Evidence map›Paper›PMID 28086219›Full record

ArticleOncotarget2017

Gadd45a deficiency accelerates BCR-ABL driven chronic myelogenous leukemia.

Kaushiki Mukherjee, Xiaojin Sha, Andrew Magimaidas, Silvia Maifrede, Tomasz Skorski, Ravi Bhatia, Barbara Hoffman, Dan A Liebermann

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Gadd45 in Normal Hematopoiesis and Leukemia.Advances in experimental medicine and biology · 2022
    Article
  5. Roles for GADD45 in Development and Cancer.Advances in experimental medicine and biology · 2022
    Review
  6. GADD45 in Stress Signaling, Cell Cycle Control, and Apoptosis.Advances in experimental medicine and biology · 2022
    Article
  7. Gadd45 Proteins in Immunity 2.0.Advances in experimental medicine and biology · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

8 authors at 3 institutions in 1 country.

Kaushiki MukherjeeFels Institute for Cancer Research and Molecular Biology, Philadelphia, PA, USA.
Xiaojin ShaFels Institute for Cancer Research and Molecular Biology, Philadelphia, PA, USA.
Andrew MagimaidasFels Institute for Cancer Research and Molecular Biology, Philadelphia, PA, USA.
Silvia MaifredeFels Institute for Cancer Research and Molecular Biology, Philadelphia, PA, USA.
Tomasz SkorskiFels Institute for Cancer Research and Molecular Biology, Philadelphia, PA, USA.
Ravi BhatiaDivision of Hematology and Oncology, University of Alabama, Tuscaloosa, AL, USA.
Barbara HoffmanFels Institute for Cancer Research and Molecular Biology, Philadelphia, PA, USA.
Dan A LiebermannFels Institute for Cancer Research and Molecular Biology, Philadelphia, PA, USA.
Temple University · USTranslational Therapeutics (United States) · USUniversity of Alabama · US

Funding

Resistance of CML stem cells to STI571 (Gleevec)R01CA095684 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BHATIA, RAVI · 2003 to 2017
$4.6M
Gadd45 stress sensors in leukemiaR01CA162403 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI LIEBERMANN, DAN A · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA095684NCI NIH HHS R01 CA162403
6 · The paper itself

Abstract

The Gadd45a stress sensor gene is a member in the Gadd45 family of genes that includes Gadd45b & Gadd45g. To investigate the effect of GADD45A in the development of CML, syngeneic wild type lethally irradiated mice were reconstituted with either wild type or Gadd45a null myeloid progenitors transduced with a retroviral vector expressing the 210-kD BCR-ABL fusion oncoprotein. Loss of Gadd45a was observed to accelerate BCR-ABL driven CML resulting in the development of a more aggressive disease, a significantly shortened median mice survival time, and increased BCR-ABL expressing leukemic stem/progenitor cells (GFP+Lin- cKit+Sca+). GADD45A deficient progenitors expressing BCR-ABL exhibited increased proliferation and decreased apoptosis relative to WT counterparts, which was associated with enhanced PI3K-AKT-mTOR-4E-BP1 signaling, upregulation of p30C/EBPα expression, and hyper-activation of p38 and Stat5. Furthermore, Gadd45a expression in samples obtained from CML patients was upregulated in more indolent chronic phase CML samples and down regulated in aggressive accelerated phase CML and blast crisis CML. These results provide novel evidence that Gadd45a functions as a suppressor of BCR/ABL driven leukemia and may provide a unique prognostic marker of CML progression.

Indexed as

Gene Expression Regulation, LeukemicAnimalsApoptosisBlast CrisisBone Marrow TransplantationCell Cycle ProteinsCell ProliferationCells, CulturedFlow CytometryFusion Proteins, bcr-ablGADD45 ProteinsHumansImmunoblottingK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMice, 129 StrainCell Cycle ProteinsFusion Proteins, bcr-ablGADD45A protein, humanGadd45a protein, mouseGADD45 ProteinsNuclear ProteinsPhosphatidylinositol 3-Kinaseschronic myelogenous leukemiaGadd45astress response proteintumor suppressor

Identifiers

PMID28086219
PMCPMC5355225
OpenAlexW2572819105

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.