Evidence map›Paper›PMID 24418330›Full record

ArticleJournal of translational medicine2014

Frequent copy number variations of PI3K/AKT pathway and aberrant protein expressions of PI3K subunits are associated with inferior survival in diffuse large B cell lymphoma.

Wenli Cui, Ying Cai, Weige Wang, Zebing Liu, Ping Wei, Rui Bi, Weixiang Chen, Menghong Sun, Xiaoyan Zhou

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

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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

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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

27 citing papers in PubMed, 44 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Wenli Cui
Ying Cai
Weige Wang
Zebing Liu
Ping Wei
Rui Bi
Weixiang Chen
Menghong Sun
Xiaoyan ZhouDepartment of Pathology, Fudan University Shanghai Cancer Center, 270 Dong'an Road, Shanghai 200032, PR China. xyzhou100@yahoo.com.
Shanghai Medical College of Fudan University · CNFudan University · CNFudan University Shanghai Cancer Center · CNXinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt has been reported that the PI3K/AKT signaling pathway is activated in diffuse large B-cell lymphoma (DLBCL), PI3K constitutive activation plays a crucial role in PI3K/AKT pathway. However, the copy number variations (CNVs) of PI3K subunits on gene level remain unknown in DLBCL. Therefore, the aim of the study is to investigate the CNV of PI3K subunits and their relationship with clinicopathological features exploring the possible mechanism underlying of PI3K activation in DLBCL.

methodsCNV of 12 genes in the PI3K/AKT pathway was detected by NanoString nCounter in 60 de novo DLBCLs and 10 reactive hyperplasia specimens as controls. Meanwhile, immunohistochemistry (IHC) was performed to examine the expression of p110α, p110β, p110γ, p110δ, and pAKT on DLBCL tissue microarrays.

resultsAll PI3K and AKT subunits, except for PIK3R1, had various CNVs in the form of copy number amplifications and copy number losses. Their rates were in the range of 8.3-20.0%. Of them PIK3CA and PIK3CB gene CNVs were significantly associated with decreased overall survival (P = 0.029 and P = 0.019, respectively). IHC showed that the frequency of strong positive expression of p110α, p110β, p110γ, and p110δ were 26.7%, 25.0%, 18.3%, and 25.0% respectively, and they were found to be associated with decreased survival (P = 0.022, P = 0.015, P = 0.015, and P = 0.008, respectively). Expression of p110α was not only significantly associated with CNVs of PIK3CA (P = 0.002) but also positively correlated with strong positive expression of pAKT (P = 0.026).

conclusionsCNV of PIK3CA is highly associated with aberrant p110α protein expression and subsequent activation of PI3K/AKT pathway. CNVs of PIK3CA and PIK3CB, and aberrant protein expression of p110 isoforms are of great important value for predicting inferior prognosis in DLBCL. Frequent CNVs of PI3K/AKT subunits may play an important role in the tumorigenesis of DLBCL.

Indexed as

Class I Phosphatidylinositol 3-KinasesDNA Copy Number VariationsGenes, NeoplasmGenetic Predisposition to DiseaseHumansImmunohistochemistryLymphoma, Large B-Cell, DiffusePhosphatidylinositol 3-KinasesProtein SubunitsProto-Oncogene Proteins c-aktSignal TransductionSurvival AnalysisTissue Array AnalysisClass I Phosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesPIK3CA protein, humanProtein SubunitsProto-Oncogene Proteins c-akt

Identifiers

PMID24418330
PMCPMC3896773
OpenAlexW2135284059

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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.