Evidence map›Paper›PMID 28416485›Full record

ArticleCancer research2017

Targeting Autocrine CCL5-CCR5 Axis Reprograms Immunosuppressive Myeloid Cells and Reinvigorates Antitumor Immunity.

Yi Ban, Junhua Mai, Xin Li, Marisa Mitchell-Flack, Tuo Zhang, Lixing Zhang, Lotfi Chouchane, Mauro Ferrari, Haifa Shen, Xiaojing Ma

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

97 citing papers in PubMed, 172 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. CCR1Journal of advanced research · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Targeting Myeloid Cells for Cancer Immunotherapy.Cancer immunology research · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review

37 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

10 authors at 4 institutions in 3 countries.

Yi BanDepartment of Microbiology and Immunology, Weill Cornell Medicine, New York, New York.
Junhua MaiDepartment of NanoMedicine, Houston Methodist Research Institute, Houston, Texas.
Xin LiHunan Clinical Meditech Research Center for Breast Cancer, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Marisa Mitchell-FlackDepartment of Microbiology and Immunology, Weill Cornell Medicine, New York, New York.
Tuo ZhangDepartment of Microbiology and Immunology, Weill Cornell Medicine, New York, New York.
Lixing ZhangDepartment of Cell and Developmental Biology, Weill Cornell Medicine, New York, New York.
Lotfi ChouchaneLaboratory of Genetic Medicine and Immunology, Weill Cornell Medical College in Qatar, Doha, Qatar.
Mauro FerrariDepartment of NanoMedicine, Houston Methodist Research Institute, Houston, Texas.
Haifa ShenDepartment of NanoMedicine, Houston Methodist Research Institute, Houston, Texas.
Xiaojing MaDepartment of Microbiology and Immunology, Weill Cornell Medicine, New York, New York. xim2002@med.cornell.edu.
Cornell University · USHouston Methodist · USCentral South University · CNWeill Cornell Medical College in Qatar · QA

Funding

Transport Oncophysics CoreU54CA210181 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI WANG, RONGFU · 2016 to 2020
$9.3M
IMMUNOLOGY RESEARCH TRAINING PROGRAMT32AI007621 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI CESARMAN, ETHEL · 1999 to 2014
$3.4M
Tumor vasculature-targeted nanotherapeutics for DNA damage responseR01CA193880 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI SHEN, HAIFA · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA193880NCI NIH HHS U54 CA210181NIAID NIH HHS T32 AI007621
6 · The paper itself

Abstract

The tumor-promoting potential of CCL5 has been proposed but remains poorly understood. We demonstrate here that an autocrine CCL5-CCR5 axis is a major regulator of immunosuppressive myeloid cells (IMC) of both monocytic and granulocytic lineages. The absence of the autocrine CCL5 abrogated the generation of granulocytic myeloid-derived suppressor cells and tumor-associated macrophages. In parallel, enhanced maturation of intratumoral neutrophils and macrophages occurred in spite of tumor-derived CCL5. The refractory nature of

Indexed as

AnimalsAutocrine CommunicationBreast NeoplasmsCell Line, TumorChemokine CCL5Disease Models, AnimalFemaleHumansImmunosuppressive AgentsMiceMice, Inbred BALB CMice, Inbred C57BLMyeloid CellsCCL5 protein, humanChemokine CCL5Immunosuppressive Agents

Identifiers

PMID28416485
PMCPMC5484057
OpenAlexW2606222190

What OpenQuestion holds

Textmetadata
LicenceTDM
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.