Evidence map›Paper›PMID 27308309›Full record

ReviewMolecular & cellular oncology2014

Role of macrophage inflammatory protein (MIP)-1α/CCL3 in leukemogenesis.

Tomohisa Baba, Naofumi Mukaida

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular & cellular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 32% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Effect of Fibroblast Signaling on Macrophage Polarization.The American journal of pathology · 2025
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  9. Observational
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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

2 authors at 2 institutions in 2 countries.

Tomohisa BabaDivision of Molecular Bioregulation; Cancer Research Institute; Kanazawa University; Kanazawa, Ishikawa, Japan.
Naofumi MukaidaDivision of Molecular Bioregulation; Cancer Research Institute; Kanazawa University; Kanazawa, Ishikawa, Japan.
Kanazawa University · JPSt. Petersburg Institute of Bioregulation and Gerontology · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The biologic function of the CC chemokine macrophage inflammatory protein-1α (MIP-1α/CCL3) has been extensively studied since its initial identification as a macrophage-derived inflammatory mediator. In addition to its proinflammatory activities, CCL3 negatively regulates the proliferation of hematopoietic stem/progenitor cells (HSPCs). On the basis of this unique function, CCL3 is alternatively referred to as a stem cell inhibitor. This property has prompted many researchers to investigate the effects of CCL3 on normal physiologic hematopoiesis and pathophysiologic processes of hematopoietic malignancies. Consequently, there is accumulating evidence supporting a crucial involvement of CCL3 in the pathophysiology of several types of leukemia arising from neoplastic transformation of HSPCs. In this review we discuss the roles of CCL3 in leukemogenesis and its potential value as a target in a novel therapeutic strategy for the treatment of leukemia.

Indexed as

chemokineleukemialeukemia initiating cellmicroenvironmentMIP-1α/CCL3

Identifiers

PMID27308309
PMCPMC4905173
OpenAlexW2027286680

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.