Evidence map›Paper›PMID 26773036›Full record

ArticleBlood2016

Deletion of Pten in CD45-expressing cells leads to development of T-cell lymphoblastic lymphoma but not myeloid malignancies.

Cristina Mirantes, Maria Alba Dosil, David Hills, Jian Yang, Núria Eritja, Maria Santacana, Sònia Gatius, Felip Vilardell, Alexander Medvinsky, Xavier Matias-Guiu and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. PTEN in Regulating Hematopoiesis and Leukemogenesis.Cold Spring Harbor perspectives in medicine · 2020
    Review
  3. Review
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

11 authors at 5 institutions in 2 countries.

Cristina MirantesOncologic Pathology Group, Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, Hospital Universitari Arnau de Vilanova, Institut de Recerca Biomèdica de Lleida, Lleida, Spain; and.
Maria Alba DosilOncologic Pathology Group, Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, Hospital Universitari Arnau de Vilanova, Institut de Recerca Biomèdica de Lleida, Lleida, Spain; and.
David HillsInstitute for Stem Cell Research, Medical Research Council Center for Regenerative Medicine, Edinburgh, United Kingdom.
Jian YangInstitute for Stem Cell Research, Medical Research Council Center for Regenerative Medicine, Edinburgh, United Kingdom.
Núria EritjaOncologic Pathology Group, Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, Hospital Universitari Arnau de Vilanova, Institut de Recerca Biomèdica de Lleida, Lleida, Spain; and.
Maria SantacanaOncologic Pathology Group, Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, Hospital Universitari Arnau de Vilanova, Institut de Recerca Biomèdica de Lleida, Lleida, Spain; and.
Sònia GatiusOncologic Pathology Group, Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, Hospital Universitari Arnau de Vilanova, Institut de Recerca Biomèdica de Lleida, Lleida, Spain; and.
Felip VilardellOncologic Pathology Group, Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, Hospital Universitari Arnau de Vilanova, Institut de Recerca Biomèdica de Lleida, Lleida, Spain; and.
Alexander MedvinskyInstitute for Stem Cell Research, Medical Research Council Center for Regenerative Medicine, Edinburgh, United Kingdom.
Xavier Matias-GuiuOncologic Pathology Group, Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, Hospital Universitari Arnau de Vilanova, Institut de Recerca Biomèdica de Lleida, Lleida, Spain; and.
Xavier DolcetOncologic Pathology Group, Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, Hospital Universitari Arnau de Vilanova, Institut de Recerca Biomèdica de Lleida, Lleida, Spain; and.
Hospital Universitari Arnau de Vilanova · ESBiomedical Research Institute of Lleida · ESMRC Centre for Regenerative Medicine · GBUniversitat de Lleida · ESMedical Research Council · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since its discovery in the late 1990s, Pten has turned out to be one of the most important tumor suppressor genes. Pten loss results in increased activation of the phosphatidylinositol 3-kinase/Akt signaling pathway, which is associated with increased proliferation, survival, and neoplastic growth. Here, we have addressed the effects of conditional deletion of Pten in hematopoietic cells by crossing Pten conditional knockout mice with a knock-in mouse expressing the Cre recombinase in the CD45 locus. CD45 is also known as leukocyte common antigen, and it is expressed in virtually all white cells and in hematopoietic stem cells. Using a reporter mouse, we demonstrate that CD45:Cre mouse displays recombinase activity in both myeloid and lymphoid cells. However, deletion of Pten in CD45-expressing cells induces development of T-cell acute lymphoblastic leukemia and lymphoma, but not other hematologic malignancies.

Indexed as

AnimalsBone Marrow CellsDisease Models, AnimalFemaleFlow CytometryGene DeletionHematopoietic Stem CellsIntegrasesKaplan-Meier EstimateLeukocyte Common AntigensMaleMiceMice, KnockoutMyeloproliferative DisordersPrecursor T-Cell Lymphoblastic Leukemia-LymphomaPTEN PhosphohydrolaseCre recombinaseIntegrasesLeukocyte Common AntigensPTEN PhosphohydrolasePten protein, mousePtprc protein, mouse

Identifiers

PMID26773036
PMCPMC4874386
OpenAlexW2295809819

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.