Evidence map›Paper›PMID 22589276›Full record

ArticleCancer research2012

Loss of cell-surface laminin anchoring promotes tumor growth and is associated with poor clinical outcomes.

Armin Akhavan, Obi L Griffith, Liliana Soroceanu, Dmitri Leonoudakis, Maria Gloria Luciani-Torres, Anneleen Daemen, Joe W Gray, John L Muschler

Abstract read
In one paragraph

Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

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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.

Armin AkhavanCalifornia Pacific Medical Center Research Institute, San Francisco, CA, USA.
Obi L Griffith
Liliana Soroceanu
Dmitri Leonoudakis
Maria Gloria Luciani-Torres
Anneleen Daemen
Joe W Gray
John L Muschler
Lawrence Berkeley National Laboratory · USCalifornia Pacific Medical Center · US

Funding

Tissue and Outcomes CoreP50CA058207 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRAY, JOE W. · 1992 to 2012
$32.7M
Systems-Based Predictions of Responses to Cancer TherapyU54CA112970 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI TOMLIN, CLAIRE J · 2004 to 2014
$27.1M
Dystroglycan in Epithelial Architecture and FunctionR01CA109579 · NCI · CALIFORNIA PACIFIC MED CTR RES INSTITUTE · PI MUSCHLER, JOHN L · 2005 to 2009
$1.6M
CIHRNCI NIH HHS CA109579NCI NIH HHS P50 CA058207NCI NIH HHS R01 CA109579NCI NIH HHS U54 CA112970
6 · The paper itself

Abstract

Perturbations in the composition and assembly of extracellular matrices (ECM) contribute to progression of numerous diseases, including cancers. Anchoring of laminins at the cell surface enables assembly and signaling of many ECMs, but the possible contributions of altered laminin anchoring to cancer progression remain undetermined. In this study, we investigated the prominence and origins of defective laminin anchoring in cancer cells and its association with cancer subtypes and clinical outcomes. We found loss of laminin anchoring to be widespread in cancer cells. Perturbation of laminin anchoring originated from several distinct defects, which all led to dysfunctional glycosylation of the ECM receptor dystroglycan. In aggressive breast and brain cancers, defective laminin anchoring was often due to suppressed expression of the glycosyltransferase LARGE. Reduced expression of LARGE characterized a broad array of human tumors in which it was associated with aggressive cancer subtypes and poor clinical outcomes. Notably, this defect robustly predicted poor survival in patients with brain cancers. Restoring LARGE expression repaired anchoring of exogenous and endogenous laminin and modulated cell proliferation and tumor growth. Together, our findings suggest that defects in laminin anchoring occur commonly in cancer cells, are characteristic of aggressive cancer subtypes, and are important drivers of disease progression.

Indexed as

Cell Line, TumorCell MembraneCell ProliferationDisease ProgressionDystroglycansExtracellular MatrixGlycosylationHumansLamininN-AcetylglucosaminyltransferasesNeoplasmsDystroglycansLamininLARGE1 protein, humanN-Acetylglucosaminyltransferases

Identifiers

PMID22589276
PMCPMC3354772
OpenAlexW2142828058

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.