Evidence map›Paper›PMID 24465725›Full record

ArticlePloS one2014

DEspR roles in tumor vasculo-angiogenesis, invasiveness, CSC-survival and anoikis resistance: a 'common receptor coordinator' paradigm.

Victoria L Herrera, Julius L Decano, Glaiza A Tan, Ann M Moran, Khristine A Pasion, Yuichi Matsubara, Nelson Ruiz-Opazo

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Observational
  2. Article
  3. Expression of DEspR in acute intracerebral hemorrhage.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2022
    Observational
  4. Article
  5. Article
  6. Article
  7. Humanized anti-DEspR IgG4BMC cancer · 2021
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Victoria L HerreraDepartment of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Julius L DecanoDepartment of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Glaiza A TanDepartment of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Ann M MoranDepartment of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Khristine A PasionDepartment of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Yuichi MatsubaraDepartment of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Nelson Ruiz-OpazoDepartment of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Boston University · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR025771 · NCRR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CENTER, DAVID M. · 2008 to 2011
$17.6M
NCRR NIH HHS UL1 RR025771NCRR NIH HHS UL1RR025771
6 · The paper itself

Abstract

A priori, a common receptor induced in tumor microvessels, cancer cells and cancer stem-like cells (CSCs) that is involved in tumor angiogenesis, invasiveness, and CSC anoikis resistance and survival, could underlie contemporaneous coordination of these events rather than assume stochasticity. Here we show that functional analysis of the dual endothelin1/VEGFsignal peptide receptor, DEspR, (formerly named Dear, Chr.4q31.2) supports the putative common receptor paradigm in pancreatic ductal adenocarcinoma (PDAC) and glioblastoma (GBM) selected for their invasiveness, CD133+CSCs, and polar angiogenic features. Unlike normal tissue, DEspR is detected in PDAC and GBM microvessels, tumor cells, and CSCs isolated from PDAC-Panc1 and GBM-U87 cells. DEspR-inhibition decreased angiogenesis, invasiveness, CSC-survival and anoikis resistance in vitro, and decreased Panc1-CSC and U87-CSC xenograft tumor growth, vasculo-angiogenesis and invasiveness in nude(nu/nu) rats, suggesting that DEspR activation would coordinate these tumor progression events. As an accessible, cell-surface 'common receptor coordinator', DEspR-inhibition defines a novel targeted-therapy paradigm for pancreatic cancer and glioblastoma.

Indexed as

AnoikisAnimalsBrain NeoplasmsCell Line, TumorCell SurvivalChlorocebus aethiopsCOS CellsGlioblastomaHumansHuman Umbilical Vein Endothelial CellsLigandsMicrovesselsNeoplasm InvasivenessNeoplastic Stem CellsNeovascularization, PathologicPancreatic NeoplasmsFBXW7-AS1 non-coding RNA, humanLigandsReceptors, Cell Surface

Identifiers

PMID24465725
PMCPMC3897535
OpenAlexW2095930310

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.