Evidence map›Paper›PMID 21233314›Full record

ArticleBlood2011

Normal bone marrow signal-transduction profiles: a requisite for enhanced detection of signaling dysregulations in AML.

James Marvin, Suchitra Swaminathan, Geoffrey Kraker, Amy Chadburn, James Jacobberger, Charles Goolsby

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. 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
2.1field-weighted citation impact, top 13% 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, 28 citations in OpenAlex.

  1. Trial
  2. Single-cell transcriptome profiling of mMolecular biomedicine · 2024
    Article
  3. Crizotinib Has Preclinical Efficacy in Philadelphia-Negative Myeloproliferative Neoplasms.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  4. Aberrantly low STAT3 and STAT5 responses are associated with poor outcome and an inflammatory gene expression signature in pediatric acute myeloid leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
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  17. CREB and leukemogenesis.Critical reviews in oncogenesis · 2011
    Review
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 at 2 institutions in 2 countries.

James MarvinRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, USA.
Suchitra Swaminathan
Geoffrey Kraker
Amy Chadburn
James Jacobberger
Charles Goolsby
Northwestern University · USCase Western Reserve University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular and cytogenetic alterations are involved in virtually every facet of acute myeloid leukemia (AML), including dysregulation of major signal-transduction pathways. The present study examines 5 phosphoproteins (pErk, pAkt, pS6, pStat3, and pStat5) in response to 5 cytokine/growth factors (stem cell factor [SCF], Flt-3/Flk-2 ligand [FL], granulocyte/macrophage-colony stimulating factor [GM-CSF], interleukin-3 [IL-3], and granulocyte-CSF [G-CSF]) within 7 immunophenotypically defined populations, spanning progenitor to mature myeloid/myelomonocytic cells in normal bone marrows with further comparison to AML samples. The normal cohort showed pathway-specific responses related to lineage, maturation, and stimulus. Heterogeneous-signaling responses were seen in homogeneous immunophenotypic subsets emphasizing the additive information of signaling. These profiles provided a critical baseline for detection of dysregulated signaling in AML falling into 4 broad categories, viz lack of response, increased activation, altered constitutive expression, and dysregulated response kinetics, easily identified in 10 of 12 AMLs. These studies clearly show robust and reproducible flow cytometry phosphoprotein analyses capable of detecting abnormal signal-transduction responses in AML potentially contributing to definitive reliable identification of abnormal cells. As functional correlates of underlying genetic abnormalities, signal-transduction abnormalities may provide more stable indicators of abnormal cells than immunophenotyping which frequently changes after therapy and disease recurrence.

Indexed as

Bone MarrowExtracellular Signal-Regulated MAP KinasesGranulocyte-Macrophage Colony-Stimulating FactorHumansImmunophenotypingInterleukin-3Leukemia, Myeloid, AcuteMembrane ProteinsPhosphoproteinsProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 90-kDaSignal TransductionSTAT3 Transcription FactorSTAT5 Transcription FactorStem Cell FactorExtracellular Signal-Regulated MAP Kinasesflt3 ligand proteinGranulocyte-Macrophage Colony-Stimulating FactorIL3 protein, humanInterleukin-3Membrane ProteinsPhosphoproteinsProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 90-kDaRPS6KA1 protein, humanSTAT3 protein, humanSTAT3 Transcription FactorSTAT5 Transcription FactorStem Cell Factor

Identifiers

PMID21233314
PMCPMC3087538
OpenAlexW2059667755

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.