Evidence map›Paper›PMID 25429075›Full record

ArticleScience signaling2014

Targeting cell-intrinsic and cell-extrinsic mechanisms of intravasation in invasive breast cancer.

Jiri Keirsse, Damya Laoui, Eva Van Overmeire, Jo A Van Ginderachter

Abstract readComment
PubMed Publisher
In one paragraph

Article in Science signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 45% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Jiri KeirsseMyeloid Cell Immunology Laboratory, VIB, 1050 Brussels, Belgium, and Lab of Cellular and Molecular Immunology, Vrije Universiteit Brussel, 1050 Brussels, Belgium.
Damya LaouiMyeloid Cell Immunology Laboratory, VIB, 1050 Brussels, Belgium, and Lab of Cellular and Molecular Immunology, Vrije Universiteit Brussel, 1050 Brussels, Belgium.
Eva Van OvermeireMyeloid Cell Immunology Laboratory, VIB, 1050 Brussels, Belgium, and Lab of Cellular and Molecular Immunology, Vrije Universiteit Brussel, 1050 Brussels, Belgium.
Jo A Van GinderachterMyeloid Cell Immunology Laboratory, VIB, 1050 Brussels, Belgium, and Lab of Cellular and Molecular Immunology, Vrije Universiteit Brussel, 1050 Brussels, Belgium. jvangind@vub.ac.be.
Vrije Universiteit Brussel · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The survival of breast cancer patients with metastatic disease has not markedly improved over recent decades, highlighting the need to better understand this process. In this issue of Science Signaling, Pignatelli et al. used freshly obtained invasive ductal carcinoma cells from patients to demonstrate the need for high abundance of the invasive isoform of the Mena protein (Mena(INV)) in cancer cells and colony-stimulating factor 1 (CSF-1)-mediated paracrine signaling in macrophages for efficient transendothelial migration and metastasis formation in all clinical breast cancer subtypes. Furthermore, the triple negative and HER2(+) subtypes, but not the ERPR(+)/HER2(-) subtype, had high CSF-1 receptor (CSF-1R) abundance and also partially used autocrine CSF-1/CSF-1R signaling for invasion. These data establish Mena(INV), CSF-1/CSF-1R, and macrophages as potential therapeutic targets for most human breast cancers.

Indexed as

AnimalsBiomarkers, TumorBreast NeoplasmsCarcinoma, Ductal, BreastFemaleHumansMacrophagesMicrofilament ProteinsNeoplasm InvasivenessNeoplasm ProteinsTransendothelial and Transepithelial MigrationBiomarkers, TumorMicrofilament ProteinsNeoplasm Proteins

Identifiers

PMID25429075
OpenAlexW2090928939

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.