Evidence map›Paper›PMID 28505169›Full record

ArticlePloS one2017

Molecular basis of targeted therapy in T/NK-cell lymphoma/leukemia: A comprehensive genomic and immunohistochemical analysis of a panel of 33 cell lines.

Rufino Mondejar, Cristina Pérez, Arantza Onaindia, Nerea Martinez, Julia González-Rincón, Helena Pisonero, Jose Pedro Vaqué, Laura Cereceda, Miguel Santibañez, Margarita Sánchez-Beato and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. 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
0.6field-weighted citation impact, top 33% 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, 5 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

11 authors at 4 institutions in 1 country.

Rufino MondejarCancer Genomics Laboratory, Instituto de Investigación Marqués de Valdecilla, IDIVAL, Santander, Spain.
Cristina PérezCancer Genomics Laboratory, Instituto de Investigación Marqués de Valdecilla, IDIVAL, Santander, Spain.
Arantza OnaindiaPathology Department, Hospital Universitario Marqués de Valdecilla, Santander, Spain.
Nerea MartinezCancer Genomics Laboratory, Instituto de Investigación Marqués de Valdecilla, IDIVAL, Santander, Spain.
Julia González-RincónLymphoma Research Group (Medical Oncology Service) Oncohematology Area, Instituto Investigación Sanitaria Puerta de Hierro-Majadahonda (IDIPHIM), Madrid, Spain.
Helena PisoneroCancer Genomics Laboratory, Instituto de Investigación Marqués de Valdecilla, IDIVAL, Santander, Spain.
Jose Pedro VaquéCancer Genomics Laboratory, Instituto de Investigación Marqués de Valdecilla, IDIVAL, Santander, Spain.
Laura CerecedaCancer Genomics Laboratory, Instituto de Investigación Marqués de Valdecilla, IDIVAL, Santander, Spain.
Miguel SantibañezUniversidad de Cantabria-IDIVAL, Santander, Spain.
Margarita Sánchez-BeatoLymphoma Research Group (Medical Oncology Service) Oncohematology Area, Instituto Investigación Sanitaria Puerta de Hierro-Majadahonda (IDIPHIM), Madrid, Spain.
Miguel Angel PirisCancer Genomics Laboratory, Instituto de Investigación Marqués de Valdecilla, IDIVAL, Santander, Spain.
Instituto de Investigación Marqués de Valdecilla · ESHospital Universitario Puerta de Hierro Majadahonda · ESMarqués de Valdecilla University Hospital · ESUniversidad de Cantabria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T and NK-cell lymphoma is a collection of aggressive disorders with unfavorable outcome, in which targeted treatments are still at a preliminary phase. To gain deeper insights into the deregulated mechanisms promoting this disease, we searched a panel of 31 representative T-cell and 2 NK-cell lymphoma/leukemia cell lines for predictive markers of response to targeted therapy. To this end, targeted sequencing was performed alongside the expression of specific biomarkers corresponding to potentially activated survival pathways. The study identified TP53, NOTCH1 and DNMT3A as the most frequently mutated genes. We also found common alterations in JAK/STAT and epigenetic pathways. Immunohistochemical analysis showed nuclear accumulation of MYC (in 85% of the cases), NFKB (62%), p-STAT (44%) and p-MAPK (30%). This panel of cell lines captures the complexity of T/NK-cell lymphoproliferative processes samples, with the partial exception of AITL cases. Integrated mutational and immunohistochemical analysis shows that mutational changes cannot fully explain the activation of key survival pathways and the resulting phenotypes. The combined integration of mutational/expression changes forms a useful tool with which new compounds may be assayed.

Indexed as

Antineoplastic AgentsCell Line, TumorCluster AnalysisGene Expression ProfilingGenomicsHigh-Throughput Nucleotide SequencingHumansImmunohistochemistryLymphoma, Extranodal NK-T-CellMolecular Targeted TherapyMutationAntineoplastic Agents

Identifiers

PMID28505169
PMCPMC5432176
OpenAlexW2614753278

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.