Evidence map›Paper›PMID 30592296›Full record

ReviewBritish journal of haematology2019

CBFA2T3-GLIS2-positive acute myeloid leukaemia. A peculiar paediatric entity.

Riccardo Masetti, Salvatore N Bertuccio, Andrea Pession, Franco Locatelli

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of haematology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Extramedullary Relapse ofInternational journal of molecular sciences · 2025
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

4 authors at 2 institutions in 1 country.

Riccardo MasettiDepartment of Paediatrics, "Lalla Seràgnoli", Haematology-Oncology Unit, University of Bologna, Bologna, Italy.ORCID 0000-0002-1264-057X
Salvatore N BertuccioDepartment of Paediatrics, "Lalla Seràgnoli", Haematology-Oncology Unit, University of Bologna, Bologna, Italy.ORCID 0000-0002-5428-6716
Andrea PessionDepartment of Paediatrics, "Lalla Seràgnoli", Haematology-Oncology Unit, University of Bologna, Bologna, Italy.
Franco LocatelliDepartment of Paediatric Haematology-Oncology and Cell and Gene Therapy, IRCCS Ospedale Pediatrico Bambino Gesù, Rome, Sapienza University of Rome, Rome, Italy.ORCID 0000-0002-7976-3654
University of Bologna · ITBambino Gesù Children's Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The scenario of paediatric acute myeloid leukaemia (AML), particularly non-Down syndrome acute megakaryoblastic leukaemia (non-DS-AMKL), has been recently revolutionized by the advent of large-scale, genomic sequencing technologies. In this changing landscape, a significantly relevant discovery has been represented by the identification of the CBFA2T3-GLIS2 fusion gene, which is the result of a cryptic inversion of chromosome 16. It is the most frequent chimeric oncogene identified to date in non-DS-AMKL, although it seems not to be exclusively restricted to the French-American-British M7 subgroup. The CBFA2T3-GLIS2 fusion gene characterizes a subtype of leukaemia that is specific to paediatrics, having never been identified in adults. It characterizes an extremely aggressive leukaemia, as the presence of this fusion is associated with a grim outcome in almost all of the case series reported, with overall survival rates ranging between 15% and 30%. Although the molecular basis that underlies this leukaemia subtype is still far from being completely elucidated, unique functional properties induced by CBFA2T3-GLIS2 in the leukaemogenesis driving process have been recently identified. We here review the peculiarities of CBFA2T3-GLIS2-positive AML, describing its intriguing clinical and biological behaviour and providing some challenging targeting opportunities.

Indexed as

Chromosomes, Human, Pair 16Kruppel-Like Transcription FactorsLeukemia, Myeloid, AcuteOncogene Proteins, FusionRepressor ProteinsTumor Suppressor ProteinsAdolescentAnimalsChildChild, PreschoolDisease-Free SurvivalFemaleHumansInfantInfant, NewbornMaleCBFA2T3 protein, humanGLIS2 protein, humanKruppel-Like Transcription FactorsOncogene Proteins, FusionRepressor ProteinsTumor Suppressor Proteinsacute megakaryoblastic leukaemiaacute myeloid leukaemiaCBFA2T3-GLIS2childhood leukaemialeukaemia diagnosis

Identifiers

PMID30592296
PMCPMC6590351
OpenAlexW2907286342

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.