Evidence map›Paper›PMID 36622782›Full record

ReviewBioscience reports2023

Mechanisms associated with t(7;12) acute myeloid leukaemia: from genetics to potential treatment targets.

Denise Ragusa, Liza Dijkhuis, Cristina Pina, Sabrina Tosi

Open access · goldAbstract readReview
In one paragraph

Review in Bioscience reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
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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

4 authors at 1 institution in 1 country.

Denise RagusaCollege of Health, Medicine and Life Sciences, Division of Biosciences, Brunel University London, Uxbridge, UB8 3PH, U.K.ORCID 0000-0002-0303-8683
Liza DijkhuisCollege of Health, Medicine and Life Sciences, Division of Biosciences, Brunel University London, Uxbridge, UB8 3PH, U.K.
Cristina PinaCollege of Health, Medicine and Life Sciences, Division of Biosciences, Brunel University London, Uxbridge, UB8 3PH, U.K.ORCID 0000-0002-2575-6301
Sabrina TosiCollege of Health, Medicine and Life Sciences, Division of Biosciences, Brunel University London, Uxbridge, UB8 3PH, U.K.ORCID 0000-0002-0036-0191
Brunel University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukaemia (AML), typically a disease of elderly adults, affects 8 children per million each year, with the highest paediatric incidence in infants aged 0-2 of 18 per million. Recurrent cytogenetic abnormalities contribute to leukaemia pathogenesis and are an important determinant of leukaemia classification. The t(7;12)(q36;p13) translocation is a high-risk AML subtype exclusively associated with infants and represents the second most common abnormality in this age group. Mechanisms of t(7;12) leukaemogenesis remain poorly understood. The translocation relocates the entire MNX1 gene within the ETV6 locus, but a fusion transcript is present in only half of the patients and its significance is unclear. Instead, research has focused on ectopic MNX1 expression, a defining feature of t(7;12) leukaemia, which has nevertheless failed to produce transformation in conventional disease models. Recently, advances in genome editing technologies have made it possible to recreate the t(7;12) rearrangement at the chromosomal level. Together with recent studies of MNX1 involvement using murine in vivo, in vitro, and organoid-based leukaemia models, specific investigation on the biology of t(7;12) can provide new insights into this AML subtype. In this review, we provide a comprehensive up-to-date analysis of the biological features of t(7;12), and discuss recent advances in mechanistic understanding of the disease which may deliver much-needed therapeutic opportunities to a leukaemia of notoriously poor prognosis.

Indexed as

Leukemia, Myeloid, AcuteAgedAnimalsChildGenes, HomeoboxHomeodomain ProteinsHumansInfantMiceTranscription FactorsTranslocation, GeneticHomeodomain ProteinsMNX1 protein, humanTranscription Factorsacute myeloid leukaemiacancerchromosomal translocationpaediatric

Identifiers

PMID36622782
PMCPMC9894016
OpenAlexW4313830574

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.