Evidence map›Paper›PMID 27694894›Full record

ArticleOncogene2017

NPM-ALK phosphorylates WASp Y102 and contributes to oncogenesis of anaplastic large cell lymphoma.

C A Murga-Zamalloa, V Mendoza-Reinoso, A A Sahasrabuddhe, D Rolland, S R Hwang, S R P McDonnell, A P Sciallis, R A Wilcox, V Bashur, K Elenitoba-Johnson and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

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  9. Colony-Stimulating Factor 1 Receptor (CSF1R) Activates AKT/mTOR Signaling and Promotes T-Cell Lymphoma Viability.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
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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

11 authors at 1 institution in 1 country.

C A Murga-ZamalloaDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
V Mendoza-ReinosoDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
A A SahasrabuddheDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
D RollandDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
S R HwangDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
S R P McDonnellDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
A P SciallisDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
R A WilcoxDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
V BashurDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
K Elenitoba-JohnsonDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
M S LimDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · US

Funding

Mass spectrometry-driven systems biologic analysis of salivary MALT lymphomaR01DE019249 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELENITOBA-JOHNSON, KOJO S. J. · 2008 to 2011
$1.5M
Proteomic analysis of api2-MALT1 positive gastric MALT lymphomaR01CA136905 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELENITOBA-JOHNSON, KOJO S. J. · 2009 to 2013
$1.4M
Proteomic biomarkers of ALK+ lymphomaR01CA140806 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIM, MEGAN S. · 2010 to 2013
$1.2M
NCI NIH HHS R01 CA136905NCI NIH HHS R01 CA140806NIDCR NIH HHS R01 DE019249
6 · The paper itself

Abstract

Mechanisms by which NPM-ALK signaling regulates cell migration, invasion and contributes to the oncogenesis of anaplastic large cell lymphoma (ALCL) are not completely understood. In an attempt to identify novel actin signaling pathways regulated by NPM-ALK, a comprehensive phosphoproteome analysis of ALCL cell lines was performed in the presence or absence of NPM-ALK activity. Numerous phosphoproteins involved in actin dynamics including Wiskott-Aldrich syndrome protein (WASp) were regulated by NPM-ALK. Network analysis revealed that WASp is a central component of the NPM-ALK-dependent actin signaling pathway. Here we show that NPM-ALK phosphorylates WASp at its known activation site (Y290) as well as at a novel residue (Y102). Phosphorylation of WASp at Y102 negatively regulates its interaction with Wiskott-Aldrich interacting protein and decreases its protein stability. Phosphorylation of WASp at Y102 enhances anchorage-independent growth and tumor growth in an in vivo xenograft model and enhances invasive properties of ALCL. We show that knock-down of WASp or expression of Y102F mutant of WASp decreases colony formation and in vivo tumor growth. Our results show that WASp is a novel substrate of ALK and has a critical role in regulating invasiveness and oncogenesis of ALCL.

Indexed as

AnimalsCarcinogenesisCatalytic DomainCell Line, TumorGene Knockdown TechniquesHeterograftsHumansLymphoma, Large-Cell, AnaplasticMiceMice, SCIDPhosphorylationProtein-Tyrosine KinasesWiskott-Aldrich Syndrome Proteinp80(NPM-ALK) proteinProtein-Tyrosine KinasesWAS protein, humanWiskott-Aldrich Syndrome Protein

Identifiers

PMID27694894
OpenAlexW2528805387

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.