Evidence map›Paper›PMID 29930294›Full record

ArticleScientific reports2018

CSF-1/CSF-1R axis is associated with epithelial/mesenchymal hybrid phenotype in epithelial-like inflammatory breast cancer.

Kazuharu Kai, Takayuki Iwamoto, Dongwei Zhang, Li Shen, Yuko Takahashi, Arvind Rao, Alastair Thompson, Subrata Sen, Naoto T Ueno

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

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  14. Frontiers in cell and developmental biology · 2022
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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 2 institutions in 2 countries.

Kazuharu KaiDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Takayuki IwamotoDepartment of Breast and Endocrine Surgery, Okayama University Hospital, Okayama, Japan.
Dongwei ZhangDepartment of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Li ShenDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Yuko TakahashiDepartment of Breast and Endocrine Surgery, Okayama University Hospital, Okayama, Japan.
Arvind RaoDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Alastair ThompsonDepartment of Breast Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Subrata SenDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA. ssen@mdanderson.org.
Naoto T UenoDepartment of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA. nueno@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USOkayama University Hospital · JP

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Markers of sensivity to the EGFR inhibitor erlotinib in breast cancerR01CA123318 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI UENO, NAOTO T. · 2007 to 2012
$1.4M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA123318
6 · The paper itself

Abstract

Inflammatory breast cancer (IBC) is a rare subtype of breast cancer, accounting for 8-10% of breast cancer-associated deaths in the US. Clinical hallmarks of IBC include tumor emboli in lymphatic vessels and E-cadherin overexpression, which supports a type of metastasis referred to as cell cluster-based metastasis, prevalent in IBC. In contrast, we previously reported epithelial-to-mesenchymal transition (EMT)-based progression of IBC, utilizing in vivo xenografts and in vitro Matrigel culture models. To address these two contradictory concepts of IBC metastasis, we used Matrigel culture to induce EMT in a panel of IBC cells. Results revealed Matrigel culture induced vimentin expression in SUM149 and SUM190 IBC cells at the transcriptional and protein levels while maintaining the expression of E-cadherin, a phenomenon referred to as partial EMT. Transcriptional profiling revealed that expression of colony-stimulating factor 1 (CSF-1) was induced in Matrigel culture. When the receptor tyrosine kinase of CSF-1 (CSF-1R) was inhibited by CSF-1R inhibitor BLZ945, the partial EMT was reversed in a dose-dependent manner, indicating that the CSF-1/CSF-1R axis plays a key role in controlling partial EMT. This observation may help reconcile the two contradictory theories of IBC metastasis, EMT vs cell cluster-based metastasis.

Indexed as

Epithelial-Mesenchymal TransitionBenzothiazolesBreast NeoplasmsCadherinsCell LineFemaleHumansMacrophage Colony-Stimulating FactorMCF-7 CellsPicolinic AcidsReceptor, Macrophage Colony-Stimulating FactorReceptors, Granulocyte-Macrophage Colony-Stimulating FactorVimentin4-(2-(2-hydroxycyclohexylamino)benzothiazol-6-yloxy)pyridine-2-carboxylic acid methylamideBenzothiazolesCadherinsCSF1 protein, humanCSF1R protein, humanMacrophage Colony-Stimulating FactorPicolinic AcidsReceptor, Macrophage Colony-Stimulating FactorReceptors, Granulocyte-Macrophage Colony-Stimulating FactorVimentin

Identifiers

PMID29930294
PMCPMC6013474
OpenAlexW2808527545

What Socratic 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 Socratic graph.