tbuckley/cabot-search huggingface dataset:
Critical Role of Split Hand/Foot Malformation Type 1 (SHFM1) in Homologous Recombination and Cell Survival in Multiple Myeloma (MM)
Authors: Purushothama Nanjappa, Subodh Kumar, Srikanth Talluri, Humza Ahmad, Ahsun Bajwa, Jialan Shi, Gabriel Gonzalez, Florence Magrangeas, Stephane Minvielle, Kenneth C Anderson, Herve Avet-Loiseau, Masood Shammas, Nikhil C. Munshi
Journal: Blood (2015)
Cyclin A2 Plays a Critical Role Not Only in Self-Renewal of Hematopoietic Stem Cells, but Also in Non-Self-Renewing Proliferation of Lymphoid Progenitors.
Authors: Kentaro Kohno, Tadafumi Iino, Kyoko Ito, Shin-ichi Mizuno, Piotr Sicinski, Koichi Akashi
Journal: Blood (2009)
The in vitro synergistic cytotoxic effects of inductive, concurrent and sequential cyclooxygenase-2 inhibitor with cisplatin against A549 cell line
Authors: D. Zheng, C. Zhou, B. Su
Journal: Journal of Clinical Oncology (2004)

9693 Background: Cyclooxygenase (COX)-2 inhibitors have been shown to exert antitumor activity against human lung cancer cell lines in vitro, and suppressive effect on lung tumors implanted into recipient mice, but concurrent use of COX-2 inhibitors and antineoplastic agents has not been proven clinically to be superior to chemotherapeutic agent alone. Sequential use of COX-2 inhibitors with chemotherapeutic agent might be a possible treatment option. We initiate in vitro study on the growth-inhibitory effect of inductive, concurrent and sequential celecoxib with cisplatin against A549 cell line to determine the most effective dose and schedule for maximal synergistic cytotoxic effects. We anticipate further appropriate treatment strategies to enhance the cytotoxic effect of chemotherapeutic agents using COX-2 inhibitors in the treatment of lung cancer. Methods: A549 cells were incubated with various concentration and combination of celecoxib and cisplatin for 4 days: celecoxib 24 hours prior to cisplatin as induction, celecoxib simultaneous with cisplatin as concurrent, and celecoxib 24 hours subsequent to cisplatin as sequential treatment. Time of exposure to cisplatin for all combination was 72 hours. Cell viability was determined using MTT assay. Results: The IC50 of cisplatin and celecoxib alone to A549 cell line was 16.64μM/l and 90.42μM/l, respectively. IC50 of cisplatin with celecoxib at 1.55μM/l for induction and concurrent treatment was 23.31μM/l, and 16.52μM/l, respectively, which was not superior to cisplatin alone while that of sequential treatment was 9.98μM/l, which showed synergistic cytotoxic effect against A549 cell line. Conclusions: Sequential celecoxib subsequent to cisplatin exerted the most potent in vitro synergistic cytotoxic effect against lung cancer cells. These may provide a rationale for future clinical trial to evaluate the effect of incorporating COX-2 inhibitors into the cisplatin-based regimen for the treatment of lung cancer. No significant financial relationships to disclose.
Networks and Nosology in Posttraumatic Stress Disorder
Authors: Richard J. McNally
Journal: JAMA Psychiatry (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 Psychiatry HomeNew OnlineCurrent IssueFor Authors Podcast 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 Psychiatry journal
Characterisation of Histone Deacetylase (HDAC) Expression Profiles in Acute Myeloid Leukaemia: A Basis for the Development of Targeted Therapy Using Histone Deacetylase Inhibitors.
Authors: Charlotte A. Bradbury, Farhat L. Khanim, Priyanka Mehta, Rachel E. Hayden, Charles F. Craddock, Chris M. Bunce, Bryan M. Turner
Journal: Blood (2004)
Hodgkin’s Disease / Hodgkin-PTLD after Solid Organ Transplantation in Children: A Report on 16 Patients Treated According to Subsequent Gpoh-HD Treatment Schedules
Authors: Johanna Kampers, Rita Beier, Manuela A. Orjuela-Grimm, Tilmann Schober, Thomas Schulz, Martina Stiefel, Christoph Klein, Christine Mauz-Koerholz, Hans H. Kreipe, Britta Maecker-Kolhoff
Journal: Blood (2014)
A Pilot Phase II Study of Erlotinib for the Treatment of Patients with Refractory / Relapsed AML
Authors: Adolfo Diaz Duque, Jasleen Randhawa, Hagop M. Kantarjian, Naveen Pemmaraju, Elias Jabbour, Alessandra Ferrajoli, William G. Wierda, Zeev Estrov, Marina Konopleva, Farhad Ravandi, Yesid Alvarado, Varsha Gandhi, Gautam Borthakur, Jorge E. Cortes
Journal: Blood (2014)
Adipose type I interferon signalling protects against metabolic dysfunction
Authors: Verena Wieser, Timon Erik Adolph, Christoph Grander, Felix Grabherr, Barbara Enrich, Patrizia Moser, Alexander Rupert Moschen, Susanne Kaser, Herbert Tilg
Journal: Gut (2016)

Low-grade chronic inflammation emerges as a potent driver of insulin resistance and glucose dysregulation in obesity and associated non-alcoholic fatty liver disease (NAFLD). The liver, subcutaneous fat and the immune system participate in disturbances of metabolism. Type I interferon (IFN) signalling initiated by innate and adaptive immunity modulates inflammatory responses consequent to infection. However, little is known about the role of type I IFN signalling in metabolic diseases and the development of NAFLD.We determined the impact of type I IFN signalling by tissue-specific deletion of interferon (α and β) receptor 1 (Ifnar1) in hepatocytes (Ifnar1Δhep ), adipocytes (Ifnar1Δat ), intestinal epithelial cells (Ifnar1ΔIEC ) or myelocytes (Ifnar1Δmyel ) on glucose metabolism, obesity and hepatic disease in mice exposed to a high-fat or methionine-choline-deficient (MCD) diet. Furthermore, we investigated the expression of type I IFN-regulated genes in patients with obesity undergoing laparoscopic adjustable gastric banding (LAGB).Long chain fatty acids induce type I IFN responses in murine hepatocytes and macrophages and exposure to a high-fat diet elicited type I IFN-regulated gene expression in the liver of wild-type mice. Hepatocyte-specific, but not adipose tissue-specific deletion of Ifnar1 worsened steatosis and inflammation induced by the MCD diet. In contrast, adipose-specific, but not hepatocyte-specific deletion of Ifnar1 deteriorated metabolic dysregulation induced by a high-fat diet, indicated by increased weight gain, insulin resistance and an impaired glucose tolerance. Abrogated type I IFN signalling in myeloid or intestinal epithelial cells did not modulate susceptibility to metabolic or hepatic disease. Improved metabolic control in patients with obesity after LAGB was associated with increased expression of type I IFN-regulated genes in subcutaneous adipose tissue and liver.Our study implicates a role for adipose and hepatocyte type I IFN signalling in diet-induced metabolic dysregulation and hepatic disease. Further studies on type I IFN signalling in metabolic diseases are warranted.
Rituximab and High-Dose Cytarabine Do Not Counteract the Adverse Prognostic Value of CDKN2A and TP53 Deletions in Autografted Mantle-Cell Lymphoma Patients. a European-MCL Network Study
Authors: Marie-Hélène Delfau-Larue, Klapper Wolfram, Francoise Berger, Fabrice Jardin, Josette Briere, Catherine Thieblemont, Pierre Feugier, Corinne Haioun, Gilles Andre Salles, Vincent Ribrag, Rene-Olivier Casasnovas, Michael Unterhalt, Martin Dreyling, Christiane Pott, Elizabeth Macintyre, Olivier Hermine, Eva Hoster
Journal: Blood (2014)
Elderly patient survival is higher if doctor is female, US study finds
Authors: Michael McCarthy
Journal: BMJ (2016)

Elderly hospital patients treated by female doctors had significantly lower 30 day mortality and readmission rates than those cared for by male physicians, a US study has found.1

Previous research has suggested that male and female doctors practise medicine differently. Female doctors, for example, are more likely to adhere to clinical practice guidelines and to provide preventive care more often. But whether these differences affected outcomes was not known.

In the new study Ashish K Jha, of the Harvard TH Chan School …
Higher Mortality in Weekend Admissions to the Hospital
Authors: Nick Black
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 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
An end of life prognostic score for patients with metastatic prostate cancer receiving palliative radiotherapy
Authors: J. Donaghy, A. Lopes, M. Ali, R. Davda, J. Mascoll, J. Forgenie, S. Howard, U. McGovern, H. Payne, A. Mitra, M. Linch
Journal: Annals of Oncology (2016)
Drug‐Mediated Regulation of Glycosaminoglycan Biosynthesis
Authors: Giancarlo Ghiselli
Journal: Medicinal Research Reviews (2016)

Abstract Glycosaminoglycans (GAGs) are a heterogeneous family of unbranched polysaccharides that exist in either a free state or attached to proteins and are found on the cell surface as well as in the extracellular matrix. GAGs play essential roles in cellular and tissue homeostasis, and their metabolism is altered in response to several pathological conditions. Despite strong experimental evidence supporting the function of GAGs in various diseases, little is known about the regulation of GAG biosynthesis via pharmacological intervention. In recent studies, the effects of several experimental drugs on GAG biosynthesis in animal models of disease were examined and key enzymes involved in GAG biosynthesis were found to be druggable. In addition to experimental small‐molecule drugs that alter GAG biosynthesis, a number of clinically approved drugs modulate GAG metabolism, contributing to the therapeutic benefits associated with the use of these drugs. In this review article, we propose a classification scheme for drugs affecting GAG biosynthesis. Our goal is to present a rational approach to investigate the pharmacological regulation of these important biological molecules.
A novel mutation in hMLH1 gene in a Uruguayan Hereditary non-polyposis colorectal cancer (HNPCC-Lynch syndrome) family
Authors: A. Della Valle, C. Sarroca, R. Fresco, C. Hurtado Riveros, F. Lopez Kostner, P. Peltomaki, H. T. Lynch
Journal: Journal of Clinical Oncology (2008)

22203 Background: HNPCC is the most common colorectal cancer syndrome and is associated with germ-line mutations in DNA mismatch repair genes (MMR). To date, more than 700 MMR gene mutations have been identified. The MMR gene mutation spectrum may vary across different populations and be influenced by founder mutations that prevail in specific ethnic groups. Uruguay is a small country without considerable genetic diversity and whose population is mainly originated from Southern Europe. We have previously reported an unexpectedly low frequency of molecularly defined HNPCC cases despite advanced methodology used for mutation detection, which may suggest the involvement of novel susceptibility genes. Methods: Ten Amsterdam positive families, seven of them without microsatellite instability (MSI) in their proband´s tumours, where thoroughly evaluated for mutations in hMLH1 and hMSH2 by Single-Strand Conformation Polymorphism (SSCP) and direct sequencing of genomic DNA from peripheral blood performed in the proband. Results: We identified a novel hMLH1 mutation (c.289T>G - Y97D) in a 37 year-old colorectal cancer patient from a family with eleven affected members, Amsterdam I positive criteria and without MSI. The affected family members are descendant of a Spanish family and the mean colon cancer diagnosis was 54 years old. This mutation has not been reported to the available databases (InSiGHT or the Newfoundland database). Conclusions: We identified a novel punctual germ-line mutation in hMLH1 in an HNPCC patient with microsatellite stable colorectal cancer. Absence of MSI in HNPCC patients is found only in 10–15% of cases. Southern Europe people represent mixed populations in which no particular mutation has been enriched and therefore it is not surprising that Uruguayan mutations differ from those found in Southern Europeans. However, novel mutations and the reported unexpectedly low frequency of molecularly defined HNPCC cases can be explained by a different mutational spectrum in the Uruguayan population which should be further investigated. No significant financial relationships to disclose.
Abstract 3104: Molecular features that determine the sensitivity of cancer cells to abemaciclib, an inhibitor of CDK4 and CDK6
Authors: Xueqian Gong, Li-Chun Chio, MaryJo Lallena, Farhana Merzoug, Shaoyou Chu, Yue Webster, Jack Dempsey, Xiwen Ma, Alfonso De Dios, Richard Beckman, Sean G. Buchanan
Journal: Cancer Research (2015)

Abstract It is well established that phosphorylation of Rb-family pocket proteins by CDK4 and CDK6 is important for the commitment of cancer cells to a new cell cycle and the initiation of the G1-S phase transition. Abemaciclib is a potent inhibitor of the kinase activity of both CDK4 and CDK6 and is currently undergoing clinical testing. To better understand the molecular determinants of response to abemaciclib, we tested its anti-proliferative activity across a panel of over 500 well characterized cancer cell lines. Statistical approaches were employed to uncover genomic features associated with the response. Candidate markers of sensitivity and resistance were further tested by genetic manipulations in vitro. In vivo models representing the candidate molecular marker of sensitivity were identified and drug efficacy examined. Three broad classes of response were identified. The class of tumors cells most resistant to abemaciclib showed enrichment for RB1 mutations. Conversely, cell lines with amplification of CCND2 and CCND3 were among the very most sensitive tumor cells and tumor cells with these markers showed evidence of senescence and apoptosis after either depletion of the cognate D-cyclin or treatment with abemaciclib. In vivo models of tumors harboring CCND2 and CCND3 gene amplification were very sensitive to abemaciclib treatment and showed evidence of tumor regression. Citation Format: Xueqian Gong, Li-Chun Chio, MaryJo Lallena, Farhana Merzoug, Shaoyou Chu, Yue Webster, Jack Dempsey, Xiwen Ma, Alfonso De Dios, Richard Beckman, Sean G. Buchanan. Molecular features that determine the sensitivity of cancer cells to abemaciclib, an inhibitor of CDK4 and CDK6. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3104. doi:10.1158/1538-7445.AM2015-3104
Toll-Like Receptor-Induced Expression of the NKG2D Ligand MICA on Monocytes Modulates Their Interaction with NK Cells.
Authors: Mercedes Kloss, Patrice Decker, Matthias Krusch, Katrin M. Baltz, Tina Baessler, Lothar Kanz, Alexander Steinle, Helmut R. Salih
Journal: Blood (2007)
Effect of Fingolimod on Neural Stem Cells: A Novel Mechanism and Broadened Application for Neural Repair
Authors: Yuan Zhang, Xing Li, Bogoljub Ciric, Cun-Gen Ma, Bruno Gran, Abdolmohamad Rostami, Guang-Xian Zhang
Journal: Molecular Therapy (2016)

Inflammatory demyelination and axonal damage of the CNS are hallmarks of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Fingolimod (FTY720), the first FDA-approved oral medication for MS, suppresses acute disease but is less effective at the chronic stage, and whether it has a direct effect on neuroregeneration in MS and EAE remains unclear. Here we show that FTY720, at nanomolar concentrations, effectively protected survival of neural stem cells (NSCs) and enhanced their development into mature oligodendrocytes (OLGs) in vitro, primarily through the S1P3 and S1P5 receptors. In vivo, treatment with either FTY720 or NSCs alone had no effect on the secondary progressive stage of remitting-relapsing EAE, but a combination therapy with FTY720 and NSCs promoted significant recovery, including ameliorated clinical signs and CNS inflammatory demyelination, enhanced MBP synthesis and remyelination, inhibited axonal degeneration, and reduced astrogliosis. Moreover, FTY720 significantly improved incorporation and survival of transplanted NSCs in the CNS and drove their differentiation into more OLGs but fewer astrocytes, thus promoting remyelination and CNS repair processes in situ. Our data demonstrate a novel effect of FTY720 on NSC differentiation and remyelination, broadening its possible application to NSC-based therapy in the secondary progressive stage of MS.
Whole-exome sequencing of HER-2 positive human breast cancers: potential molecular mechanisms of response to neoadjuvant chemotherapy plus trastuzumab
Authors: M. La Ferla, L. Cantini, P. Aretini, C. Scatena, I. Bertolini, S. Fancelli, I. Ferrarini, C. De Angelis, B. Salvadori, A. Michelotti, E. Landucci, M. Ghilli, L. Fustaino, M. Lo Russo, M. Roncella, A. Falcone, G. Bevilacqua, G.A. Naccarato, C.M. Mazzanti, A. Fontana
Journal: Annals of Oncology (2015)
Physiotherapy reduced recurrent headaches linked to neck pain and dysfunction in older adults
Authors: Gabriel Gavrilescu
Journal: Annals of Internal Medicine (2016)

Source Citation Uthaikhup S, Assapun J, Watcharasaksilp K, Jull G. Effectiveness of physiotherapy for seniors with recurrent headaches associated with neck pain and dysfunction: a randomized controlled trial. Spine J. 2016 Aug 4. [Epub ahead of print]. 27497890
Allogeneic Related HLA Mismatch Mesenchymal Stem Cells for the Treatment of Engraftment Failure Following Autologous Hematopoietic Stem Cell Transplantation.
Authors: Loic Fouillard, Alain Chapel, Domnique Bories, Sandrine Bouchet Tec, Helene Rouard, Patrick Herve, Patrick Gourmelon, Dominique Thierry, Norbert C. Gorin
Journal: Blood (2006)
P42 Increased FDG uptake in areas of ‘normal’ lung in idiopathic pulmonary fibrosis
Authors: SA Aliyu, G Avery, AH Morice, SP Hart, MG Crooks
Journal: Thorax (2016)

<h3>Background</h3> Idiopathic pulmonary fibrosis (IPF) has a variable disease course and we lack biomarkers that accurately predict prognosis or treatment response. Positron Emission Tomography-Computed Tomography (PET-CT) provides structural and functional information about the lung. A study of 25 IPF patients reported increased 18[F]-FDG uptake in areas of normal lung compared to controls.<sup>1</sup> If confirmed, this raises the possibility that PET-CT can identify ‘microscopic fibrosis’ with prognostic implications. We assess 18[F]-FDG uptake in areas of lung with normal CT appearance in a second IPF cohort. <h3>Methods</h3> PET-CT scans undertaken for cancer staging at an interstitial lung disease tertiary referral centre were reviewed. IPF patients and controls without lung disease were identified. 18[F]-FDG uptake was assessed using manual region of interest (ROI) placement in areas of lung with normal CT appearance in IPF patients and controls. ROI were placed away from the mediastinum and concomitant tumours. 18[F]-FDG uptake within ROI was expressed as maximum and mean standardised uptake values (SUV) normalised using body weight. Mean Hounsfield Units (HU) were evaluated to assess for subtle differences in radiodensity within ROI. Data are presented as mean ± SD. Unpaired, 2-tailed T-tests were used to compare between group differences with a P value &lt; 0.05 considered significant. <h3>Results</h3> Forty-five subjects were included in this study (15 IPF and 30 controls). Lung cancer was the most common concomitant malignancy in both groups. There was no difference in mean HU within ROI between IPF and controls (−719 ± 79 HU in IPF and −723 ± 147 HU in controls. P = 0.92). Areas of normal lung in IPF patients exhibited increased 18[F]-FDG uptake compared to controls measured by maximum SUV (0.98 ± 0.32 in IPF and 0.70 ± 0.20 in controls, P &lt;0.01) and mean SUV (0.80 ± 0.29 in IPF and 0.57 ± 0.18 in controls, P &lt; 0.01). <h3>Conclusions</h3> We confirm that in IPF, areas of normal appearing lung exhibit increased 18[F]-FDG uptake compared with corresponding areas in controls. A longitudinal study is required to establish the relationship between 18[F]-FDG uptake, disease progression and treatment response. <h3>Reference</h3> Win T, Thomas BA, Lambrou T, <i>et al</i>. Areas of normal pulmonary parenchyma on HRCT exhibit increased FDG PET signal in IPF patients. <i>Eur J Nucl Med Mol Imaging</i> 2013;<b>41</b>(2):337–42.