Evidence map›Paper›PMID 27622061›Full record

ArticleOncoimmunology2016

Stromal CCR6 drives tumor growth in a murine transplantable colon cancer through recruitment of tumor-promoting macrophages.

Bisweswar Nandi, Mia Shapiro, Mehmet K Samur, Christine Pai, Natasha Y Frank, Charles Yoon, Rao H Prabhala, Nikhil C Munshi, Jason S Gold

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.8field-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

49 citing papers in PubMed, 79 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Bisweswar NandiResearch Service, VA Boston Healthcare System, West Roxbury, MA, USA; Harvard Medical School, Boston, MA, USA.
Mia ShapiroResearch Service, VA Boston Healthcare System, West Roxbury, MA, USA; Harvard Medical School, Boston, MA, USA.
Mehmet K SamurHarvard Medical School, Boston, MA, USA; Dana-Farber Cancer Institute, Boston, MA, USA.
Christine PaiResearch Service, VA Boston Healthcare System , West Roxbury, MA, USA.
Natasha Y FrankHarvard Medical School, Boston, MA, USA; Medicine Service, VA Boston Healthcare System, West Roxbury, MA, USA; Brigham and Women's Hospital, Boston, MA, USA.
Charles YoonHarvard Medical School, Boston, MA, USA; Dana-Farber Cancer Institute, Boston, MA, USA; Brigham and Women's Hospital, Boston, MA, USA.
Rao H PrabhalaResearch Service, VA Boston Healthcare System, West Roxbury, MA, USA; Dana-Farber Cancer Institute, Boston, MA, USA.
Nikhil C MunshiHarvard Medical School, Boston, MA, USA; Dana-Farber Cancer Institute, Boston, MA, USA; Medicine Service, VA Boston Healthcare System, West Roxbury, MA, USA.
Jason S GoldHarvard Medical School, Boston, MA, USA; Brigham and Women's Hospital, Boston, MA, USA; Surgery Service, VA Boston Healthcare System, West Roxbury, MA, USA.
Harvard University · USBrigham and Women's Hospital · USVA Boston Healthcare System · USDana-Farber Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interactions between the inflammatory chemokine CCL20 and its receptor CCR6 have been implicated in promoting colon cancer; however, the mechanisms behind this effect are poorly understood. We have previously demonstrated that deficiency of CCR6 is associated with decreased tumor macrophage accumulation in a model of sporadic intestinal tumorigenesis. In this study, we aimed to determine the role of stromal CCR6 expression in a murine syngeneic transplantable colon cancer model. We show that deficiency of host CCR6 is associated with decreased growth of syngeneic CCR6-expressing colon cancers. Colon cancers adoptively transplanted into CCR6-deficient mice have decreased tumor-associated macrophages without alterations in the number of monocytes in blood or bone marrow. CCL20, the unique ligand for CCR6, promotes migration of monocytes in vitro and promotes accumulation of macrophages in vivo. Depletion of tumor-associated macrophages decreases the growth of tumors in the transplantable tumor model. Macrophages infiltrating the colon cancers in this model secrete the inflammatory mediators CCL2, IL-1α, IL-6 and TNFα. Ccl2, Il1α and Il6 are consequently downregulated in tumors from CCR6-deficient mice. CCL2, IL-1α and IL-6 also promote proliferation of colon cancer cells, linking the decreased macrophage migration into tumors mediated by CCL20-CCR6 interactions to the delay in tumor growth in CCR6-deficient hosts. The relevance of these findings in human colon cancer is demonstrated through correlation of CCR6 expression with that of the macrophage marker CD163 as well as that of CCL2, IL1α and TNFα. Our findings support the exploration of targeting the CCL20-CCR6 pathway for the treatment of colon cancer.

Indexed as

CCR6chemokine CCL20colorectal cancermacrophagesmicereceptors

Identifiers

PMID27622061
PMCPMC5007974
OpenAlexW2406015015

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.