Evidence map›Paper›PMID 33139832›Full record

ArticleOncogene2021

Deficiency of Wiskott-Aldrich syndrome protein has opposing effect on the pro-oncogenic pathway activation in nonmalignant versus malignant lymphocytes.

Seong-Su Han, Kuo-Kuang Wen, Yatin M Vyas

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 11 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

3 authors at 1 institution in 1 country.

Seong-Su HanDivision of Pediatric Hematology-Oncology, Carver College of Medicine and the Stead Family University of Iowa Children's Hospital, Iowa City, IA, 52242, USA.
Kuo-Kuang WenDivision of Pediatric Hematology-Oncology, Carver College of Medicine and the Stead Family University of Iowa Children's Hospital, Iowa City, IA, 52242, USA.
Yatin M VyasDivision of Pediatric Hematology-Oncology, Carver College of Medicine and the Stead Family University of Iowa Children's Hospital, Iowa City, IA, 52242, USA. yatin-vyas@uiowa.edu.ORCID http://orcid.org/0000-0002-4595-0267
University of Iowa Stead Family Children’s Hospital · US

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Christopher K Laubenthal · 2000 to 2026
$70.0M
Mechanisms of R loop-mediated genome instability in Wiskott-Aldrich syndromeR01AI146380 · NIAID · UNIVERSITY OF IOWA · PI VYAS, YATIN M · 2020 to 2024
$2.1M
Role of WASp in Golgi dispersal response to DNA damage in lymphocytesR21AI138051 · NIAID · UNIVERSITY OF IOWA · PI VYAS, YATIN M · 2018 to 2019
$419k
NIAID NIH HHS R01 AI146380NIAID NIH HHS R21 AI138051
6 · The paper itself

Abstract

Immunodeficiency is associated with cancer risk. Accordingly, hematolymphoid cancers develop in Wiskott-Aldrich syndrome (WAS), an X-linked primary immunodeficiency disorder (PID) resulting from the deficiency of WAS-protein (WASp) expressed predominantly in the hematolymphoid cell lineages. Despite the correlation between WASp deficiency and hematolymphoid cancers, the molecular mechanism underlying the oncogenic role of WASp is incompletely understood. Employing the WASp-sufficient and WASp-deficient cell-pair model of human T and B lymphocytes, we show that WASp deficiency differentially influences hyperactivation versus inhibition of both CDC42:ERK1/2 and NF-κB:AP-1 pro-oncogenic signaling pathways in nonmalignant versus malignant T and B lymphocytes. Furthermore, WASp deficiency induces a cell-type specific up/down-modulation of the DNA-binding activities of NF-κB, AP-1, and multiple other transcription factors with known roles in oncogenesis. We propose that WASp functions as a putative "tumor-suppressor" protein in normal T and B cells, and "oncoprotein" in a subset of established T and B cell malignancies that are not associated with the NPM-ALK fusion.

Indexed as

B-Lymphocytescdc42 GTP-Binding ProteinCell ProliferationCells, CulturedHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BOncogene ProteinsSignal TransductionT-LymphocytesTranscription Factor AP-1Tumor Suppressor ProteinsWiskott-Aldrich SyndromeWiskott-Aldrich Syndrome Proteincdc42 GTP-Binding ProteinCDC42 protein, humanMAPK1 protein, humanMAPK3 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BOncogene ProteinsTranscription Factor AP-1Tumor Suppressor ProteinsWAS protein, humanWiskott-Aldrich Syndrome Protein

Identifiers

PMID33139832
PMCPMC7855887
OpenAlexW3095198007

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.