Evidence map›Paper›PMID 19147813›Full record

ArticleThe American journal of pathology2009

Profiling bladder cancer organ site-specific metastasis identifies LAMC2 as a novel biomarker of hematogenous dissemination.

Steven Christopher Smith, Brian Nicholson, Matthew Nitz, Henry F Frierson, Mark Smolkin, Garret Hampton, Wael El-Rifai, Dan Theodorescu

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 45 citations in OpenAlex.

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  8. Metastatic cells are preferentially vulnerable to lysosomal inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2018
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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

8 authors at 2 institutions in 1 country.

Steven Christopher SmithDepartment of Molecular Physiology and Biological Physics, University of Virginia Health System, Charlottesville, VA 22908, USA.
Brian Nicholson
Matthew Nitz
Henry F Frierson
Mark Smolkin
Garret Hampton
Wael El-Rifai
Dan Theodorescu
University of Virginia Health System · USGenomics Institute of the Novartis Research Foundation · US

Funding

Cancer Research Training Program: From Molecular Mechanisms to Therapeutic StrategiesT32CA009109 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Andrew Carl Dudley, Melanie R Rutkowski · 1985 to 2026
$13.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007267 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GARCIA-BLANCO, MARIANO A. · 1985 to 2024
$13.4M
Regulation and Targeting of CD24 in Bladder CancerR01CA075115 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI THEODORESCU, DAN · 2003 to 2024
$7.0M
MECHANISMS OF BLADDER CANCER INVANSIONR29CA075115 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI THEODORESCU, DAN · 1997 to 2001
$217k
NCI NIH HHS CA009109NCI NIH HHS CA075115NCI NIH HHS R01 CA075115NCI NIH HHS R29 CA075115NCI NIH HHS T32 CA009109NIGMS NIH HHS T32 GM007267NIGMS NIH HHS T32GM007267
6 · The paper itself

Abstract

Little is known about which genes mediate metastasis in bladder cancer, which accounts for much of the mortality of this disease. We used human bladder cancer cell lines to develop models of two clinically common metastatic sites, lung and liver, and evaluated their gene expression with respect to human tumor tissues. Parental cells were injected into either the murine spleen to generate liver metastases or tail vein to generate lung metastases with sequential progeny derived by re-injection and comparisons made of their organ-specific nature by crossed-site injections. Both genomic and transcriptomic analyses of organ-selected cell lines found salient differences and shared core metastatic profiles, which were then screened against gene expression data from human tumors. The expression levels of laminin V gamma 2 (LAMC2) contained in the core metastatic signature were increased as a function of human tumor stage, and its genomic location was in an area of gain as measured by comparative genomic hybridization. Using immunohistochemistry in a human bladder cancer tissue microarray, LAMC2 expression levels were associated with tumor grade, but inversely with nodal status. In contrast, in node-negative patients, LAMC2 expression was associated with visceral metastatic recurrence. In summary, LAMC2 is a novel biomarker of bladder cancer metastasis that reflects the propensity of cells to metastasize via either lymphatic or hematogenous routes.

Indexed as

Gene Expression ProfilingAnimalsBiomarkers, TumorCell Line, TumorComparative Genomic HybridizationHumansImmunohistochemistryLamininMiceNeoplasm MetastasisTissue Array AnalysisUrinary Bladder NeoplasmsBiomarkers, TumorLAMC2 protein, humanLaminin

Identifiers

PMID19147813
PMCPMC2630547
OpenAlexW2079667503

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.