Evidence map›Paper›PMID 20457873›Full record

ArticleBlood2010

Myeloid-specific inactivation of p15Ink4b results in monocytosis and predisposition to myeloid leukemia.

Juraj Bies, Marek Sramko, Joanna Fares, Michael Rosu-Myles, Steven Zhang, Richard Koller, Linda Wolff

Abstract read
In one paragraph

Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 38 citations in OpenAlex.

  1. CRISPR/dCas9 DNA methylation editing is heritable during human hematopoiesis and shapes immune progeny.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  2. Article
  3. Structural basis for cooperative regulation of KIX-mediated transcription pathways by the HTLV-1 HBZ activation domain.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  4. Article
  5. A combination of STI571 and BCR-ABL1 siRNA with overexpressed p15INK4B induced enhanced proliferation inhibition and apoptosis in chronic myeloid leukemia.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
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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

7 authors at 3 institutions in 3 countries.

Juraj BiesLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. biesj@mail.nih.gov
Marek Sramko
Joanna Fares
Michael Rosu-Myles
Steven Zhang
Richard Koller
Linda Wolff
National Cancer Institute · USCenter for Cancer Research · USNational Institutes of Health · US

Funding

Animal models to study the role of INK4b loss in human acute myeloid leukemiaZIABC011027 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WOLFF, LINDA · 2009 to 2013
$3.5M
Intramural NIH HHS
6 · The paper itself

Abstract

Inactivation of p15INK4b, an inhibitor of cyclin-dependent kinases, through DNA methylation is one of the most common epigenetic abnormalities in myeloid leukemia. Although this suggests a key role for this protein in myeloid disease suppression, experimental evidence to support this has not been reported. To address whether this event is critical for premalignant myeloid disorders and leukemia development, mice were generated that have loss of p15Ink4b specifically in myeloid cells. The p15Ink4b(fl/fl)-LysMcre mice develop nonreactive monocytosis in the peripheral blood accompanied by increased numbers of myeloid and monocytic cells in the bone marrow resembling the myeloproliferative form of chronic myelomonocytic leukemia. Spontaneous progression from chronic disease to acute leukemia was not observed. Nevertheless, MOL4070LTR retrovirus integrations provided cooperative genetic mutations resulting in a high frequency of myeloid leukemia in knockout mice. Two common retrovirus insertion sites near c-myb and Sox4 genes were identified, and their transcript up-regulated in leukemia, suggesting a collaborative role of their protein products with p15Ink4b-deficiency in promoting malignant disease. This new animal model demonstrates experimentally that p15Ink4b is a tumor suppressor for myeloid leukemia, and its loss may play an active role in the establishment of preleukemic conditions.

Indexed as

AnimalsCell Line, TumorCyclin-Dependent Kinase Inhibitor p15Disease Models, AnimalGenes, mybGenes, Tumor SuppressorGenetic Predisposition to DiseaseLeukemia, MyeloidMiceMice, KnockoutMonocyte-Macrophage Precursor CellsMonocytesPrecancerous ConditionsRetroviridaeSOXC Transcription FactorsSpleenCdkn2b protein, mouseCyclin-Dependent Kinase Inhibitor p15Sox4 protein, mouseSOXC Transcription Factors

Identifiers

PMID20457873
PMCPMC2924230
OpenAlexW2097160518

What OpenQuestion holds

Textmetadata
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.