Evidence map›Paper›PMID 23266888›Full record

ArticleCell research2013

A novel role of hematopoietic CCL5 in promoting triple-negative mammary tumor progression by regulating generation of myeloid-derived suppressor cells.

Yan Zhang, Dandan Lv, Ha-Jeong Kim, Robert A Kurt, Wen Bu, Yi Li, Xiaojing Ma

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
3.1field-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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Article
  8. Population Analysis and Immunologic Landscape of Melanoma in People Living with HIV.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
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  18. CD24Global medical genetics · 2022
    Article
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  20. Article

25 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Yan ZhangDepartment of Microbiology and Immunology, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, USA.
Dandan Lv
Ha-Jeong Kim
Robert A Kurt
Wen Bu
Yi Li
Xiaojing Ma
Cornell University · USBaylor College of Medicine · USLafayette College · USShanghai Jiao Tong University · CN

Funding

Oncogene susceptibility: physiological state & breast cell differentiationR01CA124820 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LI, YI · 2010 to 2014
$1.5M
NCI NIH HHS CA124820NCI NIH HHS R01 CA124820
6 · The paper itself

Abstract

CCL5 is a member of the CC chemokine family expressed in a wide array of immune and non-immune cells in response to stress signals. CCL5 expression correlates with advanced human breast cancer. However, its functional significance and mode of action have not been established. Here, we show that CCL5-deficient mice are resistant to highly aggressive, triple-negative mammary tumor growth. Hematopoietic CCL5 is dominant in this phenotype. The absence of hematopoietic CCL5 causes aberrant generation of CD11b(+)/Gr-1(+), myeloid-derived suppressor cells (MDSCs) in the bone marrow in response to tumor growth by accumulating Ly6C(hi) and Ly6G(+) MDSCs with impaired capacity to suppress cytotoxicity of CD8(+) T cells. These properties of CCL5 are observed in both orthotopic and spontaneous mammary tumors. Antibody-mediated systemic blockade of CCL5 inhibits tumor progression and enhances the efficacy of therapeutic vaccination against non-immunogenic tumors. CCL5 also helps maintain the immunosuppressive capacity of human MDSCs. Our study uncovers a novel, chemokine-independent activity of the hematopoietically derived CCL5 that promotes mammary tumor progression via generating MDSCs in the bone marrow in cooperation with tumor-derived colony-stimulating factors. The study sheds considerable light on the interplay between the hematopoietic compartment and tumor niche. Because of the apparent dispensable nature of this molecule in normal physiology, CCL5 may represent an excellent therapeutic target in immunotherapy for breast cancer as well as a broad range of solid tumors that have significant amounts of MDSC infiltration.

Indexed as

AnimalsAntibodies, NeutralizingBone Marrow TransplantationCD11b AntigenCD8-Positive T-LymphocytesCells, CulturedChemokine CCL5Disease ProgressionHumansMaleMammary Neoplasms, AnimalMiceMice, Inbred BALB CMice, KnockoutMyeloid CellsT-Lymphocytes, CytotoxicAntibodies, NeutralizingCD11b AntigenChemokine CCL5

Identifiers

PMID23266888
PMCPMC3587709
OpenAlexW2040048742

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.