tbuckley/cabot-search huggingface dataset:
Distinctive distribution of human papillomavirus type 16 and type 20 DNA in the tonsillar and the skin carcinomas of a patient with epidermodysplasia verruciformis
Authors: T. Ishiji, M. Kawase, M. Honda, M. Niimura, E. Yoshimura, T. Sata, T. Matsukura
Journal: British Journal of Dermatology (2000)

Journal Article Distinctive distribution of human papillomavirus type 16 and type 20 DNA in the tonsillar and the skin carcinomas of a patient with epidermodysplasia verruciformis Get access T. Ishiji, T. Ishiji Department of Dermatology, The Jikei University School of Medicine, 3‐25‐8 Nishi‐shimbashi, Minato‐ku, Tokyo 105‐8461, Japan Search for other works by this author on: Oxford Academic Google Scholar M. Kawase, M. Kawase Department of Dermatology, The Jikei University School of Medicine, 3‐25‐8 Nishi‐shimbashi, Minato‐ku, Tokyo 105‐8461, Japan Search for other works by this author on: Oxford Academic Google Scholar M. Honda, M. Honda Department of Dermatology, The Jikei University School of Medicine, 3‐25‐8 Nishi‐shimbashi, Minato‐ku, Tokyo 105‐8461, Japan Search for other works by this author on: Oxford Academic Google Scholar M. Niimura, M. Niimura Department of Dermatology, The Jikei University School of Medicine, 3‐25‐8 Nishi‐shimbashi, Minato‐ku, Tokyo 105‐8461, Japan Search for other works by this author on: Oxford Academic Google Scholar E. Yoshimura, E. Yoshimura Department of Otolaryngology, Japanese Red Cross Medical Center, Shibuya‐ku, Tokyo 150‐8935, Japan Department of Pathology and Search for other works by this author on: Oxford Academic Google Scholar T. Sata, T. Sata Search for other works by this author on: Oxford Academic Google Scholar T. Matsukura T. Matsukura Laboratory of Tumor Viruses, Department of Virology II, National Institute of Infectious Diseases, 1‐23‐1 Toyama, Shinjuku‐ku, Tokyo 162‐8640, Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 143, Issue 5, 1 November 2000, Pages 1005–1010, https://doi.org/10.1046/j.1365-2133.2000.03834.x Published: 01 November 2000
A dose escalation study of gemcitabine plus oxaliplatin in combination with imatinib for gemcitabine-refractory advanced pancreatic adenocarcinoma
Authors: N. Starling, E.A. Hawkes, I. Chau, D. Watkins, J. Thomas, J. Webb, G. Brown, K. Thomas, Y. Barbachano, J. Oates, D. Cunningham
Journal: Annals of Oncology (2011)
Tumor Regression and Growth Rates Determined in Five Intramural NCI Prostate Cancer Trials: The Growth Rate Constant as an Indicator of Therapeutic Efficacy
Authors: Wilfred D. Stein, James L. Gulley, Jeff Schlom, Ravi A. Madan, William Dahut, William D. Figg, Yang-min Ning, Phil M. Arlen, Doug Price, Susan E. Bates, Tito Fojo
Journal: Clinical Cancer Research (2010)

Abstract Purpose: In solid tumors such as prostate cancer, novel paradigms are needed to assess therapeutic efficacy. We utilized a method estimating tumor growth and regression rate constants from serial PSA measurements, and assessed its potential in patients with metastatic castration resistant prostate carcinoma (mCRPC). Experimental Design: Patients were enrolled in five phase II studies, including an experimental vaccine trial, representing the evolution of therapy in mCRPC. PSA measurements obtained before, and during, therapy were used. Data analysis using a two-phase mathematical equation yielded concomitant PSA growth and regression rate constants. Results: Growth rate constants (g) can be estimated while patients receive therapy and in such patients g is superior to PSA-DT in predicting OS. Incremental reductions in growth rate constants were recorded in successive trials with a 10-fold slower g in the most recent combination therapy trial (log g = 10−3.17) relative to single-agent thalidomide (log g = 10−2.08) more than a decade earlier. Growth rate constants correlated with survival, except in patients receiving vaccine-based therapy where the evidence demonstrates prolonged survival presumably due to immunity developing subsequent to vaccine administration. Conclusion: Incremental reductions in tumor growth rate constants suggest increased efficacy in successive chemotherapy trials. The derived growth rate constant correlates with survival, and may be used to assess efficacy. The PSA-TRICOM vaccine appears to have provided marked benefit not apparent during vaccination, but consistent with subsequent development of a beneficial immune response. If validated as a surrogate for survival, growth rate constants would offer an important new efficacy endpoint for clinical trials. Clin Cancer Res; 17(4); 907–17. ©2010 AACR.
Brain Metastases: The HER2 Paradigm
Authors: Nancy U. Lin, Eric P. Winer
Journal: Clinical Cancer Research (2007)

Between 100,000 and 170,000 patients with cancer develop central nervous system (CNS) metastases each year in the U.S., of which approximately 20% carry a primary diagnosis of breast cancer. As a consequence of improvements in systemic therapy, which have allowed patients to live longer with advanced cancer, CNS metastases are emerging as an important sanctuary site, and the incidence may be increasing in patients with particular tumor subtypes. Unless there are improvements in the treatment of CNS disease, a growing proportion of patients may be at risk of experiencing both morbidity and mortality as a result of uncontrolled CNS progression, often at a time when their extra-CNS disease is apparently under control. This article reviews changes in the epidemiology and natural history of women with brain metastases from HER2-positive breast cancer over the last decade and presents the therapeutic challenges and opportunities that have arisen in this setting. First, the apparent increase in CNS disease among women with HER2-positive breast cancer, relative to historical controls, is discussed, followed by consideration of potential causes of this observation. Next, the implications of CNS disease, in terms of prognosis and the potential development of preventive strategies are considered. Finally, new developments in systemic approaches to the treatment of CNS disease, including cytotoxic chemotherapy and targeted therapy, are explored.
Signaling Properties and Functions of Two Distinct Cardiomyocyte Protease-Activated Receptors
Authors: Abdelkarim Sabri, Galina Muske, HongLu Zhang, Elena Pak, Andrew Darrow, Patricia Andrade-Gordon, Susan F. Steinberg
Journal: Circulation Research (2000)

Abstract —Previous studies have established that cardiomyocytes express protease-activated receptor (PAR)-1, a high-affinity receptor for thrombin, which is also activated by the tethered-ligand domain sequence (SFLLRN) and which promotes inositol trisphosphate accumulation, stimulates extracellular signal–regulated protein kinase, and modulates contractile function. A single previous report identified PAR-1 as a hypertrophic stimulus, but there have been no subsequent investigations of the mechanism. This study reveals the coexpression of PAR-1 and PAR-2 (a second PAR, which is activated by trypsin/tryptase but not thrombin) by Northern blot analysis and compares their signaling properties in neonatal rat ventricular cardiomyocytes. SFLLRN and SLIGRL (an agonist peptide for PAR-2) promote inositol trisphosphate accumulation, stimulate mitogen-activated protein kinases (extracellular signal–regulated protein kinase and p38-mitogen-activated protein kinase), elevate calcium concentration, and increase spontaneous automaticity. SFLLRN (but not SLIGRL) also activates c-Jun NH 2 -terminal kinase and AKT. In keeping with their linkage to pathways that have been associated with growth and/or survival, SFLLRN and SLIGRL both induce hypertrophy. However, PAR agonists promote cell elongation, a morphology that is distinct from the uniform increase in cell dimension induced by α 1 -adrenergic receptor activation. These studies provide novel evidence that cardiomyocytes coexpress 2 functional PARs, which link to a common set of signals that culminate in changes in contractile function and hypertrophic growth. PAR actions may assume clinical importance in the border zone surrounding an infarction, where local proteolysis of PARs by serine proteases generated during inflammatory or thrombogenic pathways would elevate calcium concentration (setting the stage for arrhythmias), promote hypertrophic growth, and/or influence cardiomyocyte survival.
Inhibition of Tissue Factor Gene Induction and Activity Using a Hairpin Ribozyme
Authors: Erdal Cavusoglu, Irene Chen, Jay Rappaport, Jonathan D. Marmur
Journal: Circulation (2002)

Background — Tissue factor (TF) is a membrane-bound glycoprotein that initiates the clotting cascade. Inhibition of the TF pathway has been shown to prevent thrombosis and restenosis after arterial injury in a variety of animal models. Methods and Results — We describe a novel approach to inhibiting the expression of the TF protein that involves the targeted destruction of cellular TF mRNA with the use of a tetraloop hairpin ribozyme. After construction of the ribozyme and determination of its optimal length and kinetic parameters, a ribozyme expression vector that used the retroviral vector pMV12 was constructed. The ability of this expression vector to generate anti-TF ribozyme was further augmented by positioning of the anti-TF ribozyme downstream of a rat tRNA val (RNA polymerase II) promoter. The resultant construct containing the anti-TF ribozyme was then used to transfect vascular smooth muscle cells and generate a variety of clonal cell lines. Northern blot analyses performed on 3 transfected and 3 untransfected clones demonstrated markedly reduced TF mRNA levels in the transfected clones both during quiescence and after serum stimulation. Cell lysates analyzed for total TF activity by monitoring factor Xa generation similarly demonstrated a statistically significant and concordant reduction in TF activity in smooth muscle cells transfected with the ribozyme expression vector compared with both untransfected clones and clones transfected with the empty vector. Conclusions — These results demonstrate the feasibility of an antithrombotic strategy based on ribozyme technology.
Acute fatty liver of pregnancy and long-chain 3-hydroxyacyl–coenzyme A dehydrogenase deficiency
Authors: William R. Treem, Piero Rinaldo, Daniel E. Hale, Charles A. Stanley, David S. Millington, Jeffrey S. Hyams, Sandra Jackson, Douglass M. Turnbull
Journal: Hepatology (1994)

The pathogenesis of acute fatty liver of pregnancy is unknown, but similarities in the clinical presentation and the histological appearance of the liver with those found in children with metabolic defects in the intramitochondrial beta-oxidation pathway of the liver suggest that a disturbance in hepatic fatty acid oxidation may play a role. We report a woman with acute fatty liver of pregnancy who gave birth to a seemingly normal full-term infant who was seen at 4 mo of age with hypoglycemia, coma and profound hepatic steatosis. The infant had a defect in fatty acid oxidation, long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency, and the mother proved to be heterozygous for this metabolic condition. We hypothesize that the interaction of an affected fetus with a female heterozygous for this defect in fatty acid oxidation in the late third trimester accounts for some cases of acute fatty liver of pregnancy.
Abstract A72: Stat3 is a negative regulator of intestinal tumor progression in APCmin mice
Authors: Monica Musteanu, Leander Blaas, Markus Mair, Emilio Casanova, Lukas Kenner, Valeria Poli, Robert Eferl
Journal: Cancer Research (2009)

Abstract The transcription factor Stat3 has been considered to promote progression and metastasis of intestinal cancers. We investigated the role of Stat3 in intestinal tumors using mice with conditional ablation of Stat3 in intestinal epithelial cells (Stat3ΔIEC). In the APCmin mouse model of intestinal cancer, genetic ablation of Stat3 reduced the multiplicity of early adenomas. However, loss of Stat3 promoted tumor progression at later stages leading to formation of invasive carcinomas which significantly shortened the lifespan of Stat3ΔIEC APCmin/+ mice. Interestingly, loss of Stat3 in tumors of APCmin/+ mice had no significant impact on cell survival and angiogenesis but promoted cell proliferation. A genome-wide expression analysis of Stat3-deficient tumors suggested that Stat3 negatively regulates intestinal cancer progression via the cell adhesion molecule Ceacam1. Therefore, detrimental effects on tumor progression have to be considered upon therapeutic targeting of the Stat3 signaling pathway in intestinal cancer. Citation Information: Cancer Res 2009;69(23 Suppl):A72.
Evidence-Based Cardiology
Authors: M. Saleem Seyal
Journal: JAMA (2010)

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
Genetic Variants on Chromosome 15q25 Associated with Lung Cancer Risk in Chinese Populations
Authors: Chen Wu, Zhibin Hu, Dianke Yu, Liming Huang, Guangfu Jin, Jie Liang, Huan Guo, Wen Tan, Mingfeng Zhang, Ji Qian, Daru Lu, Tangchun Wu, Dongxin Lin, Hongbing Shen
Journal: Cancer Research (2009)

Recent three genome-wide association studies have mapped a lung cancer susceptibility locus to chromosome 15q25 in Caucasians. However, the reported risk single nucleotide polymorphisms (SNPs) are extremely rare in Asians, arguing against any of these being causative variants. This study sought to identify other variants on 15q25 associated with lung cancer susceptibility in Chinese. Two-stage case-control studies were conducted in subjects derived from both Northern and Southern China. The first-stage, consisting of 576 cases and 576 controls, was to discover novel risk variants using a haplotype-tagging SNP approach, and these variants were then replicated in the second-stage, consisting of 2,989 cases and 2,880 controls. Associations were estimated by logistic regression models, and function of the variants was examined by biochemical assays. We found that the three risk SNPs reported in Caucasians were not associated with lung cancer risk in Chinese. However, we identified four novel SNPs (rs2036534C>T, rs667282C>T, rs12910984G>A, and rs6495309T>C) that were associated with significantly increased lung cancer risk and smoking behavior, which were all confirmed in the replication analyses [odds ratios (95% confidence intervals) in the dominant model: 1.39 (1.23-1.57; P = 2.3 x 10(-7)), 1.52 (1.35-1.71; P = 2.0 x 10(-12)), 1.44 (1.28-1.63; P = 2.7 x 10(-9)), and 1.43 (1.27-1.61; P = 2.6 x 10(-9)), respectively]. We characterized the rs6495309T>C change in the CHRNA3 promoter as a functional variant because it affected the Oct-1 binding ability, resulting in increased CHRNA3 expression. These results support 15q25 as a susceptibility region for lung cancer in Chinese but underscore the difference in genetic markers among different ethnic populations.
Selective Inhibition of BRCA2-Deficient Mammary Tumor Cell Growth by AZD2281 and Cisplatin
Authors: Bastiaan Evers, Rinske Drost, Eva Schut, Michiel de Bruin, Eline van der Burg, Patrick W.B. Derksen, Henne Holstege, Xiaoling Liu, Ellen van Drunen, H. Berna Beverloo, Graeme C.M. Smith, Niall M.B. Martin, Alan Lau, Mark J. O'Connor, Jos Jonkers
Journal: Clinical Cancer Research (2008)

Abstract Purpose: To assess efficacy of the novel, selective poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor AZD2281 against newly established BRCA2-deficient mouse mammary tumor cell lines and to determine potential synergy between AZD2281 and cisplatin. Experimental Design: We established and thoroughly characterized a panel of clonal cell lines from independent BRCA2-deficient mouse mammary tumors and BRCA2-proficient control tumors. Subsequently, we assessed sensitivity of these lines to conventional cytotoxic drugs and the novel PARP inhibitor AZD2281. Finally, in vitro combination studies were done to investigate interaction between AZD2281 and cisplatin. Results: Genetic, transcriptional, and functional analyses confirmed the successful isolation of BRCA2-deficient and BRCA2-proficient mouse mammary tumor cell lines. Treatment of these cell lines with 11 different anticancer drugs or with γ-irradiation showed that AZD2281, a novel and specific PARP inhibitor, caused the strongest differential growth inhibition of BRCA2-deficient versus BRCA2-proficient mammary tumor cells. Finally, drug combination studies showed synergistic cytotoxicity of AZD2281 and cisplatin against BRCA2-deficient cells but not against BRCA2-proficient control cells. Conclusion: We have successfully established the first set of BRCA2-deficient mammary tumor cell lines, which form an important addition to the existing preclinical models for BRCA-mutated breast cancer. The exquisite sensitivity of these cells to the PARP inhibitor AZD2281, alone or in combination with cisplatin, provides strong support for AZD2281 as a novel targeted therapeutic against BRCA-deficient cancers.
Efficacy and cost of video-assisted thoracoscopic partial pleurectomy versus talc pleurodesis in patients with malignant pleural mesothelioma (MesoVATS): an open-label, randomised, controlled trial
Authors: Robert C Rintoul, Andrew J Ritchie, John G Edwards, David A Waller, Aman S Coonar, Maxine Bennett, Eleonora Lovato, Victoria Hughes, Julia A Fox-Rushby, Linda D Sharples
Journal: The Lancet (2014)
Extracellular matrix gene expression increases preferentially in rat lipocytes and sinusoidal endothelial cells during hepatic fibrosis in vivo.
Authors: J J Maher, R F McGuire
Journal: Journal of Clinical Investigation (1990)

Whether parenchymal or nonparenchymal liver cells play a predominant role in the pathophysiology of hepatic fibrosis has not been firmly established in vivo. We have addressed this question by quantitating the relative abundance of specific mRNAs for collagen types I, III, and IV, and laminin in purified populations of hepatocytes, sinusoidal endothelial cells, and lipocytes from normal and fibrotic rat liver. In normal liver, type I collagen gene expression was minimal in all cell types; mRNA for types III and IV collagen were apparent in endothelial cells and lipocytes, but not in hepatocytes. Laminin mRNA was present in all cell types. Induction of fibrogenesis by either bile duct ligation or carbon tetrachloride administration was associated with a substantial increase in mRNA for types I and III collagen in nonparenchymal cells. Lipocytes from fibrotic animals exhibited a greater than 30-fold increase in type I collagen mRNA relative to normal lipocytes, and greater than 40-fold relative to hepatocytes. Type III collagen mRNA reached 5 times that in normal lipocytes and greater than 120 times that in hepatocytes. Endothelial cells exhibited an isolated increase in type I collagen mRNA, reaching five times that in normal liver. Type IV collagen and laminin gene expression were not significantly increased in nonparenchymal cells during fibrogenesis; in fact, mRNA for type IV collagen and laminin decreased by up to 50% in endothelial cells. Despite the pronounced changes that occurred in matrix gene expression in nonparenchymal cells during fibrogenesis, no change was noted in hepatocytes. We conclude that nonparenchymal liver cells, particularly lipocytes, are important effectors of hepatic fibrosis in vivo.
Retargeting of adenoviral gene delivery via Herceptin–PEG–adenovirus conjugates to breast cancer cells
Authors: Yukyung Jung, Hyo-Jin Park, Pyung-Hwan Kim, Jaewon Lee, Woochan Hyung, Jaemoon Yang, Hyunju Ko, Joo-Hyuk Sohn, Joo-Hang Kim, Yong-Min Huh, Chae-Ok Yun, Seungjoo Haam
Journal: Journal of Controlled Release (2007)
Aspirin-Induced Esophageal Hemorrhage
Authors: Jonathan B. Schreiber
Journal: JAMA (1988)

To the Editor.  —Pill-induced esophagitis has been recognized with increasing frequency since it was first described in 1970. 1,2 It most commonly occurs in association with the use of doxycycline, tetracycline, quinidine, emepromium bromide, or potassium chloride. 3 Surprisingly, aspirin therapy rarely causes pill-induced esophagitis and has not been known to induce significant bleeding. We describe a case of aspirin-induced esophageal injury that presented with hematemesis and an esophageal mass.  Report of a Case.  —A 52-year-old man with a history of peptic ulcer disease and a cerebral vascular accident that resulted in paralysis developed nausea, vomiting without hematemesis, and syncope. The medications he received were aspirin, two tablets twice a day, haloperidol, benztropine mesylate, and clonidine. In the emergency department, he vomited about 1 L of blood and was hypotensive. After stabilization, he underwent esophagogastroduodenoscopy. Profuse bleeding originated from the lower part of the esophagus. The exact site of hemorrhage
Vascular Remodeling in Mice Lacking the Cytoplasmic Domain of Tissue Factor
Authors: Ilka Ott, Cornelia Michaelis, Maren Schuermann, Birgit Steppich, Isabell Seitz, Mieke Dewerchin, Dietlind Zohlnhofer, Rainer Wessely, Martina Rudelius, Albert Schömig, Peter Carmeliet
Journal: Circulation Research (2005)

Tissue factor (TF), the cell surface receptor for the serine protease FVIIa supports cell migration by interaction with the cytoskeleton. Intracellular signaling pathways dependent on the cytoplasmic domain of TF modify cell migration and may alter vascular remodeling. Vascular remodeling was analyzed in a femoral artery injury and a blood flow cessation model in mice with a targeted deletion of the 18 carboxy-terminal intracellular amino acids of TF (TF(Deltact/Deltact)) and compared with TF wild-type mice (TF(wt/wt)). Morphometric analysis revealed a decrease in the intima/media ratio after vascular injury in arteries from TF(Deltact/Deltact) compared with TF(wt/wt) mice (femoral artery injury: 2.4+/-0.3 TF(wt/wt) versus 0.6+/-0.3 TF(Deltact/Deltact), n=9 to 10, P=0.002; carotis ligation: 0.45+0.11 TF(wt/wt) versus 0.22+0.03 TF(Deltact/Deltact), n=12 to 14, P=0.09). This was caused by an increase in the media by 54% (P=0.04) in the femoral artery model and by 32% (P=0.03) after carotis ligation and was associated with an increased number of proliferating cells. Isolated aortic smooth muscle cells (SMCs) of TF(wt/wt) mice showed an increased migratory response toward the TF ligand active site-inhibited FVIIa that was abolished in TF(Deltact/Deltact) SMC. In contrast, the unstimulated proliferation rate was increased in TF(Deltact/Deltact) SMC compared with TF(wt/wt) SMCs. Thus, retention of SMCs attributable to a migratory defect and increased proliferation results in thickening of the media and in decrease in neointima formation after arterial injury. TF cytoplasmic domain signaling alters vascular remodeling and, thereby, may play a role in the development of restenosis, atherosclerotic disease, and neovascularization.