Endocrine Abstracts Vol 65
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Hypoxia and Oxygen-Sensing Signaling in Gene Regulation and Cancer Progression
International Journal of Molecular Sciences Review Hypoxia and Oxygen-Sensing Signaling in Gene Regulation and Cancer Progression Guang Yang, Rachel Shi and Qing Zhang * Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; [email protected] (G.Y.); [email protected] (R.S.) * Correspondence: [email protected]; Tel.: +1-214-645-4671 Received: 6 October 2020; Accepted: 29 October 2020; Published: 31 October 2020 Abstract: Oxygen homeostasis regulation is the most fundamental cellular process for adjusting physiological oxygen variations, and its irregularity leads to various human diseases, including cancer. Hypoxia is closely associated with cancer development, and hypoxia/oxygen-sensing signaling plays critical roles in the modulation of cancer progression. The key molecules of the hypoxia/oxygen-sensing signaling include the transcriptional regulator hypoxia-inducible factor (HIF) which widely controls oxygen responsive genes, the central members of the 2-oxoglutarate (2-OG)-dependent dioxygenases, such as prolyl hydroxylase (PHD or EglN), and an E3 ubiquitin ligase component for HIF degeneration called von Hippel–Lindau (encoding protein pVHL). In this review, we summarize the current knowledge about the canonical hypoxia signaling, HIF transcription factors, and pVHL. In addition, the role of 2-OG-dependent enzymes, such as DNA/RNA-modifying enzymes, JmjC domain-containing enzymes, and prolyl hydroxylases, in gene regulation of cancer progression, is specifically reviewed. We also discuss the therapeutic advancement of targeting hypoxia and oxygen sensing pathways in cancer. Keywords: hypoxia; PHDs; TETs; JmjCs; HIFs 1. Introduction Molecular oxygen serves as a co-factor in many biochemical processes and is fundamental for aerobic organisms to maintain intracellular ATP levels [1,2]. -
A Case of Mistaken Identity…
Gastroenterology & Hepatology: Open Access Case Report Open Access A case of mistaken identity… Abstract Volume 5 Issue 8 - 2016 Paragangliomas are rare tumors of the autonomic nervous system, which may origin from Marina Morais,1,2 Marinho de Almeida,1,2 virtually any part of the body containing embryonic neural crest tissue. Catarina Eloy,2,3 Renato Bessa Melo,1,2 Luís A 60year-old old female, with a history of resistant hypertension and constitutional Graça,1 J Costa Maia1 symptoms, was hospitalized for acute renal failure. In the investigation, a CT scan revealed 1General Surgery Department, Portugal a 63x54mm hepatic nodule in the caudate lobe. Intraoperatively, the tumor was closely 2University of Porto Medical School, Portugal attached to segment 1, but not depending directly on the hepatic parenchyma or any other 3Instituto de Patologia e Imunologia Molecular da Universidade adjacent structure, and it was resected. Histology reported a paraganglioma. Postoperative do Porto (IPATIMUP), Portugal period was uneventful. Correspondence: J Costa Maia, Sao Joao Medical Center, A potentially functional PG was mistaken for an incidentaloma, due to its location, General Surgery Department, Portugal, interrelated illnesses and unspecific symptoms. PG may mimic primary liver tumors and Email therefore should be a differential diagnosis for tumors in this location. Received: August 29, 2016 | Published: December 30, 2016 Background and hydrochlorothiazide), was admitted to the Internal Medicine Department due to gastroenteritis and dehydration-associated acute Paragangliomas (PG) are rare tumors of the autonomic nervous renal failure (ARF). She reported weight loss (more than 15%), system. Their origin takes part in the neural crest cells, which produce anorexia, asthenia, polydipsia, polyuria and frequent episodes of 1 neuropeptides and catecholamines. -
Neuroscience Product Handbook
www.MedChemExpress.com MedChemExpressMedChemExpress Neuroscience Product Handbook Pain Biological Rhythms and Sleep Neuromuscular Diseases AutonomicNeuroendocrine Somatosensation metabolism Regulation Processes transduction Behavioral Neuroethology Neuroendocrin feature soding Food Intake oral and speech From the itineraries of and Energy Balance vocal/social 8,329 attendees Touch Thirst and communication Water Balance social behavior Development peptides at the 2018 SfN meeting Ion Channels and Evolution Stress and social cognition opiates the Brain monoamines Spinal Cord Adolescent Development PTSD Injury and Plasticity Postnatal autism Developmental fear Neurogenesis Disorders human social Mood cognition ADHD, Disorders Human dystexia Anxiety Cognition and Neurogenesis depression Appetitive Behavior and Gllogenesis bipolar and Aversive timing Development of Motor, Schizophrenia Learning perception Sensory,and Limbic Systems perceptual learning Other Psychiatric executive attention Stem Cells... mitochondria Emotionfunction human Parkinson's Glial Mechanisms biomarkers reinforcement long-term Disease Synaptogenesis human human memory Huntington's Transplant and ... Development Neurotransm., Motivation decisions working and Regen Axon and Transportors, memory PNS G-Protein...Signaling animal Dendrite reward decision visual Other Movement Development Receptors learning and memory model microglia making decisions Disorders Demyelinating NMDA dopamine ataxia Disorders place cells, GABA, LT P Synaptic grid cells gly... Plasticity striatum -
Interplay Between Epigenetics and Metabolism in Oncogenesis: Mechanisms and Therapeutic Approaches
OPEN Oncogene (2017) 36, 3359–3374 www.nature.com/onc REVIEW Interplay between epigenetics and metabolism in oncogenesis: mechanisms and therapeutic approaches CC Wong1, Y Qian2,3 and J Yu1 Epigenetic and metabolic alterations in cancer cells are highly intertwined. Oncogene-driven metabolic rewiring modifies the epigenetic landscape via modulating the activities of DNA and histone modification enzymes at the metabolite level. Conversely, epigenetic mechanisms regulate the expression of metabolic genes, thereby altering the metabolome. Epigenetic-metabolomic interplay has a critical role in tumourigenesis by coordinately sustaining cell proliferation, metastasis and pluripotency. Understanding the link between epigenetics and metabolism could unravel novel molecular targets, whose intervention may lead to improvements in cancer treatment. In this review, we summarized the recent discoveries linking epigenetics and metabolism and their underlying roles in tumorigenesis; and highlighted the promising molecular targets, with an update on the development of small molecule or biologic inhibitors against these abnormalities in cancer. Oncogene (2017) 36, 3359–3374; doi:10.1038/onc.2016.485; published online 16 January 2017 INTRODUCTION metabolic genes have also been identified as driver genes It has been appreciated since the early days of cancer research mutated in some cancers, such as isocitrate dehydrogenase 1 16 17 that the metabolic profiles of tumor cells differ significantly from and 2 (IDH1/2) in gliomas and acute myeloid leukemia (AML), 18 normal cells. Cancer cells have high metabolic demands and they succinate dehydrogenase (SDH) in paragangliomas and fuma- utilize nutrients with an altered metabolic program to support rate hydratase (FH) in hereditary leiomyomatosis and renal cell 19 their high proliferative rates and adapt to the hostile tumor cancer (HLRCC). -
Mutant IDH, (R)-2-Hydroxyglutarate, and Cancer
Downloaded from genesdev.cshlp.org on October 1, 2021 - Published by Cold Spring Harbor Laboratory Press REVIEW What a difference a hydroxyl makes: mutant IDH, (R)-2-hydroxyglutarate, and cancer Julie-Aurore Losman1 and William G. Kaelin Jr.1,2,3 1Department of Medical Oncology, Dana-Farber Cancer Institute, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA; 2Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA Mutations in metabolic enzymes, including isocitrate whether altered cellular metabolism is a cause of cancer dehydrogenase 1 (IDH1) and IDH2, in cancer strongly or merely an adaptive response of cancer cells in the face implicate altered metabolism in tumorigenesis. IDH1 of accelerated cell proliferation is still a topic of some and IDH2 catalyze the interconversion of isocitrate and debate. 2-oxoglutarate (2OG). 2OG is a TCA cycle intermediate The recent identification of cancer-associated muta- and an essential cofactor for many enzymes, including tions in three metabolic enzymes suggests that altered JmjC domain-containing histone demethylases, TET cellular metabolism can indeed be a cause of some 5-methylcytosine hydroxylases, and EglN prolyl-4-hydrox- cancers (Pollard et al. 2003; King et al. 2006; Raimundo ylases. Cancer-associated IDH mutations alter the enzymes et al. 2011). Two of these enzymes, fumarate hydratase such that they reduce 2OG to the structurally similar (FH) and succinate dehydrogenase (SDH), are bone fide metabolite (R)-2-hydroxyglutarate [(R)-2HG]. Here we tumor suppressors, and loss-of-function mutations in FH review what is known about the molecular mechanisms and SDH have been identified in various cancers, in- of transformation by mutant IDH and discuss their im- cluding renal cell carcinomas and paragangliomas. -
2016 IES Annual Meeting Final Programme
ROYAL ACADEMY OF MEDICINE IN IRELAND IRISH JOURNAL OF MEDICAL SCIENCE Irish Endocrine Society 40th Annual Meeting 14th and 15th October 2016 Stormont Hotel, Belfast Local Organiser: Doctor Hamish Courtney, REVISEDRoyal Victoria Hospital, PROOF Belfast Irish Journal of Medical Science Volume XXX Supplement X DOI 10.1007/s11845-016-1482-y 123 123 Journal : Large 11845 Dispatch : 17-8-2016 Pages : 57 Article No. : 1482 h LE h TYPESET MS Code : 1482 h44CP h DISK Ir J Med Sci Disclosure statement This supplement is paid for by the Irish Endocrine Society. However the meeting costs are supported by the following commercial sponsors: Abbott Amgen Astra Zeneca Besins Healthcare BMS Boehringer Ingleheim Consilient Ipsen Janssen-Cilag Kyowa Kirin Lilly Menarini Merck Serono MSD Novartis Novo Nordisk Pfizer Sanofi REVISED PROOF 123 Journal : Large 11845 Dispatch : 17-8-2016 Pages : 57 Article No. : 1482 h LE h TYPESET MS Code : 1482 h44CP h DISK Ir J Med Sci Novo Lecture Nordisk Lecture 1976 D.K. O’Donovan 1977 S. Bloom 1978 J.H.S. Robertson 1979 A.G. Cudworth 1980 D.A.D. Montgomery 1981 Peter Watkins 1982 G. Joplin 1983 D.R. London 1984 A.X. Bertagna 1985 Malcolm Nattrass Laurence Kennedy 1986 Brian Frier JB Ferriss 1987 Maurice Scanlon TJ McKenna 1988 D.A. Heath AB Atkinson 1989 J. Ward GH Tomkin 1990 R. Volpe KD Buchanan 1991 Michael Besser PPA Smyth 1992 R.V. Ragontte DH Hadden 1993 Bruce Weintraub David Powell 1994 Oscar Croffard Patrick Bell 1995 Robert Lindsay Brian Sheridan 1996 C.R.W. Edwards Rosemary Freaney 1997 Stephanie Amiel David McCance 1998 Robert Turner Randle Hayes 1999 Ian Hay Sean K Cunningham 2000 Stephen O’Rahilly Michael Cullen 2001 Andre Lacroix Daphne Owens 2002 J. -
Protein Identities in Evs Isolated from U87-MG GBM Cells As Determined by NG LC-MS/MS
Protein identities in EVs isolated from U87-MG GBM cells as determined by NG LC-MS/MS. No. Accession Description Σ Coverage Σ# Proteins Σ# Unique Peptides Σ# Peptides Σ# PSMs # AAs MW [kDa] calc. pI 1 A8MS94 Putative golgin subfamily A member 2-like protein 5 OS=Homo sapiens PE=5 SV=2 - [GG2L5_HUMAN] 100 1 1 7 88 110 12,03704523 5,681152344 2 P60660 Myosin light polypeptide 6 OS=Homo sapiens GN=MYL6 PE=1 SV=2 - [MYL6_HUMAN] 100 3 5 17 173 151 16,91913397 4,652832031 3 Q6ZYL4 General transcription factor IIH subunit 5 OS=Homo sapiens GN=GTF2H5 PE=1 SV=1 - [TF2H5_HUMAN] 98,59 1 1 4 13 71 8,048185945 4,652832031 4 P60709 Actin, cytoplasmic 1 OS=Homo sapiens GN=ACTB PE=1 SV=1 - [ACTB_HUMAN] 97,6 5 5 35 917 375 41,70973209 5,478027344 5 P13489 Ribonuclease inhibitor OS=Homo sapiens GN=RNH1 PE=1 SV=2 - [RINI_HUMAN] 96,75 1 12 37 173 461 49,94108966 4,817871094 6 P09382 Galectin-1 OS=Homo sapiens GN=LGALS1 PE=1 SV=2 - [LEG1_HUMAN] 96,3 1 7 14 283 135 14,70620005 5,503417969 7 P60174 Triosephosphate isomerase OS=Homo sapiens GN=TPI1 PE=1 SV=3 - [TPIS_HUMAN] 95,1 3 16 25 375 286 30,77169764 5,922363281 8 P04406 Glyceraldehyde-3-phosphate dehydrogenase OS=Homo sapiens GN=GAPDH PE=1 SV=3 - [G3P_HUMAN] 94,63 2 13 31 509 335 36,03039959 8,455566406 9 Q15185 Prostaglandin E synthase 3 OS=Homo sapiens GN=PTGES3 PE=1 SV=1 - [TEBP_HUMAN] 93,13 1 5 12 74 160 18,68541938 4,538574219 10 P09417 Dihydropteridine reductase OS=Homo sapiens GN=QDPR PE=1 SV=2 - [DHPR_HUMAN] 93,03 1 1 17 69 244 25,77302971 7,371582031 11 P01911 HLA class II histocompatibility antigen, -
Urology & Kidney Disease News
CLEVELAND CLINI Urology & Kidney Disease News C Glickman Urological & Kidney Institute A Physician Journal of Developments in Urology and Nephrology Vol. 21 | Winter 2012 G lickman Urological & Kidney I n stitute | Urology & Kidney Disease News | 21 l. V o 2 012 In This Issue: 17 45 58 Robotic Surgery with the Post-Transrectal Ultrasound The ABCDs of Antibiotic Dosing Adjunctive Use of Fluorescent (TRUS)- Guided Prostate Biopsy in Continuous Dialysis Imaging for Prostate Cancer Infection – Importance of Quality and Outcomes Surveillance 60 36 The Potential Role of Stem Cells Determinants of Renal Function 51 in Relief of Urinary Incontinence After Partial Nephrectomy: Molecular Insights into Implications for Surgical Technique Salt-Sensitive Hypertension 72 NextGenSM Home Sperm Banking Kit clevelandclinic.org/glickman 44 56 for Men from Geographically Remote Gene Expression Profiling of Critical Care Nephrology – Testing Sites Seeking Fertility Preservation Prostate Cancer: First Step to the Old and Finding the New Services: An Exciting Development Identifying Best Candidates for Active Surveillance 78224_CCFBCH_Cover_ACG.indd 1 12/12/11 7:37 PM Urology & Kidney Resources for Physicians Resources for Patients Physician Directory Disease News View all Cleveland Clinic staff online at Medical Concierge clevelandclinic.org/staff. For complimentary assistance for out-of-state patients and families, call 800.223.2273, ext. Referring Physician Center Chairman’s Report ....................................................................4 55580, or email [email protected]. For help with service-related issues, information about our News from the Glickman Urological & Kidney Institute clinical specialists and services, details about CME oppor- Global Patient Services tunities, and more, contact the Referring Physician Center Chair Established in Urological Oncology Research ......................5 For complimentary assistance for national at [email protected], or 216.448.0900 or 888.637.0568. -
Top 4000 Is Marco De Best Vertegenwoordigde Nederlandse Artiest in De Grootste Hitlijst Aller Tijden!
Vanaf 1 december t/m 24 december luister je van 07.00 tot 21.00 uur naar de Top 4OOO op Radio 1O! NR Artiest Titel Jaar 4000 THE O’JAYS I LOVE MUSIC 1976 3999 KANE GANG CLOSEST THING TO HEAVEN 1984 3998 WILL DOWNING A LOVE SUPREME 1988 3997 THE BEATLES DAY TRIPPER 1965 3996 THE J. GEILS BAND CENTERFOLD 1982 3995 THE JUDDS WHY NOT ME 1989 3994 ROBBIE WILLIAMS SOMETHING BEAUTIFUL 2002 3993 DAVID DUNDAS JEANS ON 1977 3992 SHANIA TWAIN I’M GONNA GETCHA GOOD 2002 3991 MICHAEL JACKSON GONE TOO SOON 1993 3990 STEVE WINWOOD WHILE YOU SEE A CHANCE 1981 3989 LOS DEL RIO MACARENA 1996 In 1993 kwam ´Macarena´ van het Spaanse zangduo Los Del Río voor het eerst uit. Het nummer brak echter pas echt door toen de Bayside Boys er in 1996 een remix van maakten en het een wereldwijde zomerhit werd. Helaas is het daar ook bij gebleven. 3988 TIME BANDITS I’M SPECIALIZED IN YOU 1983 3987 ROD STEWART I DON’T WANT TO TALK ABOUT IT 1977 3986 A-HA THE LIVING DAYLIGHTS 1987 3985 TAMMY WYNETTE STAND BY YOUR MAN 1975 3984 KOOL & THE GANG TOO HOT 1980 3983 WENDY & LISA ARE YOU MY BABY 1989 3982 QUEEN HEAVEN FOR EVERYONE 1995 3981 KIM WILDE NEVER TRUST A STRANGER 1988 3980 ENGLAND DAN & JOHN FORD-COLEY I’D REALLY LOVE TO SEE YOU TONIGHT 1976 3979 EURYTHMICS IT’S ALRIGHT 1986 3978 THE REAL THING CAN YOU FEEL THE FORCE 1979 3977 UB40 HOMELY GIRL 1989 3976 JAKI GRAHAM BREAKING AWAY 1986 3975 THE BEACH BOYS DARLIN’ 1968 3974 THE CORRS BREATHLESS 2000 3973 JULIAN LENNON TOO LATE FOR GOODBYES 1984 3972 MARVIN GAYE LET’S GET IT ON 1973 3971 I.O.S. -
Biogenic Amine Reference Materials
Biogenic Amine reference materials Epinephrine (adrenaline), Vanillylmandelic acid (VMA) and homovanillic norepinephrine (noradrenaline) and acid (HVA) are end products of catecholamine metabolism. Increased urinary excretion of VMA dopamine are a group of biogenic and HVA is a diagnostic marker for neuroblastoma, amines known as catecholamines. one of the most common solid cancers in early childhood. They are produced mainly by the chromaffin cells in the medulla of the adrenal gland. Under The biogenic amine, serotonin, is a neurotransmitter normal circumstances catecholamines cause in the central nervous system. A number of disorders general physiological changes that prepare the are associated with pathological changes in body for fight-or-flight. However, significantly serotonin concentrations. Serotonin deficiency is raised levels of catecholamines and their primary related to depression, schizophrenia and Parkinson’s metabolites ‘metanephrines’ (metanephrine, disease. Serotonin excess on the other hand is normetanephrine, and 3-methoxytyramine) are attributed to carcinoid tumours. The determination used diagnostically as markers for the presence of of serotonin or its metabolite 5-hydroxyindoleacetic a pheochromocytoma, a neuroendocrine tumor of acid (5-HIAA) is a standard diagnostic test when the adrenal medulla. carcinoid syndrome is suspected. LGC Quality - ISO Guide 34 • GMP/GLP • ISO 9001 • ISO/IEC 17025 • ISO/IEC 17043 Reference materials Product code Description Pack size Epinephrines and metabolites TRC-E588585 (±)-Epinephrine -
AACE Annual Meeting 2021 Abstracts Editorial Board
June 2021 Volume 27, Number 6S AACE Annual Meeting 2021 Abstracts Editorial board Editor-in-Chief Pauline M. Camacho, MD, FACE Suleiman Mustafa-Kutana, BSC, MB, CHB, MSC Maywood, Illinois, United States Boston, Massachusetts, United States Vin Tangpricha, MD, PhD, FACE Atlanta, Georgia, United States Andrea Coviello, MD, MSE, MMCi Karel Pacak, MD, PhD, DSc Durham, North Carolina, United States Bethesda, Maryland, United States Associate Editors Natalie E. Cusano, MD, MS Amanda Powell, MD Maria Papaleontiou, MD New York, New York, United States Boston, Massachusetts, United States Ann Arbor, Michigan, United States Tobias Else, MD Gregory Randolph, MD Melissa Putman, MD Ann Arbor, Michigan, United States Boston, Massachusetts, United States Boston, Massachusetts, United States Vahab Fatourechi, MD Daniel J. Rubin, MD, MSc Harold Rosen, MD Rochester, Minnesota, United States Philadelphia, Pennsylvania, United States Boston, Massachusetts, United States Ruth Freeman, MD Joshua D. Safer, MD Nicholas Tritos, MD, DS, FACP, FACE New York, New York, United States New York, New York, United States Boston, Massachusetts, United States Rajesh K. Garg, MD Pankaj Shah, MD Boston, Massachusetts, United States Staff Rochester, Minnesota, United States Eliza B. Geer, MD Joseph L. Shaker, MD Paul A. Markowski New York, New York, United States Milwaukee, Wisconsin, United States CEO Roma Gianchandani, MD Lance Sloan, MD, MS Elizabeth Lepkowski Ann Arbor, Michigan, United States Lufkin, Texas, United States Chief Learning Officer Martin M. Grajower, MD, FACP, FACE Takara L. Stanley, MD Lori Clawges The Bronx, New York, United States Boston, Massachusetts, United States Senior Managing Editor Allen S. Ho, MD Devin Steenkamp, MD Corrie Williams Los Angeles, California, United States Boston, Massachusetts, United States Peer Review Manager Michael F. -
Orphanet Report Series Rare Diseases Collection
Marche des Maladies Rares – Alliance Maladies Rares Orphanet Report Series Rare Diseases collection DecemberOctober 2013 2009 List of rare diseases and synonyms Listed in alphabetical order www.orpha.net 20102206 Rare diseases listed in alphabetical order ORPHA ORPHA ORPHA Disease name Disease name Disease name Number Number Number 289157 1-alpha-hydroxylase deficiency 309127 3-hydroxyacyl-CoA dehydrogenase 228384 5q14.3 microdeletion syndrome deficiency 293948 1p21.3 microdeletion syndrome 314655 5q31.3 microdeletion syndrome 939 3-hydroxyisobutyric aciduria 1606 1p36 deletion syndrome 228415 5q35 microduplication syndrome 2616 3M syndrome 250989 1q21.1 microdeletion syndrome 96125 6p subtelomeric deletion syndrome 2616 3-M syndrome 250994 1q21.1 microduplication syndrome 251046 6p22 microdeletion syndrome 293843 3MC syndrome 250999 1q41q42 microdeletion syndrome 96125 6p25 microdeletion syndrome 6 3-methylcrotonylglycinuria 250999 1q41-q42 microdeletion syndrome 99135 6-phosphogluconate dehydrogenase 67046 3-methylglutaconic aciduria type 1 deficiency 238769 1q44 microdeletion syndrome 111 3-methylglutaconic aciduria type 2 13 6-pyruvoyl-tetrahydropterin synthase 976 2,8 dihydroxyadenine urolithiasis deficiency 67047 3-methylglutaconic aciduria type 3 869 2A syndrome 75857 6q terminal deletion 67048 3-methylglutaconic aciduria type 4 79154 2-aminoadipic 2-oxoadipic aciduria 171829 6q16 deletion syndrome 66634 3-methylglutaconic aciduria type 5 19 2-hydroxyglutaric acidemia 251056 6q25 microdeletion syndrome 352328 3-methylglutaconic