Evidence map›Paper›PMID 19351750›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009

Protumorigenic role of HAPLN1 and its IgV domain in malignant pleural mesothelioma.

Alla V Ivanova, Chandra M V Goparaju, Sergey V Ivanov, Daisuke Nonaka, Christina Cruz, Amanda Beck, Fulvio Lonardo, Anil Wali, Harvey I Pass

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 52 citations in OpenAlex.

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  12. Cancer-associated fibroblasts-derived HAPLN1 promotes tumour invasion through extracellular matrix remodeling in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 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 1 country.

Alla V IvanovaDepartment of Cardiothoracic Surgery, Langone School of Medicine, New York University, New York, New York, USA. alla.ivanova@vanderbilt.edu
Chandra M V Goparaju
Sergey V Ivanov
Daisuke Nonaka
Christina Cruz
Amanda Beck
Fulvio Lonardo
Anil Wali
Harvey I Pass
New York University · USThe Barbara Ann Karmanos Cancer Institute · US

Funding

PATHOLOGY, VIROLOGY, AND ANIMAL COREP01CA114047 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI TESTA, JOSEPH R. · 2006 to 2010
$8.0M
The North American Mesothelioma ConsortiumU01CA111295 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUFLEJT, MARGARET ELISABETH, PASS, HARVEY IRA · 2005 to 2016
$4.8M
NCI NIH HHS 5 U01 CA111295-02NCI NIH HHS P01 CA114047NCI NIH HHS U01 CA111295
6 · The paper itself

Abstract

purposeTumor extracellular matrix (ECM) plays a crucial role in cancer progression mediating and transforming host-tumor interactions. Targeting the ECM is becoming an increasingly promising therapeutic approach in cancer treatment. We find that one of the ECM proteins, HAPLN1, is overexpressed in the majority of mesotheliomas. This study was designed to characterize the protumorigenic role of HAPLN1 in mesothelioma. EXPERIMENTAL

designOverexpression of HAPLN1 was assessed and validated on a large set of normal/mesothelioma specimens on the RNA and protein levels. We also analyzed DNA copy number alterations in the HAPLN1 genomic locus using the array-based comparative genomic hybridization representational oligonucleotide microarray analysis tool. Tumorigenic activities of the HAPLN1 domains were evaluated in vitro on mesothelioma cells transfected with HAPLN1-expressing constructs.

resultsWe found that HAPLN1 is 23-fold overexpressed in stage I mesothelioma and confirmed it for 76% samples (n = 53) on RNA and 97% (n = 40) on protein levels. The majority of lung cancers showed no differential expression of HAPLN1. Analysis of DNA copy number alterations identified recurrent gain in the 5q14.3 HAPLN1 locus in approximately 27% of tumors. Noteworthy, high expression of HAPLN1 negatively correlated with time to progression (P = 0.05, log-rank test) and overall survival (P = 0.006). Proliferation, motility, invasion, and soft-agar colony formation assays on mesothelioma cells overexpressing full-length HAPLN1 or its functional domains strongly supported the protumorigenic role of HAPLN1 and its SP-IgV domain.

conclusionOverexpression of HAPLN1 and its SP-IgV domain increases tumorigenic properties of mesothelioma. Thus, targeting the SP-IgV domain may be one of the therapeutic approaches in cancer treatment.

Indexed as

Cell Line, TumorCell MovementCell ProliferationExtracellular MatrixExtracellular Matrix ProteinsGene Expression ProfilingHumansHyaluronic AcidKaplan-Meier EstimateLung NeoplasmsMesotheliomaOligonucleotide Array Sequence AnalysisPleural NeoplasmsProtein Structure, TertiaryProteoglycan Link ProteinProteoglycansExtracellular Matrix ProteinsHyaluronic AcidProteoglycan Link ProteinProteoglycans

Identifiers

PMID19351750
PMCPMC3761224
OpenAlexW2140861361

What OpenQuestion holds

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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.