Evidence map›Paper›PMID 24478815›Full record

ArticleInternational journal of molecular medical science2013

KU HAPLOINSUFFIENCY CAUSES A LYMPHOPROLIFERATIVE DISORDER OF IMMATURE T-CELL PRECURSORS DUE TO IKAROS MALFUNCTION.

Zahide Ozer, Sanjive Qazi, Rita Ishkhanian, Paul Hasty, Hong Ma, Fatih M Uckun

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular medical science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Zahide OzerSystems Immunobiology Laboratory and Developmental Therapeutics Program, Children's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, CA 90027 ; Molecular Oncology Program, Parker Hughes Institute, St. Paul, MN 55113.
Sanjive QaziSystems Immunobiology Laboratory and Developmental Therapeutics Program, Children's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, CA 90027 ; Department of Biology and Bioinformatics Program, Gustavus Adolphus College, 800 W College Avenue, St. Peter, MN 56082.
Rita IshkhanianSystems Immunobiology Laboratory and Developmental Therapeutics Program, Children's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, CA 90027.
Paul HastyDepartment of Molecular Medicine and Institute of Biotechnology, The University of Texas Health Science Center, San Antonio, Texas 78425.
Hong MaSystems Immunobiology Laboratory and Developmental Therapeutics Program, Children's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, CA 90027.
Fatih M UckunSystems Immunobiology Laboratory and Developmental Therapeutics Program, Children's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, CA 90027 ; Department of Pediatrics, University of Southern California Keck School of Medicine, Los Angeles, CA 90027, USA ; Developmental Therapeutics Program, USC Norris Comprehensive Cancer Center, Los Angeles, CA 90089.

Funding

USC/NORRIS COMPREHENSIVE CANCER CENTER (CORE) SUPPORTP30CA014089 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Fumito Ito · 1985 to 2026
$181.4M
Targeting SYK Kinase in B-Lineage ALL with CD19-Specific C-61 NanoparticlesU01CA151837 · NCI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI UCKUN, FATIH M · 2010 to 2014
$2.3M
Targeting SYK Tyrosine Kinase to Overcome Radiation Resistance in ALLR01CA154471 · NCI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI UCKUN, FATIH M · 2011 to 2015
$1.6M
Amplifying Radiation Potency Against Leukemic Stem CellsR21CA164098 · NCI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI UCKUN, FATIH M · 2012 to 2013
$377k
NCI NIH HHS P30 CA014089NCI NIH HHS R01 CA154471NCI NIH HHS R21 CA164098NCI NIH HHS U01 CA151837Wellcome Trust
6 · The paper itself

Abstract

Ikaros (IK) malfunction has been implicated in the pathogenesis of acute lymphoblastic leukemia (ALL), the most common form of childhood cancer. Therefore, a stringent regulation of IK activity is very important. Here we provide unique genetic and biochemical evidence that the Ku protein components Ku70 and Ku80 act as positive regulators of IK function via formation of IK-Ku70 and IK-Ku80 heterodimers with augmented sequence-specific DNA binding activity. siRNA-mediated depletion of Ku70 or Ku80 reduced the sequence-specific DNA binding activity of IK in EMSA as well as the RT-PCR measured IK target gene expression levels in human cells. The interaction of Ku components with IK likely contributes to the anti-leukemic effects of IK as a tumor suppressor, because Ku70 as well as Ku80 haploinsuffiency in mice caused development of a lymphoproliferative disorder (LPD) involving CD2

Identifiers

PMID24478815
PMCPMC3902664

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.