Evidence map›Paper›PMID 18794120›Full record

ArticleCancer research2008

Functional characterization of filamin a interacting protein 1-like, a novel candidate for antivascular cancer therapy.

Mijung Kwon, Engy Hanna, Dominique Lorang, Mei He, John S Quick, Asha Adem, Christina Stevenson, Joon-Yong Chung, Stephen M Hewitt, Enrique Zudaire and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

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  13. Risk factors and biomarkers of age-related macular degeneration.Progress in retinal and eye research · 2016
    Review
  14. RNA-sequencing studies identify genes differentially regulated during inflammation-driven lung tumorigenesis and targeted by chemopreventive agents.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015
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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

13 authors at 4 institutions in 1 country.

Mijung KwonTumor Angiogenesis Section, Surgery Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA.
Engy Hanna
Dominique Lorang
Mei He
John S Quick
Asha Adem
Christina Stevenson
Joon-Yong Chung
Stephen M Hewitt
Enrique Zudaire
Dominic Esposito
Frank Cuttitta
Steven K Libutti
Angiogenesis Foundation · USCenter for Cancer Research · USNational Cancer Institute · USScience Applications International Corporation (United States) · US

Funding

Trans-NIH Angiogenesis Core FacilityZICBC010964 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CUTTITTA, FRANK · 2009 to 2010
$2.1M
Trans-NIH Angiogenesis Core FacilityZ01BC010964 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CUTTITTA, FRANK · 2008 to 2008
$42k
Intramural NIH HHS NIH0011802238
6 · The paper itself

Abstract

Inhibiting angiogenesis has become a major therapeutic strategy for cancer treatment. To identify common intracellular mediators, we previously analyzed gene expression profiles of endothelial cells after treatment with angiogenesis inhibitors. Filamin A interacting protein 1-like (FILIP1L; previously known as down-regulated in ovarian cancer 1) was identified as one of the genes up-regulated in endothelial cells in response to these inhibitors. However, the expression and function of FILIP1L protein is uncharacterized. Here, we provide the first description of the expression and specific subcellular localization of FILIP1L protein in human tissue. Overexpression of FILIP1L resulted in inhibition of cell proliferation and migration and increased apoptosis. In addition, overexpression of FILIP1L truncation mutants showed differential antiproliferative activity. A COOH terminal truncation mutant (FILIP1LDeltaC103) was more potent than wild-type FILIP1L in mediating this activity. Targeted expression of FILIP1LDeltaC103 in tumor vasculature inhibited tumor growth in vivo. Overall, these findings suggest that the novel protein FILIP1L may be an important mediator of the effects of angiogenesis inhibitors and that FILIP1L has the potential to be an antivascular reagent for cancer therapy.

Indexed as

AnimalsApoptosisCell Growth ProcessesCell Line, TumorCell MovementColonic NeoplasmsCytokinesDNA, ComplementaryEndostatinsEndothelial CellsFemaleGenetic TherapyHumansIntracellular Signaling Peptides and ProteinsMaleMelanomaCytokinesDNA, ComplementaryEndostatinsFILIP1L protein, humanIntracellular Signaling Peptides and Proteins

Identifiers

PMID18794120
PMCPMC2614293
OpenAlexW2015297482

What OpenQuestion holds

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LicenceTDM
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.