Evidence map›Paper›PMID 25622909›Full record

ArticleCancer letters2015

Phosphatidylinositol 3-kinase, class 2 beta (PI3KC2β) isoform contributes to neuroblastoma tumorigenesis.

Angela Russo, Mustafa Nazir Okur, Maarten Bosland, John P O'Bryan

Abstract read
In one paragraph

Article in Cancer letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  11. Silencing Intersectin 1 Slows Orthotopic Neuroblastoma Growth in Mice.Journal of pediatric hematology/oncology · 2017
    Article
  12. Article
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  14. Intersectin scaffold proteins and their role in cell signaling and endocytosis.Biochimica et biophysica acta. Molecular cell research · 2017
    Review
  15. 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

4 authors at 1 institution in 1 country.

Angela RussoDepartment of Pharmacology, University of Illinois at Chicago, Chicago, IL 60612.
Mustafa Nazir OkurDepartment of Biochemistry, University of Illinois at Chicago, Chicago, IL 60612.
Maarten BoslandDepartment of Pathology, University of Illinois at Chicago, Chicago, IL 60612; University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL 60612.
John P O'BryanDepartment of Pharmacology, University of Illinois at Chicago, Chicago, IL 60612; University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL 60612; Jesse Brown VA Medical Center, Chicago, IL 60612. Electronic address: obryanj@uic.edu.
University of Illinois Chicago · US

Funding

Center for Clinical and Translational ScienceUL1TR000050 · NCATS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI AZAR, DIMITRI T, MERMELSTEIN, ROBIN J. · 2012 to 2014
$9.8M
Cath B and uPAR si RNA constructs regressed glioma growthR01CA116708 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI O'BRYAN, JOHN P · 2005 to 2014
$2.9M
Regulation Of Ischemic Preconditioning By Compartmentalized Signal TransductionR01HL090651 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI O'BRYAN, JOHN P · 2009 to 2012
$1.1M
Novel Functions for Ras Family GTPasesI01BX002095 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI O'BRYAN, JOHN P · 2014 to 2024
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BLRD VA I01 BX002095NCATS NIH HHS UL1 TR000050NCATS NIH HHS UL1TR000050NCI NIH HHS CA116708NCI NIH HHS R01 CA116708NHLBI NIH HHS HL090651NHLBI NIH HHS R01 HL090651
6 · The paper itself

Abstract

Phosphatidylinositol 3-kinases (PI3Ks) play important roles in human tumorigenesis. Activation of the PI3K target AKT is frequent in neuroblastoma (NB) and correlates with poor prognosis. PI3K pan-inhibitors reduce NB tumor formation but present severe toxicity, which limits their therapeutic potential. Therefore, defining the importance of specific PI3K isoforms may aid in developing more effective therapeutic strategies. We previously demonstrated that PI3K Class IIβ (PI3KC2β) and its regulator intersectin 1 (ITSN1) are highly expressed in primary NB tumors and cell lines. Silencing ITSN1 dramatically reduced the tumorigenic potential of NB cells. Interestingly, overexpression of PI3KC2β rescued the anchorage-independent growth of ITSN1-silenced cells suggesting that PI3KC2β mediates ITSN1's function in NB cells. To address the importance of PI3KC2β in NBs, we generated PI3KC2β-silenced lines and examined their biologic activity. Herein, we demonstrate that PI3KC2β-silencing inhibits early stages of NB tumorigenic growth. We also show that loss of endogenous PI3KC2β or ITSN1 reduces AKT activation but does not impact ERK-MAPK activation. These data reveal a novel role for PI3KC2β in human NB tumorigenesis.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsCarcinogenesisCell Line, TumorCell ProliferationClass II Phosphatidylinositol 3-KinasesGene Knockdown TechniquesHumansIsoenzymesMAP Kinase Signaling SystemMice, NudeNeoplasm TransplantationNeuroblastomaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAdaptor Proteins, Vesicular TransportClass II Phosphatidylinositol 3-KinasesIsoenzymesITSN1 protein, humanPhosphatidylinositol 3-KinasesPIK3C2B protein, humanProto-Oncogene Proteins c-aktAKTITSN1NeuroblastomaOncogenesisPediatric tumorsPIK3C2β

Identifiers

PMID25622909
PMCPMC4351744
OpenAlexW1978309326

What OpenQuestion holds

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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.