Evidence map›Paper›PMID 25511680›Full record

ArticleLeukemia & lymphoma2015

Induction of TAp73 by platinum-based compounds to overcome drug resistance in p53 dysfunctional chronic lymphocytic leukemia.

Sanne H Tonino, Chantal E Mulkens, Jacoline van Laar, Ingrid A M Derks, Guangli Suo, Fransien Croon-de Boer, Marinus H J van Oers, Eric Eldering, Jean Y Wang, Arnon P Kater

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Leukemia & lymphoma, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. Trial
  2. Article
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

10 authors at 3 institutions in 2 countries.

Sanne H Toninoa Department of Hematology , Academic Medical Center , Amsterdam , The Netherlands.
Chantal E Mulkensc Laboratory for Experimental Immunology, Academic Medical Center , Amsterdam , The Netherlands.
Jacoline van Laarc Laboratory for Experimental Immunology, Academic Medical Center , Amsterdam , The Netherlands.
Ingrid A M Derksc Laboratory for Experimental Immunology, Academic Medical Center , Amsterdam , The Netherlands.
Guangli Suod Division of Hematology-Oncology, Department of Medicine , Moores Cancer Center, University of California , San Diego, La Jolla , CA , USA.
Fransien Croon-de Boere Department of Internal Medicine , Ikazia Hospital , Rotterdam , The Netherlands.
Marinus H J van Oersa Department of Hematology , Academic Medical Center , Amsterdam , The Netherlands.
Eric Elderingb Lymphoma and Myeloma Center Amsterdam (LYMMCARE) , Amsterdam , The Netherlands.
Jean Y Wangd Division of Hematology-Oncology, Department of Medicine , Moores Cancer Center, University of California , San Diego, La Jolla , CA , USA.
Arnon P Katera Department of Hematology , Academic Medical Center , Amsterdam , The Netherlands.
Academic Medical Center · NLUniversity of California, San Diego · USIkazia Ziekenhuis · NL

Funding

STRUCTURE AND FUNCTION OF THE C-ABL PROTO-ONCOPROTEINR01CA043054 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WANG, JEAN Y.J. · 1986 to 2018
$4.4M
NCI NIH HHS R01 CA043054
6 · The paper itself

Abstract

In chronic lymphocytic leukemia (CLL), strategies to overcome drug resistance due to p53 dysfunction are highly needed. Platinum-based compounds such as cisplatinum (CDDP) are active in fludarabine-refractory CLL through a largely unknown mechanism. We analyzed the mechanism of action of CDDP in the context of p53 dysfunctionality. In vitro treatment with CDDP did not induce death in quiescent CLL cells, but did induce apoptosis in CD40-ligand (and CpG) stimulated and proliferating cells, irrespective of p53 function. In the p53 dysfunctional prolymphocytic cell-line MEC1, CDDP treatment resulted in apoptosis, cell cycle arrest and ABL1-dependent expression of TAp73, CDKN1A, PUMA and BID. TAp73 RNA-interference decreased sensitivity to CDDP. Finally, both in vitro stimulated CLL cells and lymph node (LN) derived CLL cells showed increased TAp73 expression in comparison with quiescent peripheral blood derived cells. Activity of CDDP may therefore be mediated by TAp73, especially in the context of activation such as occurs in the LN microenvironment.

Indexed as

Drug Resistance, NeoplasmAntigens, SurfaceAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsBH3 Interacting Domain Death Agonist ProteinBiomarkersCell CycleCell Cycle CheckpointsCell Line, TumorCell ProliferationCisplatinCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsGene Expression Regulation, NeoplasticGene Knockdown TechniquesAntigens, SurfaceAntineoplastic AgentsApoptosis Regulatory ProteinsBBC3 protein, humanBH3 Interacting Domain Death Agonist ProteinBiomarkersCisplatinCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsNuclear ProteinsPlatinumProto-Oncogene ProteinsProto-Oncogene Proteins c-ablTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor ProteinsCDDPChronic lymphocytic leukemiadrug resistancep53TAp73

Identifiers

PMID25511680
PMCPMC4592483
OpenAlexW2039711032

What OpenQuestion holds

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Registered trials

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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.