tbuckley/cabot-search huggingface dataset:
THU0160 Semi-quantitative and standardised sonographic investigations of the activity of inflamation in patients with rheumatoid arthritis
Authors: C Weidekamm, F Kainberger, M Koeller, L Erlacher, H Imhof
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> With high-resolution sonography (US) of joints affected by rheumatoid arthritis (RA) a detailed delineation of intra- and extraarticular soft-tissue abnormalities is possible. Power-Doppler is useful for the analysis of the vascularisation of inflamed tissue. The aim of the study was to evaluate the diagnostic value of Power-Doppler and B-Mode US in context with clinical examinations and conventional radiography. <h3>Objectives</h3> <h3>Methods</h3> To date, in 22 patients (5 males, 17 females) with different grades of RA (17 RF+, 5RF-) the wrists and MCP I-V and PIP II-V were scored with sonography (ATL HDI 5000, 5‑12 MHz Transducer, synthetic plastic blocks) with B-Mode and Power-Doppler application in standardised technique. Extension and severity of the inflamed tissue as well as vascularisation were scored. The results were correlated with benchmarks of the clinical and radiologic investigations. Radiographs were assessed according to the Larsen Score. The amount of time of US investigation was measured. <h3>Results</h3> With sonography, both extension and severity of wrist lesions could be delineated to better advantage than with radiography and clinical examination. This was also true for the MCP joints with the exception of MCP II, where most of the lesions detected by radiography were found. From 484 joints, 29% were found to be abnormal by clinical investigations. Erosions were detected in 26% with radiography, in 37% with sonography. Hypervascularisation was found in 36%. No significant difference of US abnormalities between patient groups with positive and negative RF could be found. A modern state-of-the-art Power Doppler program release is a necessary tool for semi-quantification. A standardised investigation technique with a median amount of time of 18 min provides sufficient quality measures. <h3>Conclusion</h3> Sonography detects more bone erosions than radiography and clinical examination. It supports the diagnosis of RA manifestations of the hand. <h3>References</h3> Fitzgerald O, Bresnihan B. Synovial vascularity is increased in rheumatoid arthritis: comment on the article by Stevens, et al.[letter]. Arthritis Rheum. 1992;35:1540–41 Hau M, Schultz H, Tony HP, Keberle M, Jahns R, Haerten R, Jenett M. Evaluation of pannus and vascularization of the metacarpophalangeal and proximal interphalangeal joints in rheumatoid arthritis by high-resolution ultrasound (multidimensional linear array). Arthritis Rheum. 1999;42(11):2303–8 Grassi W, Tittarelli E, Pirani O, Avaltroni D, Cervini C. Ultrasound examination of metacarpophalangeal joints in rheumatoid arthritis. Scand J Rheumatol. 1993;22:243–7
Abstract MP174: Cardiomyocyte-specific Deletion of Parathyroid Hormone Receptor 1 During Development Leads to Left Ventricular Hypoplasia
Authors: Desiree Leach, Ryan Jorgensen, Jayne Wolfe, Lisa D Wilsbacher
Journal: Circulation Research (2020)

Congenital heart defects occur in approximately 1% of all births and signify the most common human birth defects. Our lab previously demonstrated that cardiomyocyte specific deletion of Sphingosine 1-Phosphate Receptor 1 (S1P 1 ), a G protein-coupled receptor (GPCR) that couples exclusively to Gαi, leads to ventricular noncompaction in mice. Gαs- and Gαi-coupled GPCRs activate and inhibit adenylate cyclase, respectively, thereby regulating cAMP production. These GPCRs play important roles in adult cardiac health and disease, but their contributions to heart development are not well understood. We hypothesized that tight regulation of cAMP via Gαs- and Gαi-coupled GPCRs is a critical determinant of cardiomyocyte maturation and cardiac development. Here, we report that Parathyroid Hormone Receptor 1 (Pth1r) which couples to Gαs, is a mediator of cardiomyocyte maturation. Using mice with a Cre allele in the myosin light chain 2a locus ( Myl7 Cre/+, also known as Mlc2a Cre/+ ), we found that cardiomyocyte-specific deletion of Pth1r during development led to reduced postnatal survival. Hearts collected from surviving Pth1r cardiomyocyte mutant mice displayed left ventricular (LV) hypoplasia, and fetal cardiac genes Nppa (natriuretic peptide A) and β myosin heavy chain (Myh7) were upregulated in the hearts of surviving mutants. At 14.5 days post coitus (dpc) and 18.5 dpc, Pth1r cardiomyocyte mutant mice also showed LV hypoplasia. Furthermore, we observed decreased cardiomyocyte proliferation in Pth1r cardiomyocyte mutant hearts during development. Isolated cardiomyocytes from C57BL/6 wild-type embryos showed increased cAMP production after stimulation of Pth1r; Pth1r-dependent cAMP increases were inhibited by activation of S1P 1 . Overall, our results indicate a critical role for Pth1r signaling during heart development and suggest that cAMP levels must be tightly controlled in cardiomyocytes for normal cardiac development. LV hypoplasia is one of the key features of hypoplastic left heart syndrome (HLHS), one of the most severe forms of congenital heart disease; these studies may provide new approaches for the study and treatment of LV hypoplasia and HLHS.
Efficacy and Safety of Voxelotor in Sickle Cell Disease: A Systematic Review
Authors: Muhammad Ashar Ali, Anam Khan, Sana Irfan Khan, Sobia Aamir, Saad Ur Rahman, Anum Waqar, Hafsa Tahir Chaudry, Muhammad Yasir Anwar, Wajeeha Aiman, Faiz Anwer
Journal: Blood (2020)
SGN-CD30C, an Investigational CD30-Directed Camptothecin Antibody-Drug Conjugate (ADC), Shows Strong Anti Tumor Activity and Superior Tolerability in Preclinical Studies
Authors: Maureen Ryan, Ryan Lyski, Lauren Bou, Ryan Heiser, Bryan Grogan, Dave Meyer, Steven Jin, Jessica Simmons, Melissa Conerly, Peter Senter, Scott Jeffrey
Journal: Blood (2020)
Structural and Biochemical Studies Confirming the Mechanism of Action of Asciminib, an Agent Specifically Targeting the ABL Myristoyl Pocket (STAMP)
Authors: Peter Schuld, Stephan Grzesiek, Johannes Schlotte, Judith M Habazettl, Wolfgang Jahnke, Louise Barys, Sandra W Cowan-Jacob, Alice Loo, Andrea Wiget, Paul W. Manley
Journal: Blood (2020)
The Impact of Sorafenib on Phospho-FLT3 Inhibition and <i>FLT3</i>-ITD MRD after Chemotherapy: Correlative Studies from the Phase 2 Randomized Study of Sorafenib Versus Placebo in Combination with Intensive Chemotherapy in Previously Untreated Patients with <i>FLT3</i>-ITD Acute Myeloid Leukemia (ALLG AMLM16)
Authors: Natasha S Anstee, Giovanna Pomilio, Mark Levis, Sarah MacRaild, Michael Murray, Tristan Rawling, Glen A Kennedy, Andrew Grigg, Anthony Schwarer, Anoop Kumar Enjeti, James D'Rozario, Paula Marlton, Ian Bilmon, Adam Ivey, Doen Ming Ong, Andrew W Roberts, Andrew H Wei
Journal: Blood (2020)
A Phase II Study of Pembrolizumab in Combination with Romidepsin Demonstrates Durable Responses in Relapsed or Refractory T-Cell Lymphoma (TCL)
Authors: Swami P. Iyer, Jie Xu, Melody R. Becnel, Ranjit Nair, Raphael Steiner, Lei Feng, Hun Ju Lee, Paolo Strati, Sairah Ahmed, Simrit Parmar, Yago Nieto, Chitra Hosing, Jason Westin, Loretta J. Nastoupil, Ann Vo, Felipe Samaniego, Nathan H. Fowler, Neeraj Saini, Issa F. Khouri, Jin S. Im, Preetesh Jain, Luis Fayad, Michael Wang, Roberto N. Miranda, Francisco Vega, Christopher Flowers, Sattva S. Neelapu
Journal: Blood (2020)
Stromal Notch Ligands Drive Notch2-Dependent Transdifferentiation of Follicular B Cells into Marginal Zone-like B Cells in Lymphopenic Environments
Authors: Daniela Gómez Atria, Brian T. Gaudette, Eric Perkey, Jennifer Londregan, Samantha Kelly, Burkhard Ludewig, Chris Siebel, Russell J. H. Ryan, Warren S. Pear, David Allman, Ivan Maillard
Journal: Blood (2020)
Abstract MP171: Transcription Start Site Profiling Defines Promoter and Enhancer Regions for Cardiomyopathy Genes
Authors: Anthony M Gacita, Lisa Dellefave-Castillo, Patrick G Page, David Y Barefield, Andrew Wasserstrom, Megan Puckelwartz, Marcelo A Nobrega, Elizabeth M McNally
Journal: Circulation Research (2020)

Background: Mutations in more than 100 genes lead to dilated, hypertrophic and other forms of cardiomyopathy. Autosomal dominant mutations in the MYH7 and LMNA genes cause autosomal dominant hypertrophic and dilated cardiomyopathy, respectively. Individual mutations display a range of clinical expression from severe early onset disease to minimal or no symptoms. Genetic variation in noncoding gene regulatory regions including enhancers is expected to modify expression of cardiomyopathy genes and disease expressivity. In addition, heart failure is associated a fetal gene re-expression program, mediated by genetic regulatory regions. The contribution of noncoding genetic variation to cardiomyopathy and heart failure has been hampered by limited genome wide descriptions of human cardiac regulatory regions. Methods and Results: We used C ap A nalysis of G ene E xpression by sequencing (CAGE-seq) to profile the transcriptional start sites in healthy and failed human hearts. CAGE-seq detects the unidirectional signals of gene promoters and the bidirectional signal of transcribed enhancer regions. We identified ~17,000 transcriptional start sites associated with gene promoters and ~1,500 putative enhancer regions active in cardiac tissue. These CAGE-defined regulatory regions carried histone modifications and transcription factor binding properties characteristic of enhancers or promoters. We specifically identified promoter switching and differential enhancer usage between healthy and failed hearts. We intersected CAGE-defined enhancers with additional epigenomic datasets to identify regulatory regions for MYH7 and LMNA genes. We identified 13 putative enhancer regions and validated the functionality of a subset of these regulatory regions using reporter assays and gene editing. Conclusions: This CAGE-seq dataset defines the regulatory environment for heart failure. These promoter and enhancer regions could be used to target heart-failure associated gene expression changes. Additionally, this data can be used to identify enhancer regions regulating cardiomyopathy genes.
Dasatinib Increases MHCII Surface Levels and Can Synergize with Anti-PD1 Therapy to Increase the Anti-Tumor Effect in a Pre-Clinical Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia Model
Authors: Paul Koller, Karine Harutyunyan, Antonio Cavazos, Natalia Baran, Saradhi Mallampati, Renee Chin, Zhou Jiang, Heng-Huan Lee, Michael Curran, Mien-Chie Hung, Marina Konopleva
Journal: Blood (2020)
Predictors of Healthcare Utilization in Newly Diagnosed Myeloma
Authors: Shane Toolan, Mark Griffin, Mark Coyne, Kate O'Mahony, Joy Lewis, Chandan D'Souza, Daniel G Connaghan, Karen Murphy, Kamal Fadalla, Joan Marie Fitzgerald, Conor Collins, Niall Swan, Crotty Tom, Gibbons David, Liam Smyth
Journal: Blood (2020)
African-Americans Multiple-Myeloma Patients Undergoing Upfront Autologous Stem Cell Transplant Have Similar Survival Outcomes Compared to Whites: A Propensity-Score Matched Analysis
Authors: Neeraj Saini, Junsheng Ma, Qaiser Bashir, Ruby Delgado, Gabriela Rondon, Uday R. Popat, Chitra Hosing, Yago Nieto, Partow Kebriaei, Amin M. Alousi, Rohtesh S. Mehta, Samer A. Srour, Issa F. Khouri, Donna M. Weber, Sheeba K. Thomas, Hans C. Lee, Krina K. Patel, Robert Z. Orlowski, Richard E. Champlin, Muzaffar H. Qazilbash
Journal: Blood (2020)
Examination and Validation of a Patient-Centric Joint Metric: "Problem Joint"; Empirical Evidence from the CHESS US Dataset
Authors: Tom Burke, Idaira Rodriguez Santana, Pratima Chowdary, Randall Curtis, Kate Khair, Michael Laffan, Paul McLaughlin, Declan Noone, Brian O'Mahony, John Pasi, Mark W Skinner, Jamie O'Hara
Journal: Blood (2020)
Consolidation with Nivolumab and Brentuximab Vedotin after Autologous Hematopoietic Cell Transplantation in Patients with High-Risk Hodgkin Lymphoma
Authors: Alex F. Herrera, Lu Chen, Yago Nieto, Leona Holmberg, Patrick B. Johnston, Matthew Mei, Leslie Popplewell, Saro H. Armenian, Thai Cao, Len Farol, Firoozeh Sahebi, Ricardo Spielberger, Robert Chen, Auayporn P. Nademanee, Lacolle Peters, Neena Kennedy, Steven T. Rosen, Larry W Kwak, Stephen J. Forman, Tatyana A. Feldman
Journal: Blood (2020)
HPN217-3001: A Phase 1/2 Open-Label, Multicenter, Dose Escalation and Dose Expansion Study of the Safety, Tolerability, and Pharmacokinetics of HPN217, a Bcma-Targeting T-Cell Engager, in Patients with Relapsed/Refractory Multiple Myeloma
Authors: Henning Schade, Sumit Madan, Eva Medvedova, Rajneesh Nath, Lisa Knapp, Bryan Lemon, Liping Laura Sun
Journal: Blood (2020)
Targeted Sequencing of 7 Genes Can Help Reduce Pathologic Misclassification of MDS
Authors: Johannes B Goll, Travis L Jensen, R. Coleman Lindsley, Rafael Bejar, Jason Walker, Robert Fulton, Gregory A. Abel, Tareq Al Baghdadi, H. Joachim Deeg, Amy E. DeZern, Benjamin L. Ebert, James M. Foran, Edward J. Gorak, Steven D. Gore, Rami Komrokji, Jane Jijun Liu, Jaroslaw P. Maciejewski, Eric Padron, Wael Saber, Daniel Starczynowski, Myron Waclawiw, Steffanie H. Wilson, Donnie Hebert, Harrison Reed, Nancy L. DiFronzo, Mikkael A. Sekeres, Alexandra M. Harrington, Steven H. Kroft, Ling Zhang, Matthew J. Walter
Journal: Blood (2020)
Phenotypic and Proliferative Analysis of T Cell and Monocyte Populations in Patients with Intermediate/High/Very High-Risk MDS Compared to Age-Matched Healthy Donors
Authors: Hannah Fields, Valentina Ferrari, Alison Tarke, Randy Guo-Shi Tsai, Timothy Luger, Colin McCarthy, Ruifeng Chen, Xinlian Zhang, Thomas A Lane, Antonella Vitiello, Rafael Bejar, Tiffany N Tanaka
Journal: Blood (2020)
Prolactin signaling in Nb2-11 T-lymphoma cells: A role for HRPAP20
Authors: Manasi N. Shukla, Cristina M. Karp, Donna J. Buckley, Arthur R. Buckley
Journal: Cancer Research (2004)

2882  Previous studies of the recently identified protein, HRPAP20 (Hormone Responsive Proliferation Associated Protein, 20 KD), revealed its regulation by growth factor stimulation in responsive T-lymphoma and breast adenocarcinoma cells. In this setting, the anterior pituitary hormone, prolactin (PRL), rapidly increased HRPAP20 expression, which was also coupled to its serine phosphorylation. Stable transfection of HRPAP20 significantly increased proliferation and prolonged survival following an apoptotic stimulus, similar to the effects of PRL treatment. These observations suggested that HRPAP20 may represent an intermediate in PRL signaling. The present study was conducted to determine whether HRPAP20 could be co-localized with known PRL signaling proteins. Amino acid sequence analysis of HRPAP20 indicated a potential calmodulin (CaM) binding motif (amino acids 54-73) that overlapped with a putative protein kinase C (PKC)-phosphorylation site (amino acids 55-57; motif SXK) suggesting possible interactions among it, CaM, and PKC. Co-immunoprecipitation/ immunoblotting (co-IP/IB) experiments showed that HRPAP20 was associated with CaM in quiescent rat Nb2-11 T-lymphoma cells. Treatment with PRL rapidly (5 min) caused dissociation of the HRPAP20/CaM complex. Results from other experiments showed that phorbol ester (TPA)-induced PKC activation similarly disrupted the association of HRPAP20/CaM suggesting that the phosphorylation status of HRPAP20 may regulate its interaction with cellular proteins. Since previous studies linked PKC activation to PRL receptor stimulation, experiments were conducted to determine whether HRPAP20 was a substrate for PKC in PRL-treated cells. Stationary Nb2-11 cultures, exposed to pharmacological kinase antagonists, were treated with PRL prior to immunoblot analysis of HRPAP20 phosphorylation using anti-phosphoserine specific antibodies. Inhibition of PKC with RO-31-8220 significantly reduced HRPAP20 phosphorylation (p
mTOR-dependent translation amplifies microglia priming in aging mice
Authors: Lily Keane, Ignazio Antignano, Sean-Patrick Riechers, Raphael Zollinger, Anaelle A. Dumas, Nina Offermann, Maria E. Bernis, Jenny Russ, Frederike Graelmann, Patrick Neil McCormick, Julia Esser, Dario Tejera, Ai Nagano, Jun Wang, Claude Chelala, Yvonne Biederbick, Annett Halle, Paolo Salomoni, Michael T. Heneka, Melania Capasso
Journal: Journal of Clinical Investigation (2020)

Microglia maintain homeostasis in the brain. However, with age, they become primed and respond more strongly to inflammatory stimuli. We show here that microglia from aged mice had upregulated mTOR complex 1 signaling controlling translation, as well as protein levels of inflammatory mediators. Genetic ablation of mTOR signaling showed a dual yet contrasting effect on microglia priming: it caused an NF-κB–dependent upregulation of priming genes at the mRNA level; however, mice displayed reduced cytokine protein levels, diminished microglia activation, and milder sickness behavior. The effect on translation was dependent on reduced phosphorylation of 4EBP1, resulting in decreased binding of eIF4E to eIF4G. Similar changes were present in aged human microglia and in damage-associated microglia, indicating that upregulation of mTOR-dependent translation is an essential aspect of microglia priming in aging and neurodegeneration.
Metastatic Poorly Differentiated Thyroid Cancer With Heterogeneous Distribution of 18F-FDG, 68Ga-DOTATATE, and 68Ga-PSMA on PET/CT
Authors: Caner Civan, Emine Goknur Isik, Duygu Has Simsek
Journal: Clinical Nuclear Medicine (2020)

We present a case of a 55-year-old man with a history of poorly differentiated metastatic thyroid cancer, which is rare and shows aggressive behavior. The patient had radioactive iodine-negative multiple metastasis on 18F-FDG PET/CT, therefore 68Ga-DOTATATE and 68Ga-PSMA PET/CT were performed whether an opportunity exist for DOTATATE or PSMA-directed radionuclide therapy. Different patterns of tumoral uptakes were detected on 18F-FDG, 68Ga-DOTATATE, and 68Ga-PSMA PET/CT, as a demonstration of tumor heterogeneity.
A Machine Learning Approach for the Differential Diagnosis between Sars-COV19 Infection and Influenza Viruses with Hematological Morphologic DATA (CELL MORPHOLOGIC DATA)
Authors: Fernando Calvo Boyero, Sandra Gomez Gomez Rojas, Gloria Perez Segura, Ana Lopez Jimenez, Miguel Pedrera Jimenez, Gonzalo Carreño Gomez-Tarragona, Buenaventura Buendía Ureña, Joaquin Martinez Lopez
Journal: Blood (2020)
Abstract MP140: Epigenetic Silencing of SERCA2a by Long Noncoding RNA <i>Lnc-SYNPO</i> Contributes to Impaired Ca <sup>2+</sup> Homeostasis and Contractility in the Failing Heart
Authors: Min-Yi You, Pei-Jin Ho, Hui-Chun Ku, Shu-Ping Wang, Kai-chien Yang
Journal: Circulation Research (2020)

Abnormal sarcolemmal Ca 2+ handling and impaired contractile function owing to sarcoplasmic reticulum/endoplasmic reticulum ATPase 2a (SERCA2a, encoded by ATP2A2 ) downregulation and/or dysfunction are pathognomonic hallmarks of heart failure (HF). There is, however, no clinically proven HF therapy that targets SERCA2a/ ATP2A2 dysregulation directly. Exploiting gene co-expression network analysis using an RNA sequencing dataset generated from human failing and non-failing left ventricular (LV) tissues, we identified long noncoding RNA lnc-SYNPO , transcribed from the 3’ untranslated region of SYNPO2 , as a potential regulator of SERCA2a/ ATP2A2 . Myocardial lnc-SYNPO was markedly upregulated during HF and its expression level showed a strong negative correlation (Pearson correlation coefficient=-0.60) with that of SERCA2a/ ATP2A2 in both mouse and human LV. Knockdown of lnc-SYNPO in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM) increased, whereas overexpression of lnc-SYNPO reduced, SERCA2a/ ATP2A2 expression. In addition, lnc-SYNPO knockdown reversed endothelin-1 (ET-1) treatment-induced SERCA2a/ ATP2A2 downregulation, impaired Ca 2+ homeostasis and contractile dysfunction in hiPSC-CM. Mechanistically, the depletion of lnc-SYNPO, a chromatin-associated nuclear lncRNA, led to increased H3K4me3 and reduced H3K27me3 occupancy at SERCA2a/ ATP2A2 promoter. Chromatin isolation by RNA purification showed direct physical binding between lnc-SYNPO and the promoter of SERCA2a/ ATP2A2 . In addition, RNA pull-down assays showed that lnc-SYNPO binds to EZH2 and SUZ12, two core components of the polycomb repressor complex 2 (PRC2), suggesting that lnc-SYNPO represses SERCA2a/ ATP2A2 expression by recruiting PRC2 complex to the promoter of SERCA2a/ ATP2A2 , leading to epigenetic silencing of SERCA2a/ ATP2A2 . Taken together, these results unveiled a previously undiscovered epigenetic regulatory mechanism of SERCA2a/ ATP2A2 by lnc-SYNPO , contributing to impaired myocardial Ca 2+ homeostasis and contractile dysfunction observed with HF. Targeting lnc-SYNPO , therefore, could be a novel therapeutic approach to improve Ca 2+ homeostasis and contractile function in the failing human heart.
Efficacy of Modified Vrd-Lite for Transplant Ineligible Multiple Myeloma
Authors: Mizuki Ogura, Tadao Ishida, Moe Nomura, Hirofumi Irita, Junichiro Nashimoto, Kota Sato, Kanji Miyazaki, Yu Abe, Nobuhiro Tsukada, Kenshi Suzuki
Journal: Blood (2020)
COVID-19 in Chronic Myeloid Leukemia Patients - Brazilian Experience
Authors: Katia B Pagnano, Ana Carolina Mourão Toreli, Leila Martins Perobelli, Acy TS Quixada, Fernanda S Seguro, Israel Bendit, Marcia Torresan Delamain, Jaqueline Sapelli, Muriel Silva Moura, Jaisson Bortolini, André LG Lourenço, Natália N Gonçalves, Monika Conchon, Fabio Moore Nucci, Luciene Da Cruz Oliveira, Gustavo HR Magalhães, Vaneuza Funke, Renato Tavares, Renato Torrescasana Centrone, Fabio PS Santos, Laura Fogliatto, Leonardo Carvalho Palma, Nelma D Clementino, Paula OM Hokama, Carla M Boquimpani
Journal: Blood (2020)
Disparities in the Use of Allogeneic Hematopoietic Stem Cell Transplant Among Children, Adolescents, and Young Adults with Acute Leukemia in California
Authors: Lena E. Winestone, Qian Li, Lori S. Muffly, Kelly D Getz, Elysia Alvarez, Ted Wun, Theresa Keegan
Journal: Blood (2020)
Abstract NT-086: PRELIMINARY IDENTIFICATION OF LACTATE DEHYDROGENASE INHIBITORS TOWARDS ANTICANCER DRUG DEVELOPMENT
Authors: Adegbite Emmanuel, Joseph O Sanya, Olujide O Olubiyi
Journal: Clinical Cancer Research (2019)

Abstract In tumor cells undergoing rapid cellular division, significantly increased quantities of lactic acid are produced in an anaerobic respiration via the Cori cycle. While this produces a lower of the pH in the local environment, the hepatic conversion of the generated lactate into glucose places a huge energy demand on the body which makes the patient weaker and results in cancer cachexia in all ovarian malignancies. Thus, instead of producing acetyl CoA, the dividing tumorous cells synthesize lactic acid catalyzed by the enzyme lactate dehydrogenase (LDH). LDH's involvement in tumor initiation and metabolism primarily involves a state of fermentative glycolysis catalyzed by the A form of the enzyme which allows tumorous cells convert the majority of their glucose stores into lactate even under anaerobic conditions which invariably shifts the utilization of glucose metabolites from simple energy production to an active promotion of accelerated cell growth and replication. This makes LDH a vital target for malignant ovarian drug development. And in the present work a combination of virtual screening, database scouting and biophysical analysis of binding site properties have been employed in analysis the interaction of about 30,000 compounds with LDH. Using a synthetic NADH inhibitor, as a reference, only four compounds were found to demonstrate stronger binding features than the inhibitor. This preliminary in silicon screening represents the foundational effort in a ovarian cancer drug discovery project aimed at generating specific inhibitors of LDH for use in ovarian cancer therapeutics. Note: This abstract was not presented at the symposium. Citation Format: Adegbite Emmanuel, Joseph O Sanya, and Olujide O Olubiyi. PRELIMINARY IDENTIFICATION OF LACTATE DEHYDROGENASE INHIBITORS TOWARDS ANTICANCER DRUG DEVELOPMENT [abstract]. In: Proceedings of the 12th Biennial Ovarian Cancer Research Symposium; Sep 13-15, 2018; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2019;25(22 Suppl):Abstract nr NT-086.