tbuckley/cabot-search huggingface dataset:
LAMC2 as a prognostic marker that promotes metastasis of lung adenocarcinoma through epithelial-mensenchymal transition (EMT).
Authors: Yongwha Moon, Kang-seo Park, John Kim, Sami Sarfaraz, Donna Voeller, Pham Trung, Yisong Wang, Giuseppe Giaccone
Journal: Journal of Clinical Oncology (2013)

11034 Background: Metastasis is the main cause of death in non-small cell lung cancer (NSCLC) patients. Genes responsible for NSCLC metastasis are unknown. LAMC2 is one of the 3 chains (α3, β3, γ2) of laminin 332, an important component of basement membranes, and LAMC2 involvement in metastasis is unclear. Methods: We have established a metastasis model in nude mice by repeated intracardiac injection of A549 lung adenocarcinoma cells. After 3-4 rounds of intracardiac injections, 100% metastasis penetrance was obtained. Microarray analysis was performed to identify genes differentially expressed between parental (A549P) and round-3 (A549R3) cells. In vitro migration/invasion and in vivo metastasis assays were performed in LAMC2-overexpressed A549P, LAMC2-knockdown A549R4, PC9, H358, and H322 cells. Public RNA microarray data of human NSCLC (GSE8894, GSE3141; n=249) and LAMC2 immunohistochemistry (IHC) of stage I NSCLC TMA samples (n=250) were analyzed to correlate LAMC2 and prognosis. Results: We identified LAMC2 as a putative metastasis marker of NSCLC through gene expression profiling of A549 cells enriched for metastasis in mice. Ectopic LAMC2 expression increased migration/invasion, whereas LAMC2 knockdown decreased migration/invasion in vitro. Conditioned media containing secreted LAMC2 promoted cell migration/invasion, which were blocked by LAMC2 knockdown or LAMC2 neutralizing antibody. Ectopic LAMC2 expression induced mesenchymal but decreased epithelial markers, indicating EMT, whereas LAMC2 knockdown elicited the opposite. A549R4 LAMC2 knockdown cells showed less metastatic activity than A549R4shRNA control cells in mice. In public microarray data high LAMC2 mRNA predicted high risk of recurrence (GSE8894, P=0.022; GSE3141, P=0.029) in adenocarcinoma (AC) but not squamous carcinoma (SC). Our IHC study showed that high LAMC2 predicted high risk of recurrence (hazard ratio =1.8; P=0.040) and death (hazard ratio=1.9; P=0.028) in AC but not SC by multivariate analysis. Conclusions: LAMC2 promotes metastasis through activation of EMT pathways, and is a potential prognostic marker and therapeutic target of metastasis in lung adenocarcinoma.
CLO20-068: Incidence and Potential Predictors of Thromboembolic Events in Epithelial Ovarian Carcinoma Patients During Perioperative Period
Authors: Qingqing Zhou, Chenchen Zhu, Zhen Shen, Jing Zhu, Tianjiao Zhang, Min Li, Jiwei Qin, Lili Qian, Chuan Chen, Hanyuan Liu, Zhihao Xu, Dabao Wu, Björn Nashan, Ying Zhou
Journal: Journal of the National Comprehensive Cancer Network (2020)

"CLO20-068: Incidence and Potential Predictors of Thromboembolic Events in Epithelial Ovarian Carcinoma Patients During Perioperative Period" published on 20 Mar 2020 by National Comprehensive Cancer Network.
SOMALOGIC ST2 AND NTPROBNP ASSAYS PREDICT HEART FAILURE MORTALITY AS EFFECTIVELY AS THE ELISA ASSAY
Authors: Joseph Debbs, Timothy D. Bryson, Nicole Zeld, Lindsey Aurora, Hongsheng Gui, Jasmine A. Luzum, Edward Peterson, Ruicong She, L Keoki Williams, David E. Lanfear
Journal: Journal of the American College of Cardiology (2020)
NCIC CTG MA.17: Intent to treat analysis (ITT) of randomized patients after a median follow-up of 54 months
Authors: J. Ingle, D. Tu, L. Shepherd, M. Palmer, J. Pater, P. Goss
Journal: Journal of Clinical Oncology (2006)

549 Background: MA.17 evaluated letrozole (LET) or placebo (PLAC) after 5 years of tamoxifen (Tam) and showed [median follow-up 30 months (mos)] significant improvement in disease-free survival (DFS) for LET [hazard ratio (HR) 0.57, p = 0.00008]. The trial was unblinded and PLAC patients (pts) were offered LET. An ITT analysis of all outcomes, before and after unblinding, based on the original randomization was performed. Methods: A stratified log-rank test was used to compare DFS, distant (D)DFS, overall survival (OS) and incidence of contra-lateral breast cancer (CBC). The Cox regression model used baseline stratification variables and two prespecified factors, menopausal status at the start of Tam and time on Tam. Subgroup analyses for DFS and OS were performed for the two prespecified subsets. All p-values were two-sided Results: 5187 pts were randomized at baseline and, at unblinding, 1655 of 2268 PLAC pts accepted LET. At median follow-up of 54 mos (range,16–86) 363 recurrences or CBC’s (144 LET and 219 PLAC) occurred; 118 LET and 176 PLAC pts had recurrent disease and 26 LET and 43 PLAC pts had CBC. 4 year DFS was 94.3% (LET) and 91.4% (PLAC) (HR 0.64; 95% CI, 0.52 - 0.79; p = 0.00002). Corresponding 4 year DDFS was 96.2% and 94.9% (HR 0.76; 0.58–0.99; p = 0.041). 4 year OS was 95.0% (LET) and 95.1% (PLAC) (HR 1.00; 0.78–1.28; p = 0.99). LET was equally effective in node +ve and -ve pts (i.e., similar HRs) in DFS. OS was not significantly different for LET and PLAC in any subgroup. The annual rate of CBC was 0.29% LET (0.18–0.40) and 0.47% PLAC (0.34–0.61); HR 0.61 (0.38–0.98) p = 0.037. 255 pts had died as of the data cut-off (128 LET and 127 PLAC). Conclusions: In this ITT analysis, pts originally randomized to LET within 3 months of stopping Tam did better than PLAC pts in DFS, DDFS and CBC, despite 73% of PLAC pts crossing to LET after unblinding. This highlights the strong beneficial effect of extended adjuvant therapy with LET. [Table: see text]
NATIONAL TRENDS OF SUBSTANCE USE DISORDER RELATED INFECTIVE ENDOCARDITIS FROM 2002 TO 2016: COMPARISON BETWEEN RURAL AND URBAN AREAS
Authors: Amer N. Kadri, Stephen Lynch, Ahmed Ali, Sara Khodor, Nizam Habhab, Steven W. Werns, Georges N. Nakhoul, Mohamed M. Gad, Adrian V. Hernandez, Brian P. Griffin, Gosta Pettersson, Richard A. Grimm, Jose Luis Navia, Steve M. Gordon, Samir R. Kapadia, Serge Harb
Journal: Journal of the American College of Cardiology (2020)
Genetic susceptibility to toxicity of chemotherapy in mice as pharmacokinetics-independent and drug-specific.
Authors: Ashley J Dittmar, Hayley Affronti, Maria Vittoria Sepporta, Elizabeth Gebuijs, Peter Demant
Journal: Journal of Clinical Oncology (2013)

e13549 Background: Adverse drug reactions (ADRs) are a significant obstacle in cancer chemotherapy. In spite of the advances in the development of drugs for cancer therapy, ADRs compromise their potential beneficial effects in many patients by imposing reduction of dose or cessation of treatment. Prediction of susceptibility to ADRs in individual patients could significantly improve treatment outcomes by more effectively choosing which drugs to treat with and which dose is appropriate. The pharmacokinetics (PK) of many drugs has been extensively studied and numerous enzymes and transporters that are involved in their activation and processing have been identified. However, when their role in individual susceptibility to ADRs has been tested in numerous studies, the variants of these proteins have not been able to consistently predict specific ADRs. Therefore, additional studies are required for a reliable prediction of toxicity. Methods: We used mouse strains with precisely defined limited genomic differences to evaluate genetic control of ADRs to three drugs commonly used in cancer chemotherapy - irinotecan, gemcitabine, and doxorubicin. We compared strain distribution of susceptibility to ADRs caused by each of these drugs and tested whether there is a correlation with genotypes at the major processing/transport (PK) genes that were reported in humans to affect toxicity of these drugs. Results: The major genetic differences in toxic reactions caused by these drugs do not correlate with the major PK loci and that the strain distribution pattern of susceptibility vs. resistance for each drug is different. Conclusions: This data suggests that a significant part of genetic susceptibility to ADRs is controlled by genes other than the presently known PK-related genes, and that many responsible genes are drug specific, with some possible overlaps. We hypothesize that these genes are likely involved in downstream pharmacodynamic (PD) processes and have remained largely unknown, because most studies in humans have been limited to known PK-related genes. We are proceeding towards identification of these novel genes, as they could help to optimize the selection of therapy for individual patients.
EXTRINSIC COMPRESSION OF THE LEFT MAIN CORONARY ARTERY BY A DILATED PULMONARY ARTERY IN A PATIENT
Authors: Fabio Akio Nishijuka, Nickolas Oliveira Dohmann, Renata R T Castro, Danuze Pereira De Carvalho Moura, Monica Medeiros Luna, José Geraldo Athayde, Marcia Queiroz, Carolina Cunto De Athayde, Rodrigo Musa De Mesquita Rodrigues Pereira, Leonardo Marinho, Paulo André da Silva, Ramon Nunes Vieira
Journal: Journal of the American College of Cardiology (2020)
Molecular classification and therapeutic targets in extrahepatic cholangiocarcinoma
Authors: Robert Montal, Daniela Sia, Carla Montironi, Wei Q. Leow, Roger Esteban-Fabró, Roser Pinyol, Miguel Torres-Martin, Laia Bassaganyas, Agrin Moeini, Judit Peix, Laia Cabellos, Miho Maeda, Carlos Villacorta-Martin, Parissa Tabrizian, Leonardo Rodriguez-Carunchio, Giancarlo Castellano, Christine Sempoux, Beatriz Minguez, Timothy M. Pawlik, Ismail Labgaa, Lewis R. Roberts, Manel Sole, Maria I. Fiel, Swan Thung, Josep Fuster, Sasan Roayaie, Augusto Villanueva, Myron Schwartz, Josep M. Llovet
Journal: Journal of Hepatology (2020)
COST, RESOURCE UTILIZATION, QUALITY OF LIFE, MENTAL HEALTH, AND FINANCIAL TOXICITY AMONG YOUNG ADULTS WITH STROKE IN THE UNITED STATES
Authors: Javier Valero Elizondo, Rohan Khera, Farhaan Vahidy, Haider Warraich, Shiwani Mahajan, Michael Blaha, Ron Blankstein, Salim Virani, Miguel Caínzos Achirica, Bita Kash, Harlan Krumholz, Khurram Nasir
Journal: Journal of the American College of Cardiology (2020)
Splenogonadal Fusion in Children
Authors: Isa Burak Guney, Abdulkerim Temiz, Mahmut Oksuzler, Murat Alkan
Journal: Clinical Nuclear Medicine (2020)

Splenogonadal fusion (SGF) is a rare congenital malformation, which can be of a continuous or discontinuous type. It is characterized by splenic tissue fused with gonadal tissue. Because it lacks characteristic features, very few cases of SGF have been diagnosed preoperatively. Herein, we present a case with left side SGF who was diagnosed by Tc-nanocolloid spleen scintigraphy.
EFFECT ON PATIENT ADHERENCE TO PRIMARY PREVENTION RECOMMENDATIONS FOR STATIN THERAPY BASED ON THE NATIONAL GUIDELINES-SUPPORTED POOLED COHORT RISK EQUATION OR A CORONARY ARTERY CALCIUM SCORE: PRELIMINARY FINDINGS FROM THE VANGUARD STUDY FOR THE CORCAL RANDOMIZED CLINICAL OUTCOMES TRIAL
Authors: J. Brent Muhlestein, Kirk Knowlton, Viet T. Le, Donald Lappe, Heidi May, David Min, Kevin Johnson, Shanelle T. Cripps, Lesley H. Schwab, Shelbi B. Braun, Tami Bair, Jeffrey L. Anderson
Journal: Journal of the American College of Cardiology (2020)
FUNCTIONAL RECOVERY AFTER PERCUTANEOUS REVASCULARIZATION OF CORONARY CHRONIC TOTAL OCCLUSIONS: INSIGHTS FROM CARDIAC MAGNETIC RESONANCE TISSUE TRACKING
Authors: Henk Everaars, Stefan Schumacher, Wijnand Stuijfzand, Martijn Basten Batenburg, Jennifer Huynh, Pepijn van Diemen, Michiel Bom, Ruben de Winter, Roel Driessen, Peter van de Ven, R.B. van Loon, Albert van Rossum, Maksymilian P. Opolski, Alexander Nap, Paul Knaapen
Journal: Journal of the American College of Cardiology (2020)
Abstract 17203: Exosomes From Induced Pluripotent Stem Cell-Derived Cardiomyocytes Salvage the Injured Myocardium by Modulation of Autophagy
Authors: Michelle R Santoso, Yuko Tada, Gentaro Ikeda, Ji-Hye Jung, Evgeniya Vaskova, Raymond G Sierra, Cornelius Gati, Andrew B Goldstone, Daniel V Bornstaedt, Praveen Shukla, Joseph C Wu, Soichi Wakatsuki, Joseph Woo, Phillip C Yang
Journal: Circulation (2018)

Background: Induced pluripotent stem cells (iPSCs) and their differentiated cardiomyocytes (iCMs) have tremendous potential as patient-specific therapy for myocardial injury (MI). Our previous work showed that the iCMs restore the injured murine myocardium through secretion of paracrine factors, modulating apoptotic pathways to restore the murine peri-infarct region (PIR). Hypothesis: iCM-derived exosomes (iCM-Ex), a major constituent of the iCM secretome, may salvage the injured cardiomyocytes in the PIR. Methods: iCM-Ex were precipitated from iCM supernatant and characterized using various molecular analyses. Immunodeficient mice sustained MIs and received iCMs, iCM-Ex, or PBS control via direct intramyocardial injection into the PIR. Cardiac MRI assessed LV ejection fraction (LVEF) and viability at 2- and 4-week post-injection. iCMs, iCM-Ex, and PIR tissue were isolated for molecular and histological analyses. Results: iCM-Ex measured approximately 142 nm and expressed CD63 and CD9. iCM and iCM-Ex miRNA profiles had significant overlap, indicating that exosomal content was reflective of the parent cell. In vitro iCM apoptosis was increased significantly by hypoxia and exosome biogenesis inhibition while iCM-Ex or rapamycin reduced iCM apoptosis (p&lt;0.05, vs. control). Mice treated with iCMs or iCM-Ex had significantly improved LVEF and LV viability compared to the control (p&lt;0.05). Apoptosis and fibrosis were significantly reduced in iCM- and iCM-Ex treated mice. Autophagy and associated mTOR signaling pathway were significantly enhanced in iCM-Ex treatment group. Conclusions: iCM-Ex demonstrated similar efficacy as the iCMs in improving post-MI cardiac function by regulating autophagy and apoptosis of hypoxia injured cardiomyocytes. This finding represents the potential of cell-free, patient-specific biologic to treat ischemic cardiomyopathy by stimulation of an endogenous repair mechanism.
Measuring the functional decline of people with advanced-stage non-small cell lung cancer (NSCLC).
Authors: Linda Denehy, Andrew Murnane, Meinir Krishnasamy, Karla Gough, Catherine Granger, Linda R. Mileshkin
Journal: Journal of Clinical Oncology (2012)

e19605 Background: People affected by lung cancer maybe highly symptomatic. This study aimed to quantify changes in physical function and health-related quality of life (HRQoL) in patients with advanced NSCLC. Methods: A prospective cohort study was performed. Patients with stage III and IV NSCLC were recruited within one month of starting treatment and assessed at baseline, 2, 4 and 6 months or until they became too unwell. HRQoL and functional status were measured using the EORTC QLQ-C30, the 6-minute walk test (6MWT) and timed up and go test (TUG). Comparisons between baseline and follow-up assessments were carried out by fitting linear mixed models to each outcome separately. Results: 39 patients (21 male) were included in the analysis; median age of 63 (range 40-80). 59% were receiving treatment with curative intent. 28% had stage 4 disease with 26% deceased by 4 months. Response rates at 2 and 4 months were 71.8% and 53.8% for 6MWT and TUG and 87.2% and 64.1% for EORTC. The mean 6MWT at baseline was significantly lower than predicted for the age, sex and height of the cohort (417.9 versus 550.4 metres, p&lt;0.0005). Significant decline in mean 6MWT distance was seen at 2 (decrease of 42.4m, 95%CI -59.0, -25.7, p&lt;0.0005) and 4 month follow-ups (decrease of 63.6m, 95%CI -85.6, -41.5, p&lt;0.0005) compared to baseline. Significant increases in time taken to complete the TUG were also seen at 2 (increase of 0.76 sec, 95%CI 0.54 – 0.98, p&lt;0.0005) and 4 month follow-ups (increase of 1.01 sec, 95%CI 0.76 – 1.27, p&lt;0.0005) compared with baseline. In contrast, global health status and physical functioning as assessed by the QLQ-C30 showed small but significant decreases at the 2 month follow-up compared to baseline (decrease of 8.04, p=0.01 and decrease of 7.67, p=0.024 respectively), but no significant differences between baseline and the 4 month follow-up. Conclusions: Patients with advanced NSCLC show clinically and statistically significant decrements in physical function at commencement of treatment. This continues to decline rapidly and significantly over time, despite small changes in self-reported HRQoL. The 6MWT demonstrated clinically relevant changes in physical function. Interventions to address this problem are urgently needed.
Drug Sensitivity and Allele Specificity of First-Line Osimertinib Resistance <i>EGFR</i> Mutations
Authors: Jacqueline H. Starrett, Alexis A. Guernet, Maria Emanuela Cuomo, Kamrine E. Poels, Iris K. van Alderwerelt van Rosenburgh, Amy Nagelberg, Dylan Farnsworth, Kristin S. Price, Hina Khan, Kumar Dilip Ashtekar, Mmaserame Gaefele, Deborah Ayeni, Tyler F. Stewart, Alexandra Kuhlmann, Susan M. Kaech, Arun M. Unni, Robert Homer, William W. Lockwood, Franziska Michor, Sarah B. Goldberg, Mark A. Lemmon, Paul D. Smith, Darren A.E. Cross, Katerina Politi
Journal: Cancer Research (2020)

Abstract Osimertinib, a mutant-specific third-generation EGFR tyrosine kinase inhibitor, is emerging as the preferred first-line therapy for EGFR-mutant lung cancer, yet resistance inevitably develops in patients. We modeled acquired resistance to osimertinib in transgenic mouse models of EGFRL858R-induced lung adenocarcinoma and found that it is mediated largely through secondary mutations in EGFR—either C797S or L718V/Q. Analysis of circulating free DNA data from patients revealed that L718Q/V mutations almost always occur in the context of an L858R driver mutation. Therapeutic testing in mice revealed that both erlotinib and afatinib caused regression of osimertinib-resistant C797S-containing tumors, whereas only afatinib was effective on L718Q mutant tumors. Combination first-line osimertinib plus erlotinib treatment prevented the emergence of secondary mutations in EGFR. These findings highlight how knowledge of the specific characteristics of resistance mutations is important for determining potential subsequent treatment approaches and suggest strategies to overcome or prevent osimertinib resistance in vivo. Significance: This study provides insight into the biological and molecular properties of osimertinib resistance EGFR mutations and evaluates therapeutic strategies to overcome resistance.
A NEW ELECTROCARDIOGRAPHIC SCORE (CRAST-PE) FOR MORTALITY RISK STRATIFICATION OF PATIENTS WITH ACUTE PULMONARY EMBOLISM
Authors: Baris Bugan, Elif Ijlal Cekirdekci, Erkan Yildirim, Cagatay Onar, Uygar Yuksel
Journal: Journal of the American College of Cardiology (2020)
British Association of Dermatologists guidelines for biologic therapy for psoriasis 2020: a rapid update
Authors: C.H. Smith, Z.Z.N. Yiu, T. Bale, A.D. Burden, L.C. Coates, W. Edwards, E. MacMahon, S.K. Mahil, A. McGuire, R. Murphy, C. Nelson‐Piercy, C.M. Owen, R. Parslew, O.A. Uthman, R.T. Woolf, L. Manounah, M.C. Ezejimofor, L.S. Exton, M.F. Mohd Mustapa
Journal: British Journal of Dermatology (2020)

Linked Comment:Ormerod. Br J Dermatol 2020; 183:604. Plain language summary available online
SEASONAL VARIATION OF ACUTE PERICARDITIS AND PREDICTORS OF ADVERSE OUTCOMES IN THE UNITED STATES: AN ANALYSIS OF THE NATIONAL INPATIENT SAMPLE
Authors: Adebayo Christian Atanda, Lily Dastmalchi, Olajide Buhari, Ariel Faiwiszewski, Tran Nguyen, Joseph Krepp
Journal: Journal of the American College of Cardiology (2020)
Cardio-Oncology and the Patient–Physician Relationship
Authors: Bonnie Ky, MD, MSCE, FACC
Journal: JACC CardioOncology (2020)

![Figure][1] 

“I am a survivor. Bring it on.”—From my patient, a survivor of 4 cancers, cardiac arrest, and heart failure in response to the question, “What first comes to mind when hearing cancer and heart disease?”

The resiliency and strength of my patients inspire and motivate me
BETA-BLOCKER USE IS ASSOCIATED WITH AN INCREASED EARLY RISK OF MAJOR ADVERSE CARDIOVASCULAR EVENTS AFTER ORTHOTOPIC LIVER TRANSPLANTATION
Authors: Anoop Ninan Koshy, Paul J. Gow, Benjamin Cailes, Jefferson Ko, Hui-Chen Han, Laurence Weinberg, Adam Testro, Andrew W. Teh, Omar Farouque
Journal: Journal of the American College of Cardiology (2020)
Diapedesis-Induced Integrin Signaling via LFA-1 Facilitates Tissue Immunity by Inducing Intrinsic Complement C3 Expression in Immune Cells
Authors: Martin Kolev, Erin E. West, Natalia Kunz, Daniel Chauss, E. Ashley Moseman, Jubayer Rahman, Tilo Freiwald, Maria L. Balmer, Jonas Lötscher, Sarah Dimeloe, Elizabeth C. Rosser, Lucy R. Wedderburn, Katrin D. Mayer-Barber, Andrea Bohrer, Paul Lavender, Andrew Cope, Luopin Wang, Mariana J. Kaplan, Niki M. Moutsopoulos, Dorian McGavern, Steven M. Holland, Christoph Hess, Majid Kazemian, Behdad Afzali, Claudia Kemper
Journal: Immunity (2020)
DIAGNOSTIC ROLE OF CARDIAC MAGNETIC RESONANCE IMAGING IN A PATIENT WITH MYOCARDIAL INFARCTION AND NORMAL CORONARY ARTERIES PRESENTING AS A ST-ELEVATION MYOCARDIAL INFARCTION
Authors: Elie Ghasb, Akash Patel, Balaji Natarajan, Prashant Patel, Ramdas Pai
Journal: Journal of the American College of Cardiology (2020)
A role for the general transcriptional factor II -I (TFII-I) in Src-mediated transcriptional suppression of SSeCKS/Gravin/AKAP12
Authors: Yahao Bu, Irwin Gelman
Journal: Cancer Research (2008)

168  SSeCKS (Src-suppressed Ckinase substrate), also called gravin/AKAP12, is a large scaffolding protein with metastasis suppressor activity. Two major isoforms of SSeCKS are expressed in most cell and tissue types under the control of two independent promoters, designated α and β (a third promoter, γ, is expressed only in the testes). SSeCKS transcript and protein levels are severely decreased in Src-transformed fibroblasts and in many epithelial tumors. Previously, we reported that repression of SSeCKS by v-Src is primarily controlled at the level of transcription and mediated by recruitment of HDAC1 into an USF1-Sp1-Sp3 complex binding to the SSeCKS α proximal promoter (1). We sought to identify proteins whose abundance on the SSeCKS α proximal promoter was affected by v-Src. Therefore, proteins from NIH3T3/v-Src nuclear lysates pulled down by SSeCKS α proximal promoter oligonucleotides (containing both the E- and GC-boxes) were subjected to Liquid Chromatography-Mass Spectrometry/Mass Spectrometry (LC-MS/MS) analysis, resulting in the identification of the General Transcriptional Factor II-I (TFII-I). v-Src does not alter the protein abundance and nuclear translocation of TFII-I but it enhances TFII-I binding levels at the α proximal promoter at least 5-fold, correlating with an increase in TFII-I tyrosine phosphorylation. The requirement for TFII-I for Src-mediated suppression of SSeCKS transcription in both NIH3T3/v-Src and prostate cancer cells, as determined by siRNA-mediated knockdown experiments, will be presented. These data suggest that TFII-I may complex with Sp1, Sp3, HDAC1, and USF1 to facilitate Src-mediated downregulation of SSeCKS.  1. Bu, Y. and Gelman, I. H. (2007) J. Biol. Chem.282, 26725-26739.  Supported by Department of Defense grant PC040256 and National Institutes of Health grant CA94108.
IMPORTANCE OF THE ANALYTIC APPROACH WHEN COMPARING THE EFFECTIVENESS OF TREATMENTS: AN APPLICATION TO REDUCED DOSE NOACS FOR STROKE PREVENTION IN ATRIAL FIBRILLATION
Authors: Peter Brønnum Nielsen, Mette Søgaard, Flemming Skjøth, Torben Bjerregaard Larsen, Gregory Y.H. Lip, Miguel Hernán
Journal: Journal of the American College of Cardiology (2020)
TISSUE PHASE MAPPING ANALYSIS IN PATIENTS WITH INCREASED CARDIOPULMONARY PRESSURES AFTER HEART TRANSPLANTATION
Authors: Roberto Sarnari, Ashitha Pathrose, Julie Blaisdell, Alyssa Singer, Kambiz Ghafourian, Jane Wilcox, Sadiya Khan, Esther Vorovich, Jonathan Rich, Allen S. Anderson, Clyde Yancy, Michael Markl, James C. Carr
Journal: Journal of the American College of Cardiology (2020)
METABOLIC SIGNATURE OF HUMAN RIGHT VENTRICULAR MYOCARDIUM IN END STAGE HEART FAILURE
Authors: Giovanni Davogustto, Jean Wassenaar, Fan Run, Haocan Song, Fei Ye, Megha Talati, Kelsey Tomasek, Tarek Absi, Yan Ru Su, Anna Hemnes, Evan L. Brittain
Journal: Journal of the American College of Cardiology (2020)