Evidence map›Paper›PMID 27741277›Full record

ArticlePloS one2016

Chromothripsis Is a Recurrent Genomic Abnormality in High-Risk Myelodysplastic Syndromes.

María Abáigar, Cristina Robledo, Rocío Benito, Fernando Ramos, María Díez-Campelo, Lourdes Hermosín, Javier Sánchez-Del-Real, Jose M Alonso, Rebeca Cuello, Marta Megido and 9 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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Chromothripsis in myeloid malignancies.Annals of hematology · 2024
    Review
  4. Spatial-Temporal Genome Regulation in Stress-Response and Cell-Fate Change.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Review
  7. Insight into the Molecular Basis Underlying Chromothripsis.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. International journal of molecular sciences · 2020
    Review
  15. BCOR involvement in cancer.Epigenomics · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

19 authors at 12 institutions in 2 countries.

María AbáigarUnidad de Diagnóstico Molecular y Celular del Cáncer, Centro de Investigación del Cáncer-IBMCC (USAL-CSIC), Salamanca, Spain.
Cristina RobledoUnidad de Diagnóstico Molecular y Celular del Cáncer, Centro de Investigación del Cáncer-IBMCC (USAL-CSIC), Salamanca, Spain.
Rocío BenitoUnidad de Diagnóstico Molecular y Celular del Cáncer, Centro de Investigación del Cáncer-IBMCC (USAL-CSIC), Salamanca, Spain.
Fernando RamosIBIOMED, Instituto de Biomedicina, Universidad de León, León, Spain.
María Díez-CampeloServicio de Hematología, Hospital Universitario de Salamanca, Salamanca, Spain.
Lourdes HermosínServicio de Hematología, Hospital Jerez de la Frontera, Cádiz, Spain.
Javier Sánchez-Del-RealServicio de Hematología, Hospital Universitario de León, León, Spain.
Jose M AlonsoServicio de Hematología, Hospital Río Carrión, Palencia, Spain.
Rebeca CuelloServicio de Hematología, Hospital Clínico Universitario de Valladolid, Valladolid, Spain.
Marta MegidoServicio de Hematología, Hospital del Bierzo, Ponferrada, Spain.
Juan N RodríguezServicio de Hematología, Hospital Juan Ramón Jiménez, Huelva, Spain.
Guillermo Martín-NúñezServicio de Hematología, Hospital Virgen del Puerto, Plasencia, Spain.
Carlos AguilarServicio de Hematología, Hospital General de Soria, Soria, Spain.
Manuel VargasServicio de Hematología, Hospital Comarcal de Jarrio, Jarrio-Coaña, Spain.
Ana A MartínServicio de Hematología, Hospital Universitario de Salamanca, Salamanca, Spain.
Juan L GarcíaUnidad de Diagnóstico Molecular y Celular del Cáncer, Centro de Investigación del Cáncer-IBMCC (USAL-CSIC), Salamanca, Spain.
Alexander KohlmannAstraZeneca, Personalized Healthcare and Biomarkers, Innovative Medicines and Early Development, Cambridge, United Kingdom.
M Consuelo Del CañizoServicio de Hematología, Hospital Universitario de Salamanca, Salamanca, Spain.
Jesús M Hernández-RivasUnidad de Diagnóstico Molecular y Celular del Cáncer, Centro de Investigación del Cáncer-IBMCC (USAL-CSIC), Salamanca, Spain.
Centro de Investigación del Cáncer · ESComplejo Hospitalario de Salamanca · ESInstituto de Investigación Biomédica de Salamanca · ESAstraZeneca (United Kingdom) · GBHospital Clínico Universitario de Valladolid · ESHospital de León · ESHospital El Bierzo · ESHospital Jerez Puerta del Sur · ESHospital Juan Ramón Jiménez · ESHospital Rio Carrion · ESHospital Virgen del Puerto · ESUniversidad de León · ES

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI MEINZEN-DERR, JAREEN, STRAWN, JEFFREY ROBERT · 2015 to 2024
$37.5M
NCATS NIH HHS UL1 TR001425
6 · The paper itself

Abstract

To explore novel genetic abnormalities occurring in myelodysplastic syndromes (MDS) through an integrative study combining array-based comparative genomic hybridization (aCGH) and next-generation sequencing (NGS) in a series of MDS and MDS/myeloproliferative neoplasms (MPN) patients. 301 patients diagnosed with MDS (n = 240) or MDS/MPN (n = 61) were studied at the time of diagnosis. A genome-wide analysis of DNA copy number abnormalities was performed. In addition, a mutational analysis of DNMT3A, TET2, RUNX1, TP53 and BCOR genes was performed by NGS in selected cases. 285 abnormalities were identified in 71 patients (23.6%). Three high-risk MDS cases (1.2%) displayed chromothripsis involving exclusively chromosome 13 and affecting some cancer genes: FLT3, BRCA2 and RB1. All three cases carried TP53 mutations as revealed by NGS. Moreover, in the whole series, the integrative analysis of aCGH and NGS enabled the identification of cryptic recurrent deletions in 2p23.3 (DNMT3A; n = 2.8%), 4q24 (TET2; n = 10%) 17p13 (TP53; n = 8.5%), 21q22 (RUNX1; n = 7%), and Xp11.4 (BCOR; n = 2.8%), while mutations in the non-deleted allele where found only in DNMT3A (n = 1), TET2 (n = 3), and TP53 (n = 4). These cryptic abnormalities were detected mainly in patients with normal (45%) or non-informative (15%) karyotype by conventional cytogenetics, except for those with TP53 deletion and mutation (15%), which had a complex karyotype. In addition to well-known copy number defects, the presence of chromothripsis involving chromosome 13 was a novel recurrent change in high-risk MDS patients. Array CGH analysis revealed the presence of cryptic abnormalities in genomic regions where MDS-related genes, such as TET2, DNMT3A, RUNX1 and BCOR, are located.

Indexed as

Chromosome AberrationsAdolescentAdultAgedAged, 80 and overChildChromosomes, Human, Pair 13Comparative Genomic HybridizationCore Binding Factor Alpha 2 SubunitDioxygenasesDNADNA-Binding ProteinsDNA Copy Number VariationsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNA Mutational AnalysisCore Binding Factor Alpha 2 SubunitDioxygenasesDNADNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanProto-Oncogene ProteinsRUNX1 protein, humanTET2 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID27741277
PMCPMC5065168
OpenAlexW2531304375

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.