Evidence map›Paper›PMID 30446625›Full record

ArticleMolecular cancer research : MCR2019

CCR2 Chemokine Receptors Enhance Growth and Cell-Cycle Progression of Breast Cancer Cells through SRC and PKC Activation.

Min Yao, Wei Fang, Curtis Smart, Qingting Hu, Shixia Huang, Nehemiah Alvarez, Patrick Fields, Nikki Cheng

Abstract read
In one paragraph

Article in Molecular cancer research : MCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–field-weighted citation impact
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

40 citing papers in PubMed.

  1. Assessment of CCR2 PET as a Biomarker for Head and Neck Squamous Cell Carcinoma.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026
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  18. Chemokine signaling in cancer-stroma communications.Journal of cell communication and signaling · 2021
    Review
  19. Anesthetic Propofol Promotes Tumor Metastasis in Lungs via GABAAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Article
  20. Review
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.

Min Yao *Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas.
Wei Fang *Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas.
Curtis SmartDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas.
Qingting HuDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas.
Shixia HuangDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.
Nehemiah AlvarezDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas.ORCID 0000-0003-4067-4387
Patrick FieldsDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas.
Nikki ChengDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas. ncheng@kumc.edu.

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
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 P30 CA125123NCI NIH HHS R01 CA172764NCI NIH HHS R01 CA207445
6 · The paper itself

Abstract

Basal-like breast cancers are an aggressive breast cancer subtype, which often lack estrogen receptor, progesterone receptor, and Her2 expression, and are resistant to antihormonal and targeted therapy, resulting in few treatment options. Understanding the underlying mechanisms that regulate progression of basal-like breast cancers would lead to new therapeutic targets and improved treatment strategies. Breast cancer progression is characterized by inflammatory responses, regulated in part by chemokines. The CCL2/CCR2 chemokine pathway is best known for regulating breast cancer progression through macrophage-dependent mechanisms. Here, we demonstrated important biological roles for CCL2/CCR2 signaling in breast cancer cells. Using the MCF10CA1d xenograft model of basal-like breast cancer, primary tumor growth was significantly increased with cotransplantation of patient-derived fibroblasts expressing high levels of CCL2, and was inhibited with CRISP/R gene ablation of stromal

Indexed as

AnimalsBreast NeoplasmsCell CycleCell Growth ProcessesCell Line, TumorChemokine CCL2Disease ProgressionEnzyme ActivationFemaleHeterograftsHumansMiceMice, NudeProtein Kinase CReceptors, CCR2Signal TransductionCCL2 protein, humanCCR2 protein, humanChemokine CCL2Protein Kinase CReceptors, CCR2src-Family Kinases

Identifiers

PMID30446625
PMCPMC6359961

What OpenQuestion holds

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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.