tbuckley/cabot-search huggingface dataset:
Inverted Meckel’s diverticulum mimicking an ulcerated pedunculated polyp: detection by single-balloon enteroscopy
Authors: T.-Y. Huang, Y.-C. Liu, H.-S. Lee, H.-C. Chu, P.-J. Chen, J.-W. Weng, C.-K. Fu, K.-F. Hsu
Journal: Endoscopy (2011)

A 19-year-old woman was referred to our hospital because of recurrent obscure gastrointestinal bleeding. Abdominal computed tomography revealed one heterogeneous lesion with soft tissue and accumulation of fluid over the distal ileum ([Fig. 1]).
Abstract 1141: p19Arf represses Pdgfrβ-driven pericyte proliferation in vivo
Authors: Ryan C. Widau, Anna Zelivianskaia, Stephen X. Skapek
Journal: Cancer Research (2011)

Abstract p19Arf, encoded by the mouse Arf gene, is a critical tumor suppressor with roles regulating cell cycle arrest in embryo development and suppressing oncogenesis. Previous studies established that p19Arf controls pericyte-like cells in the hyaloid vascular system (HVS) in the primary vitreous of the developing eye. Arf-deficient mice have hyperplasic expansion of pericytes in the vitreous, a developmental defect driven by excessive Pdgfrβ signaling. We have used complementary studies of cultured cells and mouse embryos to further explore the functional interactions between p19Arf and Pdgfrβ. To address whether Pdgfrβ acts as a mitogenic or a survival factor in the Arf-deficient mouse eye, we quantified cell proliferation and apoptosis at 13.5 days post coitum (dpc) in ArfGFP/GFP embryos that had or lacked Pdgfrβ. Cell proliferation, measured by BrdU incorporation, was increased by two-fold in the vitreous in the presence of Pdgfrβ. The presence or absence of Pdgfrβ did not change the small number of apoptotic cells in the vitreous of the eye. To explore mechanisms by which Arf expression impeded Pdgfrβ signaling, we used the 10T1/2 pericyte-like cell culture model to show that retroviral expression of p19Arf significantly repressed Pdgfrβ protein. Conversely, shRNA-mediated knockdown of p19Arf enhanced Pdgfrβ in serial-passaged mouse embryo fibroblasts (MEFs). In vivo measurements of Arf mRNA extracted from vitreous samples isolated by laser capture microdissection (LCM) from mouse embryos at 13.5 dpc demonstrated increased Pdgfrβ mRNA in Arf-deficient embryos as compared to wild-type. To confirm that p19Arf repressed Pdgfrβ transcription, we demonstrated that both mature and primary Pdgfrβ RNA transcripts were repressed in 10T1/2 cells. Co-transfection of p19Arf with a luciferase reporter plasmid driven by the Pdgfrβ promoter demonstrated that a 1.6kb segment of DNA conferred Arf-dependent regulation. Chromatin immunoprecipitation (ChIP) showed that p19Arf reduced RNA Pol II binding to the proximal Pdgfrβ promoter. Overall our data show that, in the absence of Arf, Pdgfrβ drives excess proliferation in cells that would normally express Arf in the developing eye. p19Arf acts to repress Pdgfrβ transcription, in part by blocking RNA Pol II binding to the proximal Pdgfrβ promoter. We are currently using additional ChIP assays to identify how the presence or absence of Arf influences the binding of several transcription factors known or suspected of regulating Pdgfrβ expression, and we are exploring the importance of the Arf-Pdgfrβ pathway deregulation in cancer models. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1141. doi:10.1158/1538-7445.AM2011-1141
Cardiac Features of an Unusual X-Linked Humeroperoneal Neuromuscular Disease
Authors: David D. Waters, Donald O. Nutter, Linton C. Hopkins, Edward R. Dorney
Journal: New England Journal of Medicine (1975)

To characterize an unusual, sex-linked recessive neuromuscular disease, we studied two families with 37 males who had involvement of distal leg and proximal arm muscle groups. Electromyography and muscle biopsy in five subjects showed features of both neuropathy and myopathy. Bradycardia and syncope in 15 involved subjects were associated with early death (before the age of 50 years). Electrocardiograms in 15 others showed a spectrum of atrial abnormalities that ranged from abnormal P waves to permanent atrial paralysis and from first-degree atrioventricular block to complete heart block. No patient exhibited clinical muscle disease without electrocardiographic atrial disease. Dilated, hypertrophied left ventricles with normal indexes of function were found in three cases with permanent atrial paralysis and chronic junctional bradycardia. Cardiomegaly and cardiac failure were not present in the other cases. We conclude that permanent ventricular pacing (instituted four patients) is indicated in many of these patients to prevent serious sequelae.
1034 REAL-WORLD MANAGEMENT OF HCC WITH SORAFENIB AND TACE IN EUROPE FROM GIDEON (GLOBAL INVESTIGATION OF THERAPEUTIC DECISIONS IN HCC AND OF ITS TREATMENT WITH SORAFENIB)
Authors: P. Stal, A. Hubert, B. Daniele, J.-P. Bronowicki, P. Mathurin, R. Gerolami, G. Bodoky, J.T. Vázquez, F. Serejo, A. Croitoru, L. Castells, V. Gorbunova, V. Ratziu, C. Papandreou
Journal: Journal of Hepatology (2012)
Differentiation Agents Yield Treatment, Prevention Options
Authors: N. S. Larsen
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Differentiation Agents Yield Treatment, Prevention Options Get access Natalie S. Larsen Natalie S. Larsen Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 23, 1 December 1993, Pages 1900–1902, https://doi.org/10.1093/jnci/85.23.1900 Published: 01 December 1993
P5-14-23: Clinical Outcomes of Different Subtypes Detected by Immunohistochemistry of Early Invasive Breast Cancers in a Monoinstitutional Series.
Authors: A Ferro, C Eccher, A Caldara, R Triolo, M Barbareschi, LV Cuorvo, D Aldovini, M Dipasquale, E Galligioni
Journal: Cancer Research (2011)

Abstract Background Early invasive breast cancer (EIBC) is an heterogeneous disease. Immunohistochemical (IHC) markers can be used to classify tumors in different biological subtypes with different clinical behavior. Purpose: The aim of our study was to evaluate survival outcomes for patients (pts) with different subtypes of EIBC as classified using four ICH markers (ER, PR, HER2 and Ki67). Methods: We evaluated data from 3403 consecutive cases of EIBC treated from 1995 to 2008 and classified as: luminal A (positive ER and PR, negative HER2 and Ki67&amp;lt; 14%), luminal B (positive ER and/or PR, negative HER2 and Ki67&amp;gt;14%), luminal C (positive ER and/or PR, positive HER2, any Ki67), HER2+ (negative ER and PR, positive HER2, any ki67), triple negative (negative ER and PR, negative HER2, any ki67). Log-rank test and Kaplan-Meyer estimator were performed to evaluate the impact of ICH subtypes on overall survival (OS), Event Free Survival (EFS) and their correlation with other known prognostic factors such as N, G, Size, Age. Results: We identified 917 luminal A (26.9%), 1731 luminal B (50.9%), 279 (8.2%) luminal C, 183 HER2 + (5.4%) and 293 triple negative (8.6%). Median age was 61 years. Luminal A was more frequently (p&amp;lt;0.001) associated with older age, smaller size, negative axilla involvement, low grading. Observed events (relapses, contralateral and second tumors) were: 54 in luminal A (6%), 215 in luminal B (16%), 40 in luminal C (14%), 42 in HER2+ (23%) and 59 in triple negative (20%). Disease free interval (DFI) was shorter in luminal C, HER2 and TN (median DFI: 30, 26 and 19 months) than in Luminal A and B (median DFI: 51 and 41 month). Luminal A and B presented more bony and less visceral recurrences than luminal C, HER2 and triple negative tumors. At median follow up of 51 months EFS was 94.1% in luminal A, 87.5% in luminal B, 85.5% in luminal C, 76.8% in HER2+ and 79.7% in triple negative. Corresponding OS was 95.3% in luminal A, 89% in luminal B, 89.2% in luminal C, 80.9% in HER2+, 81.9% in triple negative. Different subtypes EFS according to nodal status, grading, tumor size and age, was reported in table 1. Considering only Luminal subtypes, Luminal B and C were significantly associated with poor EFS vs Luminal A EIBCs in both N0 (p=0.046) and N+ pts (p&amp;lt;0.001), in T1 (p=0.013) and T2 (p=0.03) pts, in pts older than 40 years (p=0.002). Conclusions: Luminal A showed better prognosis in term of EFS and OS than other subtypes regardless other prognostic factors as clinical features (age) and tumor extent (T and N). Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P5-14-23.
Reauthorization Hearing Hits Major Biomedical Research Issues
Authors: C. Vanchieri, D. A. Tisevich
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Reauthorization Hearing Hits Major Biomedical Research Issues Get access Cori Vanchieri, Cori Vanchieri Search for other works by this author on: Oxford Academic PubMed Google Scholar Dorothy A. Tisevich Dorothy A. Tisevich Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 9, 1 May 1991, Page 608, https://doi.org/10.1093/jnci/83.9.608 Published: 01 May 1991
TCTAP A-122 Transcatheter Aortic Valve Implantation (TAVI) in Japanese Patients with Very Small Body Size, Data from OCEAN TAVI Registry
Authors: Hideyuki Kawashima, Yusuke Watanabe, Ken Kozuma, Takaaki Isshiki, Kensuke Takagi, Kentaro Hayashida
Journal: Journal of the American College of Cardiology (2015)
Malignant cell contamination may lead to false-positive findings at endosonographic fine needle aspiration for tumor staging
Authors: Wilson Kwong, Walter Coyle, Farnaz Hasteh, Michael Peterson, Thomas Savides, Mary Krinsky
Journal: Endoscopy (2014)

Endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) of lymph nodes is used for staging of gastrointestinal malignancies. False-positive rates of 5 % - 7 % are not well understood. Elements of EUS examinations that contribute to false-positive cytological findings were investigated.13 patients undergoing EUS staging of gastrointestinal luminal malignancy were consecutively enrolled together with 3 patients with extraluminal tumors (pancreas, lung) defined as controls. After EUS, cellular debris and fluid were collected from the FNA needle catheter, instrument channel, and endoscope tip for cytologic and histologic investigation.6 of 13 patients (46 %) had malignant cells contaminating the FNA needle catheter, instrument channel, or endoscope tip. Malignant cells were present in the instrument channel in 5 cases (38 %), exterior tip of echoendoscope in 4 (31 %) and needle catheter in 2 (15 %).Echoendoscopes used for FNA in patients with luminal tumors are at risk for malignant cell contamination of the instrument channel, FNA needle catheter, and echoendoscope tip. FNA needle contamination can contribute to false-positive findings.
AB0650 Is there an “ideal” score for cardio-vascular risk evaluation on lupus patients?
Authors: C.M. Ancuta, C. Belibou, E. Ancuta, R. Chirieac
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Summary</h3> <h3>Background</h3> Malaria was eliminated from Southern and Southeastern Brazil over 50 years ago. However, an increasing number of autochthonous episodes attributed to <i>Plasmodium vivax</i> have been recently reported in the Atlantic forest region of Rio de Janeiro State. <i>As P. vivax</i>-like non-human primate malaria parasite species <i>Plasmodium simium</i> is locally enzootic, we performed a molecular epidemiological investigation in order to determine whether zoonotic malaria transmission is occurring. <h3>Methods</h3> Blood samples of humans presenting signs and/or symptoms suggestive of malaria as well as from local howler-monkeys were examined by microscopy and PCR. Additionally, a molecular assay based on sequencing of the parasite mitochondrial genome was developed to distinguish between <i>P. vivax</i> and <i>P. simium</i>, and applied to 33 cases from outbreaks occurred in 2015 and 2016. <h3>Results</h3> Of 28 samples for which the assay was successfully performed, all were shown to be <i>P. simium</i>, indicating the zoonotic transmission of this species to humans in this region. Sequencing of the whole mitochondrial genome of three of these cases showed that <i>P. simium</i> is most closely related to <i>P. vivax</i> parasites from South American. <h3>Findings</h3> The explored malaria outbreaks were caused by <i>P. simium</i>, previously considered a monkey-specific malaria parasite, related to but distinct from <i>P. vivax</i>, and which has never conclusively been shown to infect humans before. <h3>Interpretation</h3> This unequivocal demonstration of zoonotic transmission, 50 years after the only previous report of <i>P. simium</i> in man, leads to the possibility that this parasite has always infected humans in this region, but that it has been consistently misdiagnosed as <i>P. vivax</i> due to a lack of molecular typing techniques. Thorough screening of the local non-human primate and anophelines is required to evaluate the extent of this newly recognized zoonotic threat to public health and malaria eradication in Brazil. <h3>Funding</h3> Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado de Rio de Janeiro (Faperj), The Brazilian National Council for Scientific and Technological Development (CNPq), JSPS Grant-in-Aid for scientific research, Secretary for Health Surveillance (SVS) of the Ministry of Health, Global Fund, and PRONEX Program of the CNPq.
Acquired Iron-Deficiency Anemia Caused by an Antibody against the Transferrin Receptor
Authors: James W. Larrick, Edward S. Hyman
Journal: New England Journal of Medicine (1984)

We report a case of anemia due to autoantibodies to the transferrin receptor interfering with iron incorporation by erythroid progenitors. A previously healthy woman with severe acquired microcytic anemia had increased serum iron levels, electrophoretically normal transferrin concentrations, and very high levels of free protoporphyrin in red cells. The bone marrow had no stainable iron but had an excess of normal-appearing plasma cells. Erythroid precursors stained with fluorescent mouse antihuman IgM. The serum contained an antibody that reduced 59Fe incorporation by erythroleukemia K562 cells in vitro but did not inhibit iron transferrin binding. An IgM fraction of the patient's serum immunoprecipitated the human transferrin receptor obtained from solubilized [35S]methionine-labeled K562 membranes. Binding of [59Fe]transferrin or fluorescent iron transferrin was not diminished by the patient's serum at 4 degrees C, but at 37 degrees C uptake was markedly reduced, as was the binding of fluorescent monoclonal antibodies to either surface transferrin or the human transferrin receptor. A complete clinical and hematologic remission occurred with azathioprine and prednisone therapy. We conclude that the patient's autoreactive IgM down-regulated the number of transferrin receptors and diminished iron incorporation by erythroblasts, leading to an iron-deficiency anemia.
Abstract 1308: Achaete-scute homolog 1 (Ascl1) lineage in the lung gives rise to multiple cell types
Authors: Yan Li, Ilona Linnoila
Journal: Cancer Research (2012)

Abstract Lung contains many highly specialized cells. Type I pneumocytes are responsible for gas exchange, while type II pneumocytes secrete surfactant which prevents alveoli from collapsing. Airways are lined by non-ciliated secretory (Clara) and ciliated cells that eliminate excess mucus and harmful particles, and rare pulmonary neuroendocrine cells (PNECs) which regulate breathing and contribute to carcinogenesis. PNECs have unknown histogenesis but differentiate prior to the other cells. The neural transcription factor achaete-scute homolog 1 (Ascl1) is critical for PNEC development and is associated with stem cell marker expression in normal and neoplastic lung. Hence, we used in vivo lineage and fate tracing strategy to investigate Ascl1-defined cells (ASDCs) during lung development and injury repair. R26R-stop-lacZ (Rosa) reporter mice were crossed with Ascl1-Cre and Ascl1-CreERTM mice, in which the Ascl1 promoter drives the expression of Cre or inducible Cre recombinase, respectively (Battiste et al., Development (2007) 134:285-93). Following recombination, ASDCs and their descendants will be permanently labeled and were further characterized by immunohistochemistry using cellular differentiation markers. Labeled cells in Ascl1-Cre/Rosa mice gave rise not only to PNECs but also to neural, Clara, ciliated, alveolar type I and type II cells. Interestingly, tamoxifen (TM) administration to Ascl1-CreERTM/Rosa dams at embryonic day E9.5 labeled both airway and alveolar cells, while TM injected at E11.5 only labeled airway cells. Moreover, adult Ascl1-CreERTM/Rosa mice were administered TM followed by naphthalene (Nap), which kills Clara cells. It is notable that in addition to PNECs which are resistant to Nap, regenerating Clara cells were now labeled during the injury repair. We conclude that ASDCs are not limited to giving rise to neural cells or PNECs during pulmonary development, but they also contribute to a range of non-neuroendocrine cells such as Clara and ciliated cells as well as alveolar pneumocytes. Further, the lineage participates in injury repair of the airway lining in mature lung. The current Ascl1 lineage study provides a basis for recent studies on mouse small cell lung cancer (Sutherland et al., Cancer Cell (2011) 19:754-64) which suggested that both PNECs and non-neuroendocrine cells such as alveolar type II pneumocytes may serve as progenitors for this very virulent lung cancer type. 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 1308. doi:1538-7445.AM2012-1308
Challenges to targeting epidermal growth factor receptor in glioblastoma: escape mechanisms and combinatorial treatment strategies
Authors: P. Roth, M. Weller
Journal: Neuro-Oncology (2014)

Epidermal growth factor receptor (EGFR) gene amplification and activating mutations are common findings in glioblastomas. EGFR is at the top of a downstream signaling cascade that regulates important characteristics of glioblastoma cells, including cellular proliferation, migration, and survival. Targeting EGFR has therefore been regarded as a promising therapeutic strategy in glioblastoma for decades. However, although various pharmacological inhibitors and anti-EGFR antibodies are available, the antiglioma activity of these agents has been largely limited to preclinical models, whereas their administration to glioblastoma patients was characterized by lack of clinical benefit. Comprehensive efforts have been made within the last years to understand the underlying mechanisms that confer resistance to EGFR inhibition in glioma cells. The absence of well-known mutations that predict response to EGFR tyrosine kinase inhibitors (TKIs) in gliomas as well as the presence of redundant and alternative compensatory pathways are among the most important escape mechanisms that prevent potent antiglioma effects of EGFR-targeting drugs. Accordingly, an increasing number of in vitro and in vivo studies are aimed at overcoming this resistance by combinatorial approaches using anti-EGFR treatment together with one or more additional drugs. Novel insights into the molecular mechanisms mediating resistance to anti-EGFR treatment and promising combinatorial approaches may help to better define a future role for EGFR inhibition in the treatment of glioblastoma.
P01.22 * GENERATION OF GENETICALLY ENGINEERED INDUCED PLURIPOTENT STEM CELL-DERIVED NEURAL STEM CELLS WITHOUT USING VIRAL VECTORS
Authors: T. Yamasaki, H. Kawaji, Y. Kamio, S. Amano, T. Sameshima, N. Sakai, T. Tokuyama, H. Namba
Journal: Neuro-Oncology (2014)

Suicide gene therapy using genetically engineered stem cells are is one of the most feasible and promising approaches for glioma therapy. Various stem cells, such as neural and mesenchymal stem cells, have been tested for their tumor tropic activity. We have tested stem cells transduced with the herpes simplex virus-thymidine kinase gene (HSV-TK, suicide gene) encoding a viral thymidine kinase which phosphorylates prodrug ganciclovir (GCV) for experimental glioma in rodents, because the HSV-TK/GCV system generates a potent bystander effect. Recently we found that induced pluripotent stem cells (iPSs) also had tumor tropic activity under both in vitro and in vivo conditions. One of the major limitations of use of HSV-TK gene-trasnduced iPSs in clinical field is the use of virus vectors that randomly integrate into the host genome and are associated with the risk of malignant transformation due to insertional mutagenesis. In the present study, we present a non-viral transfection method for obtaining HSV-TK expressing iPS-derived neural stem cells to circumvent the concerns associated with use of viral vectors. Mouse iPS cells were generated from somatic cells by the plasmid vectors expressing Oct4, Sox2, Klf4, c-Myc and Nanog-GFP-IRES-Puror. We differentiated the mouse iPS cells into neural stem cells and then transfected with the plasmid containing HSV-TK gene using electroporation method. In this way, we obtained HSV-TK gene-trasnduced iPSs-derived neural stem cells without using viral vectors for further pre-clinical expariments of glioma therapy.
AB1042 Synergistic effect of NSAIDS in bisphosphonate treatment, compared to COX-2 inhibitor
Authors: S.Y. Lee, S.W. Lee, W.T. Chung, C.W. Lee, E.J. Kang
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> In humans, NSAIDs appear to slow bone loss in periodontal disease by inhibiting synthesis of prostaglandins, known stimulators of osteoclastic resorption. This suggest a possible clinical application for NSAIDs in prevention of bone loss <h3>Objectives</h3> To investigate the bisphosphonate effects on bone mineral density and T-score in NSAIDs used Patients, compared to COX-2 inhibitor used group <h3>Methods</h3> Between January 2005 and September 2011, 319 women and 104 men were enrolled who were osteoarthritis or rheumatoid arthritis(taken below prednisolone 5mg) with osteoporosis, treated with NSAIDs or COX-2 inhibitors. The subjects were taken bisphosphonate and bone mineral density was measured by Dual-emission absorptiometry every one year. We observed the difference of bone mineral density, T-Score in NSAIDs and COX-2 used groups, spacing 2 years <h3>Results</h3> The efficacy of bisphosphonate on bone mineral density and T-Score was better in NSAIDs group than COX-2 inhibitors group (P&lt;0.05). other factros were not affected to bone mineral density and T-Score in both groups <h3>Conclusions</h3> In our single center study, we observed the combination bisphosphonate with NSAIDs was better response in osteoporosis treatment than COX-2 inhibitors. Further multicenter studies are needed to confirm our results <h3>References</h3> Journal of Bone and Mineral Research, Volume 13, Number 12, 1998 Osteoporos Int (2006) 17:1410–1419 <h3>Disclosure of Interest</h3> None Declared