Evidence map›Paper›PMID 31827233›Full record

ArticleOncogene2020

CCR2 signaling in breast carcinoma cells promotes tumor growth and invasion by promoting CCL2 and suppressing CD154 effects on the angiogenic and immune microenvironments.

Gage Brummer, Wei Fang, Curtis Smart, Brandon Zinda, Nadia Alissa, Cory Berkland, David Miller, Nikki Cheng

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 44 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

8 authors at 4 institutions in 1 country.

Gage Brummer *Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Wei Fang *Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Curtis SmartDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Brandon ZindaDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Nadia AlissaDepartment of Cancer Biology, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Cory BerklandDepartment of Pharmaceutical Chemistry, University of Kansas, Lawrence, KS, 66045, USA.
David MillerDepartment of Engineering Technology, Pittsburg State University, Pittsburg, KS, 66762, USA.
Nikki ChengDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA. ncheng@kumc.edu.
University of Kansas Medical Center · USPittsburg State University · USThe University of Kansas Cancer Center · USUniversity of Kansas · US

Funding

Progression of DCIS to Invasive Breast Cancer through CCR2 Chemokine SignalingR01CA172764 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI CHENG, NIKKI · 2013 to 2024
$4.2M
Identifying the Molecular and Cellular Basis of Invasive Phenotype in Human DCISR01CA207445 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BEHBOD, FARIBA · 2017 to 2019
$1.7M
NCI NIH HHS R01 CA172764NCI NIH HHS R01 CA207445
6 · The paper itself

Abstract

Breast cancer is the second leading cause of cancer-related deaths for women, due mainly to metastatic disease. Invasive tumors exhibit aberrations in recruitment and activity of immune cells, including decreased cytotoxic T cells. Restoring the levels and activity of cytotoxic T cells is a promising anticancer strategy; but its success is tumor type dependent. The mechanisms that coordinate recruitment and activity of immune cells and other stromal cells in breast cancer remain poorly understood. Using the MMTV-PyVmT/FVB mammary tumor model, we demonstrate a novel role for CCL2/CCR2 chemokine signaling in tumor progression by altering the microenvironment. Selective targeting of CCR2 in the PyVmT mammary epithelium inhibited tumor growth and invasion, elevated CD8+ T cells, decreased M2 macrophages and decreased angiogenesis. Co-culture models demonstrated these stromal cell responses were mediated by tumor-derived CCL2 and CCR2-mediated suppression of the T-cell activating cytokine, CD154. Coculture analysis indicated that CCR2-induced stromal reactivity was important for tumor cell proliferation and invasion. In breast tumor tissues, CD154 expression inversely correlated with CCR2 expression and correlated with relapse free survival. Targeting the CCL2/CCR2 signaling pathway may reprogram the immune angiogenic and microenvironments and enhance effectiveness of targeted and immunotherapies.

Indexed as

AnimalsBreast NeoplasmsCD40 LigandCell Growth ProcessesCell Line, TumorChemokine CCL2FemaleHumansMammary Neoplasms, ExperimentalMiceMice, Inbred BALB CNeoplasm InvasivenessRAW 264.7 CellsReceptors, CCR2Signal TransductionTumor MicroenvironmentCD40 LigandChemokine CCL2Receptors, CCR2

Identifiers

PMID31827233
PMCPMC7071973
OpenAlexW2996596704

What Socratic 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 Socratic graph.