occurs. Breast cancer cells in vitro selected for trastuzumab resistance exhibit over-expression of t-Darpp, a truncated form of the 32 kDa dopamine and cAMP-regulated phosphoprotein (Darpp-32). t-Darpp over-expression has previously been demonstrated to confer trastuzumab resistance and to result in increased protein kinase A (PKA) activity and signaling. Phosphorylation of Darpp-32 at threonine 75 has been shown to promote inhibition (not activation) of PKA by a yet unknown mechanism. T75 phosphorylation on t-Darpp is required for its trastuzumab resistance activity but the role of T75 phosphorylation in PKA activation by t-Darpp is not known and the molecular mechanism by which t-Darpp enhances PKA activity has not been reported. We used cells stably over-expressing either wild type t-Darpp or a T75A mutant of t-Darpp. Using proximity ligation assays, we found that t-Darpp binds directly to the RI regulatory subunit of PKA leading to 75% less RI subunit bound to the catalytic subunit of PKA (PKAc), compared to parental cells. In contrast, the t-Darpp-T75A mutant does not bind RI and those cells have only 34% less RI bound to PKAc compared to parental. These results suggest a direct effect of t-Darpp on PKA activation by binding the regulatory subunit RI and thereby preventing RI from inhibiting PKAc. The T75 phosphorylation site appears to be required for this activity. Using enzymatic and caspase activity assays, we also show that cells over-expressing t-Darpp, but not t-Darpp-T75A, have increased proliferation, up to 4-fold more cellular ATP, and diminished apoptotic response to etoposide, relative to parental cell controls. So far, this data suggests a dual mode of t-Darpp action: modulation of cell metabolism (possibly via effects on ATP production) and direct effects on PKA holoenzyme. Ultimately, pro-apoptotic response is diminished. Further studies will determine whether PKA activation by t-Darpp is responsible for, or separately influenced by, the metabolic effects of t-Darpp. Citation Format: Lenz G, Theile D, Kane SE. t-Darpp enhances protein kinase A signaling through direct effects on PKA holoenzyme and indirectly influences cell metabolism, proliferation and apoptosis. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P3-06-10.
Abstract A44: Clinical value of immunohistochemical expression of EGFL7 within high-grade serous ovarian cancer tissue.
Authors: Jacek Jan Sznurkowski, Anton Zawrocki, Maciej Pawlowski
Journal: Clinical Cancer Research (2016)

Abstract Epidermal growth factor like domain 7 (Egfl7) is expressed by endothelial cells in normal tissues and by malignant cells in various human tumors. Aim: to analyze patterns of immunohistochemical (IHC) staining of Egfl7 within high grade serous ovarian cancer (HGSOC) tissue and to assess clinical value of this biomarker. Material and methods: The IHC staining and pathological analyses were performed on paraffin-embedded primary tumours collected from 73 HGSOC patients with verified clinical history. Mouse anti-human monoclonal antibody against Egfl7, was used. Egfl7 expressing tumors were classified qualitatively in accordance to intense of staining (HSCORE). The appropriate statistical analyses were performed. P-values of &amp;lt;0.05 were regarded as significant. Results: Egfl7 was expressed by the cancer cells within 63 of 73 primary HGSOC tumors (68.3%). Endothelial expression of this biomarker was sporadic. Cancer cells presented two patterns of staining: cytoplasmic only in 50/72 cases (69.4%) and nuclear/cytoplasmic in 13/72 cases (18%). Median duration of the follow-up was 47.25 months (range 17–79 months) Cytoplasmic expression of Egfl7 was not correlated with any of clinico-pathological features as well as with prognosis. The presence of nuclear/cytoplasmic staining within HGSOC predicts worse response for chemotherapy and correlates with increased preoperative levels of CA125. Conclusion: Cancer endogenous expression of Egfl7 is frequent within HGSOC tissue. Predictive value of nuclear/cytoplasmic staining of Egfl7 for chemoresistance should be further evaluated. Citation Format: Jacek Jan Sznurkowski, Anton Zawrocki, Maciej Pawlowski. Clinical value of immunohistochemical expression of EGFL7 within high-grade serous ovarian cancer tissue. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr A44.
An international outbreak of Shiga toxin-producing Escherichia coli O157 infection due to lettuce, September – October 2007
Authors: I Friesema, G Sigmundsdottir, K van der Zwaluw, A Heuvelink, B Schimmer, C de Jager, B Rump, H Briem, H Hardardottir, A Atladottir, E Gudmundsdottir, W van Pelt
Journal: Eurosurveillance (2008)

Between 14 September and 20 October 2007, an outbreak of Shiga toxin-producing Escherichia coli (STEC) O157 simultaneously occurred in the Netherlands and Iceland. A total of 50 laboratory-confirmed cases were reported with a STEC O157 infection caused by the same clone. The strain was of type O157:H-, PT8, positive for stx 1 , stx 2 , eae and e-hly, and sorbitol negative. The most probable cause of this international outbreak was contaminated lettuce, shredded and pre-packed in a Dutch food processing plant. Samples of the environment, raw produce and end products, taken at several vegetable growers and processing plants all tested negative for STEC O157. However, the only epidemiological link between the cases in the Netherlands and in Iceland was the implicated Dutch processing plant. In Europe, food products are often widely distributed posing the risk of potential spread of food borne pathogens simultaneously to several countries. This international outbreak emphasises the importance of common alert and surveillance systems in earlier detection of international outbreaks and better assessment of their spread.
Transcription factor TLX1 controls retinoic acid signaling to ensure spleen development
Authors: Elisa Lenti, Diego Farinello, Kazunari K. Yokoyama, Dmitry Penkov, Laura Castagnaro, Giovanni Lavorgna, Kenly Wuputra, Lisa L. Sandell, Naomi E. Butler Tjaden, Francesca Bernassola, Nicoletta Caridi, Anna De Antoni, Michael Wagner, Katja Kozinc, Karen Niederreither, Francesco Blasi, Diego Pasini, Gregor Majdic, Giovanni Tonon, Paul A. Trainor, Andrea Brendolan
Journal: Journal of Clinical Investigation (2016)

The molecular mechanisms that underlie spleen development and congenital asplenia, a condition linked to increased risk of overwhelming infections, remain largely unknown. The transcription factor TLX1 controls cell fate specification and organ expansion during spleen development, and Tlx1 deletion causes asplenia in mice. Deregulation of TLX1 expression has recently been proposed in the pathogenesis of congenital asplenia in patients carrying mutations of the gene-encoding transcription factor SF-1. Herein, we have shown that TLX1-dependent regulation of retinoic acid (RA) metabolism is critical for spleen organogenesis. In a murine model, loss of Tlx1 during formation of the splenic anlage increased RA signaling by regulating several genes involved in RA metabolism. Uncontrolled RA activity resulted in premature differentiation of mesenchymal cells and reduced vasculogenesis of the splenic primordium. Pharmacological inhibition of RA signaling in Tlx1-deficient animals partially rescued the spleen defect. Finally, spleen growth was impaired in mice lacking either cytochrome P450 26B1 (Cyp26b1), which results in excess RA, or retinol dehydrogenase 10 (Rdh10), which results in RA deficiency. Together, these findings establish TLX1 as a critical regulator of RA metabolism and provide mechanistic insights into the molecular determinants of human congenital asplenia.
Challenges of identifying and treating patellofemoral osteoarthritis
Authors: David T Felson
Journal: British Journal of Sports Medicine (2016)

Twenty-five per cent of persons aged 30 years and over experience knee pain on most days.1 For many, the pain is mild and avoidable but for a substantial number, it limits activity and diminishes the quality of life. The patellofemoral joint is often the source of this pain, especially among women. Among those 45 years and over, knee pain is most likely to be due to osteoarthritis (OA) and the patellofemoral joint is often affected.2 If osteoarthritic patellofemoral pain could be identified and treated successfully, it might offer opportunities to substantially reduce the burden of knee pain in the community among middle-aged and older persons.

Patellofemoral osteoarthritic pain occurs in a knee with underlying OA, and usually patellofemoral and tibiofemoral compartments are affected. It is often extremely challenging to identify whether the pain is emanating from the patellofemoral joint or elsewhere in the knee. Much osteoarthritic pain originates in an inflamed synovium and most of the synovium is located superior to the patella. Therefore, when …
Two outbreaks of trichinellosis in the state of Northrhine-Westfalia, Germany, 1998
Authors: S Rehmet, G Sinn, O Robstad, H David, D Lesser, K Nöckler, G Scherholz, k D Erkrath, D Pechmann, L Petersen, R Kundt, G Oltmans, R Lange, J Laumen, U Nogay, M Dixius, J Eichenberg, F Dinse, D Stegemann, W Lotz, D Franke, P Hagelschur, A Ammon
Journal: Eurosurveillance (1999)

Illness or death from trichinellosis is statutorily notifiable in Germany. Between nought and ten cases were reported each year from 1987 to 1997. From November 1998 to January 1999, however, 52 cases of trichinellosis were identified by the public health
Outbreak of trichinellosis in the Midi-Pyrénées region of France January - March 1998
Authors: S Haeghebaert, M Servat, C Duchen, J- C Minet, A EAgrech, I Thièse, C Leclerc, V Vaillant, C Hemery, E Maillot, C Soulé, E Pozio, P Massip, J. F. Magnaval, J C Desenclos
Journal: Eurosurveillance (1998)

Two outbreaks of trichinellosis in the Tarn et Garonne, departement, France were reported by the departmental health autorities on 2 March 1998, to the Reseau National de Sante Publique (RNSP). An epidemiological investigation began on 3 March in order to
A CASE OF ORIENTAL SORE (OF ITALIAN ORIGIN) ENCOUNTERED IN THE UNITED STATES
Journal: JAMA (1921)

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
Implementing MACRA
Authors: Jeffrey D. Clough, Mark McClellan
Journal: JAMA (2016)

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