Evidence map›Paper›PMID 26655726›Full record

ReviewAging2015

The PTEN tumor suppressor gene and its role in lymphoma pathogenesis.

Xiaoxiao Wang, Huiqiang Huang, Ken H Young

Open access · hybridAbstract readReview
In one paragraph

Review in Aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 72 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 3 institutions in 2 countries.

Xiaoxiao WangDepartment of Hematopathology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77230, USA.
Huiqiang HuangDepartment of Medical Oncology, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China.
Ken H YoungDepartment of Hematopathology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77230, USA.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
P4 -TARGETING MULTIPLE MYELOMA BY COMBINING CDK INHIBITORS AND BCL-2 ANTAGONISTSP50CA142509 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KWAK, LARRY W · 2010 to 2014
$11.1M
Convergence of MicroRNAs and p53 Signaling in Multiple Myeloma: Environmental CoR01CA138688 · NCI · UNIVERSITY OF LOUISVILLE · PI LI, YONG · 2009 to 2017
$2.9M
UT M.D. Anderson Cancer Center Lymphoma SPOREP50CA136411 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KWAK, LARRY W · 2009 to 2011
$1.5M
Deep Sequencing of Small Regulatory RNAs in Diffuse Large B cell LymphomaRC1CA146299 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI XIAO, CHANGCHUN · 2009 to 2010
$1000k
NCI NIH HHS 1RC1CA146299NCI NIH HHS CA016672NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA136411NCI NIH HHS P50CA136411NCI NIH HHS P50 CA142509NCI NIH HHS P50CA142509NCI NIH HHS R01 CA138688NCI NIH HHS R01CA138688NCI NIH HHS RC1 CA146299
6 · The paper itself

Abstract

The phosphatase and tensin homolog gene PTEN is one of the most frequently mutated tumor suppressor genes in human cancer. Loss of PTEN function occurs in a variety of human cancers via its mutation, deletion, transcriptional silencing, or protein instability. PTEN deficiency in cancer has been associated with advanced disease, chemotherapy resistance, and poor survival. Impaired PTEN function, which antagonizes phosphoinositide 3-kinase (PI3K) signaling, causes the accumulation of phosphatidylinositol (3,4,5)-triphosphate and thereby the suppression of downstream components of the PI3K pathway, including the protein kinase B and mammalian target of rapamycin kinases. In addition to having lipid phosphorylation activity, PTEN has critical roles in the regulation of genomic instability, DNA repair, stem cell self-renewal, cellular senescence, and cell migration. Although PTEN deficiency in solid tumors has been studied extensively, rare studies have investigated PTEN alteration in lymphoid malignancies. However, genomic or epigenomic aberrations of PTEN and dysregulated signaling are likely critical in lymphoma pathogenesis and progression. This review provides updated summary on the role of PTEN deficiency in human cancers, specifically in lymphoid malignancies; the molecular mechanisms of PTEN regulation; and the distinct functions of nuclear PTEN. Therapeutic strategies for rescuing PTEN deficiency in human cancers are proposed.

Indexed as

Antineoplastic AgentsGene Expression Regulation, NeoplasticGene SilencingHumansLymphomaMutationPTEN PhosphohydrolaseAntineoplastic AgentsPTEN PhosphohydrolaseAKTdiffuse large B-cell lymphomalymphoid malignanciesmTORPI3KPTENtumor suppressor

Identifiers

PMID26655726
PMCPMC4712330
OpenAlexW2315340994

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.