Evidence map›Paper›PMID 33888841›Full record

ArticleScientific reports2021

Expression of CCL2/CCR2 signaling proteins in breast carcinoma cells is associated with invasive progression.

Wei Bin Fang, Diana Sofia Acevedo, Curtis Smart, Brandon Zinda, Nadia Alissa, Kyle Warren, Garth Fraga, Li-Ching Huang, Yu Shyr, Wei Li and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-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

18 citing papers in PubMed, 30 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

15 authors at 4 institutions in 2 countries.

Wei Bin Fang *Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Diana Sofia Acevedo *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 Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Kyle WarrenDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Garth FragaDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Li-Ching HuangVanderbilt University Medical Center, Center for Quantitative Sciences, Nashville, TN, 37232, USA.
Yu ShyrVanderbilt University Medical Center, Center for Quantitative Sciences, Nashville, TN, 37232, USA.
Wei LiShanghai Center for Bioinformation Technology, Shanghai Academy of Science and Technology, Shanghai, 201203, People's Republic of China.
Lu XieShanghai Center for Bioinformation Technology, Shanghai Academy of Science and Technology, Shanghai, 201203, People's Republic of China.
Vincent StaggsHealth Services and Outcomes Research, Children's Mercy Hospital and Clinics, University of Missouri Kansas City School of Medicine, Kansas City, KS, 64108, USA.
Yan HongDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Fariba BehbodDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, 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 · USShanghai Academy of Science & Technology · CNVanderbilt University Medical Center · USChildren's Mercy Hospital · US

Funding

Using Integrated Omics to Identify Dysfunctional Genetic Mechanisms Influencing Schizophrenia and Sleep DisturbancesP20GM130423 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Kalyani Pyaram, Steven Allan Soper · 2019 to 2026
$21.5M
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 CA207445NIGMS NIH HHS P20 GM130423
6 · The paper itself

Abstract

Ductal carcinoma in situ (DCIS) is the most common type of pre-invasive breast cancer diagnosed in women. Because the majority of DCIS cases are unlikely to progress to invasive breast cancer, many women are over-treated for DCIS. By understanding the molecular basis of early stage breast cancer progression, we may identify better prognostic factors and design treatments tailored specifically to the predicted outcome of DCIS. Chemokines are small soluble molecules with complex roles in inflammation and cancer progression. Previously, we demonstrated that CCL2/CCR2 chemokine signaling in breast cancer cell lines regulated growth and invasion through p42/44MAPK and SMAD3 dependent mechanisms. Here, we sought to determine the clinical and functional relevance of CCL2/CCR2 signaling proteins to DCIS progression. Through immunostaining analysis of DCIS and IDC tissues, we show that expression of CCL2, CCR2, phospho-SMAD3 and phospho-p42/44MAPK correlate with IDC. Using PDX models and an immortalized hDCIS.01 breast epithelial cell line, we show that breast epithelial cells with high CCR2 and high CCL2 levels form invasive breast lesions that express phospho-SMAD3 and phospho-p42/44MAPK. These studies demonstrate that increased CCL2/CCR2 signaling in breast tissues is associated with DCIS progression, and could be a signature to predict the likelihood of DCIS progression to IDC.

Indexed as

Neoplasm InvasivenessSignal TransductionAnimalsBreast NeoplasmsCarcinoma, Ductal, BreastChemokine CCL2Disease ProgressionFemaleHeterograftsHumansMiceMiddle AgedReceptors, CCR2CCL2 protein, humanCCR2 protein, humanChemokine CCL2Receptors, CCR2

Identifiers

PMID33888841
PMCPMC8062684
OpenAlexW3153222633

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.