Evidence map›Paper›PMID 17890451›Full record

ArticleBlood2008

High TCL1 expression and intact T-cell receptor signaling define a hyperproliferative subset of T-cell prolymphocytic leukemia.

Marco Herling, Kaushali A Patel, Michael A Teitell, Marina Konopleva, Farhad Ravandi, Ryuji Kobayashi, Dan Jones

Open access · greenAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

  1. Advances and Perspectives in the Treatment of T-PLL.Current hematologic malignancy reports · 2020
    Pooled it
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  14. T-Cell Prolymphocytic Leukemia: Diagnosis, Pathogenesis, and Treatment.International journal of molecular sciences · 2023
    Review
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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

7 authors at 2 institutions in 2 countries.

Marco HerlingDepartment of Hematopathology, University of Texas M. D. Anderson Cancer Center, Houston, USA.
Kaushali A Patel
Michael A Teitell
Marina Konopleva
Farhad Ravandi
Ryuji Kobayashi
Dan Jones
The University of Texas MD Anderson Cancer Center · USUniversity of California, Los Angeles · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TCL1 ONCOGENE IN B LYMPHOCYTE DEVELOPMENT AND NEOPLASIAR01CA090571 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TEITELL, MICHAEL A · 2002 to 2015
$3.8M
A NOVEL MECHANISM OF TCL1 TUMORIGENESISR01CA107300 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TEITELL, MICHAEL A · 2004 to 2008
$1.4M
NCI NIH HHS CA107300NCI NIH HHS CA16672NCI NIH HHS CA90571NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA090571NCI NIH HHS R01 CA107300
6 · The paper itself

Abstract

The T-cell leukemia 1 (TCL1) oncoprotein is overexpressed by chromosomal rearrangement in the majority of cases of T-cell prolymphocytic leukemia (T-PLL). In vitro, TCL1 can modulate the activity of the serine-threonine kinase AKT, a downstream effector of T-cell receptor (TCR) signaling. In a series of 86 T-PLL tumors, we show that expression of TCR, and levels of TCL1 and activated AKT are adverse prognostic markers. High-level TCL1 in TCR-expressing T-PLL is associated with higher presenting white blood cell counts, faster tumor cell doubling, and enhanced in vitro growth response to TCR engagement. In primary tumors and TCL1-transfected T-cell lines, TCR engagement leads to rapid recruitment of TCL1 and AKT to transient membrane activation complexes that include TCR-associated tyrosine kinases, including LCK. Pharmacologic inhibition of AKT activation alters the localization, stability, and levels of these transient TCL1-AKT complexes and reduces tumor cell growth. Experimental introduction and knockdown of TCL1 influence the kinetics and strength of TCR-mediated AKT activation. We propose that in T-PLL, TCL1 represents a highly regulated, targetable modulator of TCR-mediated AKT growth signaling.

Indexed as

Cell DivisionGene Expression Regulation, LeukemicHumansImmunophenotypingLeukemia, ProlymphocyticLeukemia, T-CellPhosphorylationProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptors, Antigen, T-CellSignal TransductionT-LymphocytesProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptors, Antigen, T-CellTCL1A protein, human

Identifiers

PMID17890451
PMCPMC2200815
OpenAlexW2042358998

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.