tbuckley/cabot-search huggingface dataset:
Thomas Davidson Veitch Lawrie
Authors: Ian Hutton, Ross Lorimer
Journal: BMJ (2015)

Thomas Davidson Veitch Lawrie, who died a few days before his 95th birthday, was appointed to the inaugural Walton chair of medical cardiology at the University of Glasgow, based at Glasgow Royal Infirmary, in 1966. He held the post until 1985.

He was born in the Springburn area of Glasgow and attended Whitehill Secondary School, where he was dux. He graduated from the University of Glasgow with BSc (Hons) in 1940 and MB ChB in 1943. War service followed where he served with the Royal Army Medical Corps in India and Burma.

On his return to the UK he decided on a career in hospital medicine, with cardiology as his specialty. His potential was recognised by J H Wright, who had the foresight to establish cardiology, firstly as a major clinical speciality, and subsequently as an academic discipline. He appointed VL, as Veitch Lawrie came to be known, as a member of …
4g/5g Prevalence in 223 Patients with Thrombosis and in 162 Healthy Controls, from the Centre Region of Portugal.
Authors: Rosa Maia, Emilia Cortesao, Catarina Geraldes, Luis Simoes, Carla Simoes, Graca Castro, Gabriel Anacleto, Vieira Barbosa, Adriana Teixeira
Journal: Blood (2004)
Abstract IA02: Cancer genomics: Translational challenges
Authors: Malachi Griffith, Obi Griffith, Nicholas Spies, Benjamin Ainscough, Zachary Skidmore, Lee Trani, Avinash Ramu, Killanin Krysiak, Elaine R. Mardis
Journal: Cancer Research (2015)

Abstract The use of next-generation sequencing and analysis has become the standard approach to studying cancer genomics in the research setting. The knowledge gained has been considerable across multiple tumor types, in many ways changing our perceptions about the genomic basis for cancer. Coincident with this new information is the continuing development and introduction of targeted therapies for cancer treatment. Bringing these two developments together is exciting and challenging for numerous reasons. My talk will focus on some of the challenges that are commonly faced, on the decision-support tools and databases we are creating to help with these challenges, and the ways in which the clinical cancer expert can contribute to these tools. Citation Format: Malachi Griffith, Obi Griffith, Nicholas Spies, Benjamin Ainscough, Zachary Skidmore, Lee Trani, Avinash Ramu, Killanin Krysiak, Elaine R. Mardis. Cancer genomics: Translational challenges. [abstract]. In: Proceedings of the AACR Special Conference on Translation of the Cancer Genome; Feb 7-9, 2015; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(22 Suppl 1):Abstract nr IA02.
Abstract 3776: HnRNP A1 regulates cell cycle and proliferation in oral squamous cancer cells
Authors: Cheng Yu, Jihua Guo, Jun Jia, Rong Jia, Mingwen Fan
Journal: Cancer Research (2015)

Abstract Oral squamous cell carcinoma (OSCC) is the most common malignant tumor in human head and neck neoplasms. Despite the improvement of therapeutic approaches, reducing high mortality is still the major challenge of OSCC. However, the molecular pathogenesis of OSCC remains largely unclear, which hinders the development of effective preventive and therapeutic methods. Alternative splicing of pre-mRNA has been implicated to be involved in tumorigenesis. Splicing factors play key roles in the regulation of alternative splicing. HnRNP A1 is an important multi-function splicing factor and closely related to tumorigenesis. It has been reported to be overexpressed in multiple types of tumors. However, the function of A1 in cell cycle and proliferation remains unclear. We found that hnRNP A1 was overexpressed in OSCC tissues and cells by immunohistochemistry and western blotting. Down-regulation of hnRNP A1 with siRNA significantly retarded the growth of OSCC cells and induced G2/M arrest. DNA chip assay showed that the expression of a number of target genes associated with G2/M phase are regulated by hnRNP A1. These findings suggest that hnRNP A1 plays key roles in the regulation of cell cycle progression and pathogenesis of OSCC. Citation Format: Cheng Yu, Jihua Guo, Jun Jia, Rong Jia, Mingwen Fan. HnRNP A1 regulates cell cycle and proliferation in oral squamous cancer cells. [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 3776. doi:10.1158/1538-7445.AM2015-3776
Lenalidomide and Novel Immunomodulatory Drugs (IMiDs®): A New Approach to the Regulation of Erythropoiesis and Hemoglobin Synthesis in Anemia.
Authors: Laure Moutouh de Parseval, Helen Brady, Dominique Verhelle, Laura G. Corral, Emilia Glezer, Christopher L. Morris, Roger Chen, Kyle Chan
Journal: Blood (2005)
Early Prediction of Acute Gvhd Based on Molecular Profiling at the Time of Engraftment after Hematopoietic Stem Cell Transplantation.
Authors: Adriano Moraes Arantes, Gerdine Sanson, Amador Gonçalves Primo, José Salvador Rodrigues Oliveira, Maria Gerbase DeLima, Natalia Shulzhenko, Andrey Morgun
Journal: Blood (2008)
High Throughput Sequencing Following Cross-Linked Immune Precipitation (HITS-CLIP) of Argonaute (AGO) Identifies Mir-9 As a Regulator of MMP2 in the Marrow Microenvironment (ME)
Authors: Ilango Balakrishnan, Xiaodong Yang, Beverly Torok-Storb, Jay Hesselberth, Manoj M Pillai
Journal: Blood (2011)
Re-Evaluation of the Efficacy of Azacitidine (AZA) In Patients From the AZA-001 Study with Higher-Risk Myelodysplastic Syndromes (MDS) Classified by WHO Criteria and WPSS Risk
Authors: Norbert Gattermann, Guillermo F. Sanz, Aristoteles Giagounidis, John F Seymour, Pierre Fenaux, Valeria Santini, Ghulam J. Mufti, Petra Muus, Fernando Ramos, Lela M. Lucy, CL Beach, Lewis R. Silverman
Journal: Blood (2010)
Systematic Identification of Personal Mutated Tumor-Specific Neoantigens in CLL
Authors: Mohini Rajasagi, Derin Keskin, Jintaek Kim, Wandi Zhang, Sachet Shukla, David DeLuca, John Sidney, Vladimir Brusic, Donna S. Neuberg, Gad Getz, Eric S. Lander, Nir Hacohen, Catherine J. Wu
Journal: Blood (2012)
Abstract 4183: Differential expression of VEGF in breast cancer cells induced by gp130 cytokines
Authors: Danielle S. Hedeen, Ken Tawara, Madhuri Nandakumar, Ryan Fox, David Chang, Alex Ide, Andrew Oler, Dollie LaJoie, Cheryl L. Jorcyk
Journal: Cancer Research (2015)

Abstract Glycoprotein 130 (gp130) is a glycosylated type 1 membrane protein and functions as a cytokine receptor modulating activity of the interleukin-6 (IL-6) family cytokines, which include IL-6, IL-11, IL-27, oncostatin M (OSM), leukemia inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), cardiotrophin 1 (CT-1), cardiotrophin-like cytokine (CLC), and neuropoietin (NP). This study was designed to determine differential expression of VEGF in breast cancer cells by IL-6 family cytokines, and to elucidate the molecular mechanisms and signaling pathways involved in cytokine-mediated VEGF induction. Triple negative breast cancer (TNBC) MDA-MB-231 and estrogen receptor positive/progesterone receptor positive/Her2 negative (ER+/PR+/Her2-) T47D cells were treated with three cytokines (25 ng/mL), OSM, IL-6, and LIF, and analyzed. Our results showed that all three cytokines increased levels of HIF1α by Western blot analysis. OSM lead to a greater production of VEGF compared to IL-6 and LIF, as measured by enzyme-linked immunosorbent assay (ELISA) and as seen by luciferase reporter assay. Of the three cytokines, OSM alone induced VEGF in TNBC MDA-MB-231 cells, and this effect was mediated by signal transducer activator of transcription 3 (STAT3) signaling. However, both OSM and IL-6 increased VEGF secretion levels in ER+/PR+/Her2- T47D breast cancer cells, and this signaling was mediated by both HIF1α and pSTAT3, utilizing ELISA and Western blot analysis. These results implicate OSM as the key gp130 cytokine inducing VEGF secretion, and also suggest that this induction is not always HIF1α dependent and is cell-line specific. Citation Format: Danielle S. Hedeen, Ken Tawara, Madhuri Nandakumar, Ryan Fox, David Chang, Alex Ide, Andrew Oler, Dollie LaJoie, Cheryl L. Jorcyk. Differential expression of VEGF in breast cancer cells induced by gp130 cytokines. [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 4183. doi:10.1158/1538-7445.AM2015-4183
387. Transfer of Hyaluronic Acid Synthase-2 Gene into Canine Joints Using Adeno-Associated Viral Vectors
Authors: Monica D. Figueiredo, Patricia Berthelette, Cathy Sookdeo, Donna Armentano, Sirkka Kyostio-Moore
Journal: Molecular Therapy (2016)

Osteoarthritis (OA) is one of the more common causes of lameness in dogs and is estimated to affect approximately 20% of dogs >1 year old. OA is a progressive and degenerative disease that results in pain, inflammation and reduced joint mobility. Novel, safe and efficacious therapies that improve joint lubrication and reduce the extent of inflammation and pain are potential solutions for the management of canine OA. Here, we evaluated the efficiency of gene transfer to canine joint by intra-articular injections of recombinant adeno-associated virus (rAAV) vectors encoding therapeutic genes. Specifically, we generated rAAV vectors (either AAV2 and AAV5 serotypes vectors) encoding canine codon-optimized hyaluronic acid (HA) synthase-2 (HAS2) to provide local and continuous synthesis of HA in the joint. Twenty-two adult healthy dogs that were seronegative for anti-AAV2 and -AAV5 antibodies were injected intra-articularly with rAAV2/HAS2 (1, 5 and 10×1011 vg/joint), rAAV5/HAS2 (5×1011 vg/joint) or PBS (control). No adverse clinical signs were observed following the 28-day study period. Histopathological analysis showed minimal synovial inflammation in the joints of dogs treated with rAAV5/HAS2 and no significant changes in the rAAV2/HAS2 treated dogs. Vector genomes (VG) were detected in the synovium of all the rAAV-treated joints and in the majority of cartilage samples tested. The rAAV5/HAS2 vector resulted in findings of higher and more consistent detection of VG and transcripts compared to rAAV2/HAS2 in both the synovial and cartilage samples. Preliminary analysis also showed a trend towards increased HA levels in the synovial fluid of the treated joints. In summary, our study demonstrated that rAAV2 and rAAV5-mediated gene transfer to canine joint tissues is feasible and that both vectors present an acceptable safety profile following a single intra-articular injection.
Genomic Profiling of Patient-Derived Xenografts for Lung Cancer Identifies <i>B2M</i> Inactivation Impairing Immunorecognition
Authors: Carolina Pereira, Pol Gimenez-Xavier, Eva Pros, Maria J. Pajares, Massimo Moro, Antonio Gomez, Alejandro Navarro, Enric Condom, Sebastian Moran, Gonzalo Gomez-Lopez, Osvaldo Graña, Miriam Rubio-Camarillo, Alex Martinez-Martí, Jun Yokota, Julian Carretero, Jose M. Galbis, Ernest Nadal, David Pisano, Gabriella Sozzi, Enriqueta Felip, Luis M. Montuenga, Luca Roz, Alberto Villanueva, Montse Sanchez-Cespedes
Journal: Clinical Cancer Research (2017)

Abstract Purpose: We aimed to maximize the performance of detecting genetic alterations in lung cancer using high-throughput sequencing for patient-derived xenografts (PDXs). Experimental Design: We undertook an integrated RNA and whole-exome sequencing of 14 PDXs. We focused on the genetic and functional analysis of β2-microglobulin (B2M), a component of the HLA class-I complex. Results: We identified alterations in genes involved in various functions, such as B2M involved in immunosurveillance. We extended the mutational analysis of B2M to about 230 lung cancers. Five percent of the lung cancers carried somatic mutations, most of which impaired the correct formation of the HLA-I complex. We also report that genes such as CALR, PDIA3, and TAP1, which are involved in the maturation of the HLA-I complex, are altered in lung cancer. By gene expression microarrays, we observed that restitution of B2M in lung cancer cells upregulated targets of IFNα/IFNγ. Furthermore, one third of the lung cancers lacked the HLA-I complex, which was associated with lower cytotoxic CD8+ lymphocyte infiltration. The levels of B2M and HLA-I proteins correlated with those of PD-L1. Finally, a deficiency in HLA-I complex and CD8+ infiltration tended to correlate with reduced survival of patients with lung cancer treated with anti-PD-1/anti-PD-L1. Conclusions: Here, we report recurrent inactivation of B2M in lung cancer. These observations, coupled with the mutations found at CALR, PDIA3, and TAP1, and the downregulation of the HLA-I complex, indicate that an abnormal immunosurveillance axis contributes to lung cancer development. Finally, our observations suggest that an impaired HLA-I complex affects the response to anti-PD-1/anti-PD-L1 therapies. Clin Cancer Res; 23(12); 3203–13. ©2016 AACR.
Abstract 597: Coding and noncoding gene targets in pediatric soft tissue sarcomas
Authors: Sheetal A. Mitra, Anirban P. Mitra, Jonathan D. Buckley, Timothy J. Triche
Journal: Cancer Research (2015)

Abstract BACKGROUND: Genomic studies on pediatric soft tissue sarcomas (STS) such as rhabdomyosarcoma (RMS) and Ewing family of tumors (EFT) have shown that the overall burden of somatic mutations in these tumors is relatively low when compared to most adult tumors. This observation along with recent studies suggest that other features such as chromosomal translocations that appear predominantly in these tumors may play an important role in their biology. Genes resulting from these translocations are known to regulate protein-coding genes that are required for tumor formation. Our studies on these tumors show that these chimeric fusion genes can hijack the cellular machinery that comprises both protein-coding and non-coding networks for tumorigenesis. RESULTS: Gene expression signature of the more aggressive RMS subset that comprises of PAX-FKHR-positive alveolar RMS suggested that the protein-coding NOS1 is most strongly associated and prognostically significant gene in this group. Functional assays confirmed that PAX-FKHR directly regulated its expression. Decreasing NOS1 expression using lentiviral vectors resulted in a decrease in cell survival and reduced tumor growth in vivo. Similar expression analyses comparing EFT, which express the fusion gene EWS-FLI1, with other tumors and normal tissues showed that the non-coding features were more strongly associated with EFT than the coding genes. EWS-FLI1 directly regulates a long intergenic non-coding RNA (lincRNA), FEZF1-AS1. Matrigel assays and tail vein injection models suggested that the lincRNA promotes cell invasion and migration. Chromatin-RNA immunoprecipitation assays revealed interaction of the lincRNA with DNA regions, both coding and non-coding, which are involved in invasion and metastasis. CONCLUSIONS: Fusion genes in pediatric STS activate genomic regions that facilitate tumor pathogenesis by regulating the interactive network between coding and non-coding genes. While fusion-positive RMS are dependent on NOS1 for survival, EFT need lincRNA FEZF1-AS1 for cell migration and tumor propagation. EFT are known to be highly metastatic tumors and our results underscore the complex regulatory networks that are required for cellular migration in these tumors. Understanding the importance of these gene interactions will help development of effective tumor-specific drug therapies that improve treatment while decreasing unwanted side-effects. Citation Format: Sheetal A. Mitra, Anirban P. Mitra, Jonathan D. Buckley, Timothy J. Triche. Coding and noncoding gene targets in pediatric soft tissue sarcomas. [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 597. doi:10.1158/1538-7445.AM2015-597
Secondary Malignancies after Hematopoietic Stem Cell Transplantation in Patients Treated with Total Body Irradiation.
Authors: Cristina de la Fuente, Maria I. Berrocal, J. Rafael Cabrera, Carlos A. Regueiro, Rafael Fores, Carmen Regidor, Isabel Millan, Luis Nuñez, Francisco Valcarcel, Manuel N. Fernandez, Isabel Sanjuan, Alejandro de la Torre
Journal: Blood (2005)
High dose fish oil supplements in late pregnancy reduce asthma in offspring, finds study
Authors: Susan Mayor
Journal: BMJ (2016)

Taking supplements containing high doses of n-3 long chain polyunsaturated fatty acids derived from fish oil in the last three months of pregnancy reduced the risk of persistent wheeze or asthma and infections of the lower respiratory tract in offspring by nearly a third in the first five years of life, a randomised study has found.1

A diet deficient in n-3 long chain polyunsaturated fatty acids during pregnancy has previously been suggested to be associated with an increased risk of asthma and wheeze in children, but results from randomised trials …
Remobilization with G-CSF Is Less Effective Than the Initial Mobilization in Healthy Donors Undergoing Peripheral Blood Stem Cell Collection for Allogeneic Transplantation
Authors: Mark A Fiala, Soo Park, Camille N. Abboud, Amanda F. Cashen, Meagan Jacoby, Iskra Pusic, Rizwan Romee, Mark A. Schroeder, Geoffrey L. Uy, Ravi Vij, Peter Westervelt, Tanya M Wildes, John F. DiPersio, Keith E. Stockerl-Goldstein
Journal: Blood (2014)
Reduction of aGVHD using chicken antibodies directed against intestinal pathogens in a murine model
Authors: Abdellatif Bouazzaoui, Elisabeth Huber, Alexander Dan, Faisal A. Al-Allaf, Jochen Pfirstinger, Günter Sprotte, Josef Köstler, Andreas Hiergeist, Andre Gessner, Wolfgang Herr, Ernst Holler
Journal: Blood (2016)
Abstract 3484: Synergism from combination of targeted therapy with tumor active phytochemicals in ovarian tumor models and changes in protein expression
Authors: Fazlul Huq
Journal: Cancer Research (2015)

Abstract Introduction Ovarian cancer is most lethal cause of gynecological types of cancer mainly because of acquired drug resistance and poor diagnosisis. In majority of cases it is detected at an advanced stage when it is likely to have spread beyond ovaries. Combination of platinum drugs with paclitaxel is the current mode of treatment. Although cancer cells respond well to the drug combination, relapse often occurs for which drugs fail to function. We have designed a number of novel platinums aimed to overcome platinum resistance in ovarian cancer. We also applied combinations of platinums and tumor active phytochemicals such as curcumin, EGCG, thymoquinone, resveratrol, ursolic acid and genistein to overcom drug resistance. This presentation will provide a brief overview of novel platinums designed in our lab with special emphasis on recent studies on combinations of platinum with phytochemicals and protein expression. Methods Activity of the compounds alone and in sequenced combination in ovarian cancer cell lines including A2780, A2780cisR and A2780ZD0473R were determined using MTT reduction assay. Drug uptake and drug-DNA binding were determined using developed protocols. Proteomic studies involving 2D gel electrophoresis and mass spectrometry were carried out to characterize key proteins associated with platinum resistance. Results Generally but not always sequenced combinations with 2 to 4 h time gap were found to be synergistic. The variation in combined drug action with the change in sequence of administration clearly indicates that the action of one drug has modulated that of the other. Proteomic studies have identified over thirty proteins believed to be associated with platinum resistance in ovarian cancer. They belong to six major groups including cytoskeletal proteins, molecular chaperone and stress related proteins, proteins involved in detoxification and drug resistance, proteins involved in metabolic processes and mRNA processing proteins. The proteins are restored to normalcy due to treatment with synergistic combinations. Conclusion If confirmed in vivo, the results of the study indicate that appropriate combinations of targeted therapy and tumor active phytochemicals may providing an effective and affordable means of overcoming drug resistance in ovarian cancer. Citation Format: Fazlul Huq. Synergism from combination of targeted therapy with tumor active phytochemicals in ovarian tumor models and changes in protein expression. [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 3484. doi:10.1158/1538-7445.AM2015-3484
Projecting Individualized Absolute Invasive Breast Cancer Risk in US Hispanic Women
Authors: Matthew P. Banegas, Esther M. John, Martha L. Slattery, Scarlett Lin Gomez, Mandi Yu, Andrea Z. LaCroix, David Pee, Rowan T. Chlebowski, Lisa M. Hines, Cynthia A. Thompson, Mitchell H. Gail
Journal: JNCI Journal of the National Cancer Institute (2016)

Background: There is no model to estimate absolute invasive breast cancer risk for Hispanic women. Methods: The San Francisco Bay Area Breast Cancer Study (SFBCS) provided data on Hispanic breast cancer case patients (533 US-born, 553 foreign-born) and control participants (464 US-born, 947 foreign-born). These data yielded estimates of relative risk (RR) and attributable risk (AR) separately for US-born and foreign-born women. Nativity-specific absolute risks were estimated by combining RR and AR information with nativity-specific invasive breast cancer incidence and competing mortality rates from the California Cancer Registry and Surveillance, Epidemiology, and End Results program to develop the Hispanic risk model (HRM). In independent data, we assessed model calibration through observed/expected (O/E) ratios, and we estimated discriminatory accuracy with the area under the receiver operating characteristic curve (AUC) statistic. Results: The US-born HRM included age at first full-term pregnancy, biopsy for benign breast disease, and family history of breast cancer; the foreign-born HRM also included age at menarche. The HRM estimated lower risks than the National Cancer Institute's Breast Cancer Risk Assessment Tool (BCRAT) for US-born Hispanic women, but higher risks in foreign-born women. In independent data from the Women's Health Initiative, the HRM was well calibrated for US-born women (observed/expected [O/E] ratio = 1.07, 95% confidence interval [CI] = 0.81 to 1.40), but seemed to overestimate risk in foreign-born women (O/E ratio = 0.66, 95% CI = 0.41 to 1.07). The AUC was 0.564 (95% CI = 0.485 to 0.644) for US-born and 0.625 (95% CI = 0.487 to 0.764) for foreign-born women. Conclusions: The HRM is the first absolute risk model that is based entirely on data specific to Hispanic women by nativity. Further studies in Hispanic women are warranted to evaluate its validity.
Evidence in Favor of Standard Surgical Treatment for Rectal Cancer
Authors: Heidi Nelson, Nikolaos Machairas, Axel Grothey
Journal: JAMA Oncology (2016)

This Viewpoint argues that that it is premature to practice selective withdrawal of surgery based on the curative contribution of surgery, the lack of reliable predictive biomarkers, and the scarcity of solid evidence in support of this practice.