Evidence map›Paper›PMID 26886259›Full record

ArticlePloS one2016

The Mutational Landscape of Acute Promyelocytic Leukemia Reveals an Interacting Network of Co-Occurrences and Recurrent Mutations.

Mariam Ibáñez, José Carbonell-Caballero, Luz García-Alonso, Esperanza Such, Jorge Jiménez-Almazán, Enrique Vidal, Eva Barragán, María López-Pavía, Marta LLop, Iván Martín and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

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  12. Oncology letters · 2020
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  15. Differentiation therapy revisited.Nature reviews. Cancer · 2018
    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

15 authors at 3 institutions in 1 country.

Mariam IbáñezHematology Service, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
José Carbonell-CaballeroComputational Genomics Department, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Luz García-AlonsoComputational Genomics Department, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Esperanza SuchHematology Service, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
Jorge Jiménez-AlmazánComputational Genomics Department, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Enrique VidalComputational Genomics Department, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Eva BarragánLaboratory of Molecular Biology, Department of Clinical Chemistry, Hospital Universitario La Fe, Valencia, Spain.
María López-PavíaHematology Service, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
Marta LLopLaboratory of Molecular Biology, Department of Clinical Chemistry, Hospital Universitario La Fe, Valencia, Spain.
Iván MartínHematology Service, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
Inés Gómez-SeguíHematology Service, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
Pau MontesinosHematology Service, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
Miguel A SanzHematology Service, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
Joaquín DopazoComputational Genomics Department, Centro de Investigación Príncipe Felipe, Valencia, Spain.
José CerveraHematology Service, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
Hospital Universitari i Politècnic La Fe · ESCentro de Investigacion Principe Felipe · ESCentre for Biomedical Network Research on Rare Diseases · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preliminary Acute Promyelocytic Leukemia (APL) whole exome sequencing (WES) studies have identified a huge number of somatic mutations affecting more than a hundred different genes mainly in a non-recurrent manner, suggesting that APL is a heterogeneous disease with secondary relevant changes not yet defined. To extend our knowledge of subtle genetic alterations involved in APL that might cooperate with PML/RARA in the leukemogenic process, we performed a comprehensive analysis of somatic mutations in APL combining WES with sequencing of a custom panel of targeted genes by next-generation sequencing. To select a reduced subset of high confidence candidate driver genes, further in silico analysis were carried out. After prioritization and network analysis we found recurrent deleterious mutations in 8 individual genes (STAG2, U2AF1, SMC1A, USP9X, IKZF1, LYN, MYCBP2 and PTPN11) with a strong potential of being involved in APL pathogenesis. Our network analysis of multiple mutations provides a reliable approach to prioritize genes for additional analysis, improving our knowledge of the leukemogenesis interactome. Additionally, we have defined a functional module in the interactome of APL. The hypothesis is that the number, or the specific combinations, of mutations harbored in each patient might not be as important as the disturbance caused in biological key functions, triggered by several not necessarily recurrent mutations.

Indexed as

Gene Regulatory NetworksExomeGenome, HumanHumansINDEL MutationLeukemia, Promyelocytic, AcuteMutationMutation RatePolymorphism, Single NucleotideReproducibility of Results

Identifiers

PMID26886259
PMCPMC4757557
OpenAlexW2278876799

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.