Evidence map›Paper›PMID 19458356›Full record

ArticleBlood2009

High frequency of PTEN, PI3K, and AKT abnormalities in T-cell acute lymphoblastic leukemia.

Alejandro Gutierrez, Takaomi Sanda, Ruta Grebliunaite, Arkaitz Carracedo, Leonardo Salmena, Yebin Ahn, Suzanne Dahlberg, Donna Neuberg, Lisa A Moreau, Stuart S Winter and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed, 1 pooled it
16.5field-weighted citation impact, top 1% 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

240 citing papers in PubMed, 1 synthesis or guideline pooled it, 437 citations in OpenAlex.

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  19. Acute lymphoblastic leukaemia.Nature reviews. Disease primers · 2024
    Review
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180 more citing papers are in PubMed but not listed here.

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

19 authors at 5 institutions in 1 country.

Alejandro GutierrezDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, 44 Binney St., Boston, MA 02115, USA.
Takaomi Sanda
Ruta Grebliunaite
Arkaitz Carracedo
Leonardo Salmena
Yebin Ahn
Suzanne Dahlberg
Donna Neuberg
Lisa A Moreau
Stuart S Winter
Richard Larson
Jianhua Zhang
Alexei Protopopov
Lynda Chin
Pier Paolo Pandolfi
Lewis B Silverman
Stephen P Hunger
Stephen E Sallan
A Thomas Look
Dana-Farber Cancer Institute · USCancer Genetics (United States) · USBeth Israel Deaconess Medical Center · USCenter for Cancer and Blood Disorders · USUniversity of New Mexico · US

Funding

COG FOREIGN ACCRUALU10CA098543 · NCI · NATIONAL CHILDHOOD CANCER FOUNDATION · PI ADAMSON, PETER C. · 2003 to 2013
$335.5M
Zebrafish Screens for Genetic Modifiers and Human Application in T-ALLP01CA068484 · NCI · DANA-FARBER CANCER INSTITUTE · PI ORKIN, STUART H · 1995 to 2010
$31.9M
Support for Human Specimen Banking in NCI-Supported Cancer Clinical TrialsU24CA114766 · NCI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI RAMIREZ MILAN, NILSA DEL CARMEN · 2005 to 2014
$14.5M
Zebrafish Chemical and Classical Genetics Approach to the Pathogenesis of T-ALLK08CA133103 · NCI · DANA-FARBER CANCER INST · PI GUTIERREZ, ALEJANDRO · 2008 to 2012
$705k
NCI NIH HHS K08 CA133103NCI NIH HHS P01 CA068484NCI NIH HHS U10 CA098543NCI NIH HHS U24 CA114766
6 · The paper itself

Abstract

To more comprehensively assess the pathogenic contribution of the PTEN-PI3K-AKT pathway to T-cell acute lymphoblastic leukemia (T-ALL), we examined diagnostic DNA samples from children with T-ALL using array comparative genomic hybridization and sequence analysis. Alterations of PTEN, PI3K, or AKT were identified in 47.7% of 44 cases. There was a striking clustering of PTEN mutations in exon 7 in 12 cases, all of which were predicted to truncate the C2 domain without disrupting the phosphatase domain of PTEN. Induction chemotherapy failed to induce remission in 3 of the 4 patients whose lymphoblasts harbored PTEN deletions at the time of diagnosis, compared with none of the 12 patients with mutations of PTEN exon 7 (P = .007), suggesting that PTEN deletion has more adverse therapeutic consequences than mutational disruptions that preserve the phosphatase domain. These findings add significant support to the rationale for the development of therapies targeting the PTEN-PI3K-AKT pathway in T-ALL.

Indexed as

MutationChildComparative Genomic HybridizationDrug Resistance, NeoplasmHumansPhosphatidylinositol 3-KinasesPrecursor T-Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID19458356
PMCPMC2713461
OpenAlexW2049396238

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.