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Atlas of Genetics and Cytogenetics in Oncology and Haematology Home Genes Leukemias Solid Tumours Cancer-Prone Deep Insight Portal Teaching X Y 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 NA Atlas Journal Atlas Journal versus Atlas Database: the accumulation of the issues of the Journal constitutes the body of the Database/Text-Book. TABLE OF CONTENTS Volume 5, Number 1, Jan-Mar 2001 Previous Issue / Next Issue Genes GRAF (GTPase activating protein for Rho associated with FAK) (5q31). Stig Bojesen, Arndt Borkhardt. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 1-4. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Genes/GRAFID291.html HMGIY (High mobility group protein (non histone chromosomal) isoform I and Y) (6p21.3). Gilka J.F. Gattas, Florence Pedeutour. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 5-14. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Genes/HMGIYID221.html PU.1 (11p11-22). Françoise Moreau-Gachelin. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 15-19. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Genes/SPI1ID269.html FGFR1 (Fibroblast Growth Factor Receptor 1) (8p12) - updated. Marie-Josèphe Pébusque. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 20-27. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Genes/FGFR1113.html MLL (myeloid/lymphoid or mixed lineage leukemia) (11q23) - updated. Jay L Hess, Jean-Loup Huret. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 28-38. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Genes/MLL.html PRDX1 (peroxiredoxin 1) (1p34.1) - updated. Jean-Loup Huret. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 39-44. [Full Text] [PDF] Atlas Genet Cytogenet Oncol Haematol 2001; 5 (5) I URL : http://AtlasGeneticsOncology.org/Genes/PAGID266.html PTCH1 (9q22.3) - updated. Erika Lindström, Rune Toftgård. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 45-53. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Genes/PTCH100.html TFF2 (TreFoil Factor 2) (21q22.3). Catherine Tomasetto. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 54-58. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Genes/TFF2ID264.html FGFR1OP (FGFR1 oncogene partner) (6q27). Marie-Joséphe Pébusque. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 59-63. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Genes/FOPID140.html MST1R (Macrophage stimulating 1 receptor) (3p21.31). Debora Angeloni, Michael I. Lerman. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 64-73. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Genes/RONID287.html FIM (fused in myeloproliferative disorders) (13q12) - updated. Marie-Joséphe Pébusque. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 74-79. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Genes/ZNF198ID114.html Leukaemias t(1;3)(p36;q21) - updated. Pascale Cornillet-Lefebvre, Sylvie Daliphard, Stéphanie Struski. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 80-83. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/t0103.html del(17p) in non-Hodgkin's lymphoma (NHL). Antonio Cuneo, Gianluigi Castoldi. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 84-86. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/del17pNHLID2083.html del(20q) in myeloid malignancies. Chrystèle Bilhou-Nabera. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 87-89. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/del20qID1040.html Juvenile Chronic Myelogenous Leukemia (JCML). Jay L. Hess. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 90-93. [Full Text] [PDF] Atlas Genet Cytogenet Oncol Haematol 2001; 5 (5) II URL : http://AtlasGeneticsOncology.org/Anomalies/JCMLID1099.html t(6;8)(q27;p12). Marie-Josèphe Pébusque. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 94-96. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/t68ID1090.html t(8;13)(p12;q12) - updated. Marie-Josèphe Pébusque, and Nick CP Cross. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 97-100. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/t813ID1094.html t(9;12)(q34;p13). Nyla A. Heerema. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 101-103. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/t912ID1080.html 11q23 rearrangements in leukaemia - updated. Jean-Loup Huret. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 104-114. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/11q23ID1030.html del(11q) in non-Hodgkin's lymphoma (NHL). Antonio Cuneo, Gianluigi Castoldi. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 115-117. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/del11qNHLID2020.html del(7q) in non-Hodgkin's lymphoma (NHL). Antonio Cuneo, Gianluigi Castoldi. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 118-119. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/del7qNHLID2082.html t(1;14)(p22;q32) in non Hodgkin's lymphoma (NHL). Antonio Cuneo, Gianluigi Castoldi. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 120-121. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/t114ID2044.html t(5;10)(q33;q21)E. Cristina Mecucci. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 122-123. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/t510ID1166.html +3 or trisomy 3 in non Hodgkin's lymphoma (NHL). Antonio Cuneo, Gianluigi Castoldi. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 124-126. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/tri3NHLID2008.html Atlas Genet Cytogenet Oncol Haematol 2001; 5 (5) III Y loss in leukemia. Daniel L. Van Dyke. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 127-130. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Anomalies/YlossID1089.html Solid Tumours Nervous system: Astrocytic tumors. Anne Marie Capodano. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 131-138. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Tumors/AstrocytID5007.html Cancer Prone Diseases Beckwith-Wiedemann syndrome. Marcel Mannens. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 139-144. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Kprones/BeckwithWiedemannID10037.html Hereditary breast cancer. Kaija Holli. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 146-151. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Kprones/HeredBreastCanID10062.html Variegated aneuploidy related to premature centromere division (PCD). Alberto Plaja. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 152-156. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Kprones/VariegAneuplPCDID10069.html Hereditary Pancreatic Cancer. Ralph H. Hruban, Scott E. Kern. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 157-164. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Kprones/HeredPancrCanID10068.html Li-Fraumeni Syndrome. Jenny M Varley. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (1): 165-168. [Full Text] [PDF] URL : http://AtlasGeneticsOncology.org/Kprones/LiFraumeniID10011.html Deep Insights Case Reports Educational Items © Atlas of Genetics and Cytogenetics in Oncology and Haematology Atlas Genet Cytogenet Oncol Haematol 2001; 5 (5) IV X Y 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 NA Home Genes Leukemias Solid Tumours Cancer-Prone Deep Insight Portal Teaching For comments and suggestions or contributions, please contact us [email protected]. Atlas Genet Cytogenet Oncol Haematol 2001; 5 (5) V Atlas of Genetics and Cytogenetics in Oncology and Haematology GRAF (GTPase activating protein for Rho associated with FAK) Identity Other KIAA0621 names OPHN1L Location 5q31 just centromeric of GRL DNA/RNA Description at least 24 exons Transcription two isoforms of 2277 bp (leukocytes) and 2442 bp (brain); transcripts of 4,4 and 9,5 kb Protein Description isoform A: 759 amino acids, 86 kDa; isoform B: 814 amino acids. 92 kDa Expression highly expressed in epithelial tissues i.e. pancreas islet beta-cells, testicles, prostate, mammary gland, GI glands, squamous layer of skin epithelium; highly expressed in nervous tissues including enteric ganglia; expressed in cardiomyocytes, erythropoiesis cells and liver Atlas Genet Cytogenet Oncol Haematol 2001; 1 -1- Localisation mainly cytoplasmatic Function interacts with FAK and RhoA both in vivo and in vitro; acts as GTPase activating protein (GAP) for the active GTP-bound RhoA.; negative regulator of RhoA Homology Oligophrenin-1, Beta-chimerin, BCR Mutations Germinal not known Somatic deletion of four bases (251-254, A in ATG=nt1) Insert 1158 GRAF-base 1144, 5' 1 TA GAG ACA GGA TTT CAT CAT GTT GGC CAG GTT GGT TTT GAA 42 TTC CTG ACC TCA AGT GAT CCA CCT GCC TCG GCC TCC CAA AGT 84 GGT GGG ATT TTG G 3' ......GRAF-base 1145 Insert 1299 GRAF-base 1285, 5' 1 TC ATC GTT GTC ATA TAA ATC GGC GAG GTA ATA TTC CAT CAG 42 GTA GAC ATA CG 3' ...GRAF-base 1286.Predicted STOP codon underlined. Insert 2002 GRAF-base 1988 5' 1 G GTT CAT GCG AGT TCA GCA AGC AGT TAC CAT GTC TAC GGC 41 ATG CCA GGA TAC TGT TGG GAA GGT AGT ATT CCG T 3' ...GRAF-base 1989 Implicated in Entity t(5;11)(q31;q23) / acute non lymphocytic leukemia --> MLL - GRAF Disease acute non lymphocytic leukemia and myelodysplastic syndrome with del(5q) Prognosis unknown; only a few cases unknown Cytogenetics del(5q) Hybrid/Mutated 5' MLL 3' GRAF Gene Abnormal MLL-GRAF Protein Oncogenesis basically unknown; a bi-allelic loss of GRAF has been documented in three cases of ANLL External links Nomenclature GDB ARHGAP26 Entrez_Gene ARHGAP26 23092 Rho
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  • An Extra Chromosome 9 Derived from Either a Normal

    An Extra Chromosome 9 Derived from Either a Normal

    ONCOLOGY LETTERS 18: 6725-6731, 2019 An extra chromosome 9 derived from either a normal chromosome 9 or a derivative chromosome 9 in a patient with acute myeloid leukemia positive for t(9;11)(p21.3;q23.3): A case report MAN GAO1, HUI PANG2, YOUNG MI KIM2, XIANGLAN LU2, XIANFU WANG2, JIYUN LEE2,3, MINGWEI WANG4, FANZHENG MENG1 and SHIBO LI2 1Department of Pediatrics, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China; 2Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma, OK 73104, USA; 3Department of Pathology, College of Medicine, Korea University, Seoul, South Korea; 4Clinical Medical College of Beihua University, Jilin City, Jilin 132013, P.R. China Received March 11, 2019; Accepted September 27, 2019 DOI: 10.3892/ol.2019.11035 Abstract. Translocation (9;11)(p21.3;q23.3) is one the extra chromosome 9 could serve a crucial role in AML of the most common lysine methyltransferase 2A disease progression and contribute to cellular sensitivity to (KMT2A)-rearrangements in de novo and therapy-related chemotherapy. acute myeloid leukemia (AML). Numerous in vitro and in vivo studies have demonstrated that the KMT2A/MLLT3 Introduction super elongation complex subunit (MLLT3) fusion gene on the derivative chromosome 11 serves a crucial role in leuke- Chromosomal rearrangements of the lysine methyltransferase mogenesis. Trisomy 9 as a secondary chromosome change 2A (KMT2A) gene (former MLL) at 11q23 have been reported in patients with t(9;11) is relatively rare. The present study in ~10% of patients with acute leukemias (1). Analysis of reported a unique case of AML with a chromosome 9 trisomy the KMT2A recombinome of acute leukemias has identified secondary to t(9;11)(p21.3;q23.3) through the cytogenetic 135 totally different KMT2A rearrangements, and 94 related analysis of leukemic blood and bone marrow.
  • Development and Validation of a One-Step RT-Qpcr

    Development and Validation of a One-Step RT-Qpcr

    Development and Validation of a One-Step RT-qPCR Assay for Identifying Common Fusion Gene Transcripts Associated with the Prognosis of Mexican Children with B-Lineage Acute Lymphoblastic Leukemia Juan Manuel Mejía-Aranguré ( [email protected] ) IMSS: Instituto Mexicano del Seguro Social https://orcid.org/0000-0003-0949-461X Minerva Mata-Rocha CONACYT: Consejo Nacional de Ciencia y Tecnologia Angelica Rangel-López IMSS: Instituto Mexicano del Seguro Social Juan Carlos Núñez-Enríquez IMSS: Instituto Mexicano del Seguro Social Elva Jiménez-Hernández IMSS: Instituto Mexicano del Seguro Social Blanca Angélica Morales-Castillo IMSS: Instituto Mexicano del Seguro Social Norberto Sánchez-Escobar UABJO Faculty of Medicine: Universidad Autonoma Benito Juarez de Oaxaca Facultad de Medicina Omar Alejandro Sepúlveda-Robles CONACYT: Consejo Nacional de Ciencia y Tecnologia Juan Carlos Bravata-Alcántara Hospital Juárez de México: Hospital Juarez de Mexico Alan Steve Nájera-Cortés Hospital Juárez de México: Hospital Juarez de Mexico María Luisa Pérez-Saldivar IMSS: Instituto Mexicano del Seguro Social Janet Flores-Lujano IMSS: Instituto Mexicano del Seguro Social David Aldebarán Duarte-Rodríguez IMSS: Instituto Mexicano del Seguro Social Norma Angélica Oviedo de Anda IMSS: Instituto Mexicano del Seguro Social Page 1/22 Carmen Alaez Verson INMEGEN: Instituto Nacional de Medicina Genomica Jorge Alfonso Martín-Trejo IMSS: Instituto Mexicano del Seguro Social María de Los Ángeles Del Campo-Martínez IMSS: Instituto Mexicano del Seguro Social José Esteban
  • Redefining the Specificity of Phosphoinositide-Binding by Human

    Redefining the Specificity of Phosphoinositide-Binding by Human

    bioRxiv preprint doi: https://doi.org/10.1101/2020.06.20.163253; this version posted June 21, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. Redefining the specificity of phosphoinositide-binding by human PH domain-containing proteins Nilmani Singh1†, Adriana Reyes-Ordoñez1†, Michael A. Compagnone1, Jesus F. Moreno Castillo1, Benjamin J. Leslie2, Taekjip Ha2,3,4,5, Jie Chen1* 1Department of Cell & Developmental Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801; 2Department of Biophysics and Biophysical Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205; 3Department of Biophysics, Johns Hopkins University, Baltimore, MD 21218; 4Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21205; 5Howard Hughes Medical Institute, Baltimore, MD 21205, USA †These authors contributed equally to this work. *Correspondence: [email protected]. bioRxiv preprint doi: https://doi.org/10.1101/2020.06.20.163253; this version posted June 21, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. ABSTRACT Pleckstrin homology (PH) domains are presumed to bind phosphoinositides (PIPs), but specific interaction with and regulation by PIPs for most PH domain-containing proteins are unclear. Here we employed a single-molecule pulldown assay to study interactions of lipid vesicles with full-length proteins in mammalian whole cell lysates.