Evidence map›Paper›PMID 22065599›Full record

ArticleBlood2012

Tcl1 interacts with Atm and enhances NF-κB activation in hematologic malignancies.

Eugenio Gaudio, Riccardo Spizzo, Francesco Paduano, Zhenghua Luo, Alexey Efanov, Alexey Palamarchuk, Amanda S Leber, Mohamed Kaou, Nicola Zanesi, Arianna Bottoni and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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  12. Eμ-TCL1xMyc: A Novel Mouse Model for Concurrent CLL and B-Cell Lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
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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

18 authors at 5 institutions in 3 countries.

Eugenio GaudioDepartment of Molecular Immunology, Virology and Medical Genetics, The Ohio State University, Columbus, OH 43210, USA.
Riccardo Spizzo
Francesco Paduano
Zhenghua Luo
Alexey Efanov
Alexey Palamarchuk
Amanda S Leber
Mohamed Kaou
Nicola Zanesi
Arianna Bottoni
Stefan Costinean
Laura Z Rassenti
Tatsuya Nakamura
Thomas J Kipps
Rami I Aqeilan
Yuri Pekarsky
Francesco Trapasso
Carlo M Croce
The Ohio State University · USMagna Graecia University · ITUniversity of California, San Diego · USCentro di Riferimento Oncologico · ITHebrew University of Jerusalem · IL

Funding

Tissue CoreP01CA081534 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KIPPS, THOMAS J · 2000 to 2016
$59.5M
TOWARD AN UNDERSTANDING OF CLL PROGRESSIONR01CA151319 · NCI · OHIO STATE UNIVERSITY · PI CROCE, CARLO M · 2011 to 2015
$1.5M
Novel pharmacologic agents in CLLP20CA081534 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI KIPPS, THOMAS J. · 1999 to 1999
–
NCI NIH HHS CA81534NCI NIH HHS P01 CA081534NCI NIH HHS R01 CA151319
6 · The paper itself

Abstract

The T-cell leukemia/lymphoma 1 (TCL1) oncogene is a target of chromosomal translocations and inversions at 14q31.2, and its rearrangement in T cells causes T-cell prolymphocytic leukemias. TCL1 dysregulation in B cells is responsible for the development of an aggressive form of chronic lymphocytic leukemia (CLL), the most common human leukemia. We have investigated the mechanisms underlying the oncogenic functions of Tcl1 protein using a mass spectrometry approach and have identified Atm (ataxia-telangiectasia mutated) as a candidate Tcl1-interacting protein. The Tcl1-Atm complex formation was validated by coimmunoprecipitation experiments. Importantly, we show that the association of Atm with Tcl1 leads to enhanced IκBα phosphorylation and ubiquitination and subsequent activation of the NF-κB pathway. Our findings reveal functional cross-talk between Atm and Tcl1 and provide evidence for a novel pathway that could be targeted in leukemias and lymphomas.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsBlotting, WesternCell Cycle ProteinsCell ProliferationDNA-Binding ProteinsFemaleHumansI-kappa B ProteinsImmunoprecipitationLeukemia, B-CellLeukemia, Lymphocytic, Chronic, B-CellLuciferasesMiceMice, NudeMice, TransgenicAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsI-kappa B ProteinsLuciferasesNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanNfkbia protein, mouseProtein Serine-Threonine KinasesProto-Oncogene ProteinsRNA, MessengerTCL1A protein, humanTumor Suppressor Proteins

Identifiers

PMID22065599
PMCPMC3251228
OpenAlexW2077516186

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.