Evidence map›Paper›PMID 34865701›Full record

ReviewBest practice & research. Clinical haematology2021

Redefining the biological basis of lineage-ambiguous leukemia through genomics: BCL11B deregulation in acute leukemias of ambiguous lineage.

Lindsey E Montefiori, Charles G Mullighan

Open access · greenAbstract readReview
In one paragraph

Review in Best practice & research. Clinical haematology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.5field-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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Review
  6. Dual role ofBlood science (Baltimore, Md.) · 2024
    Review
  7. Article
  8. [Clinical characteristics of 34 adult patients with acute leukemias of ambiguous lineage].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
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

2 authors at 1 institution in 1 country.

Lindsey E MontefioriDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Charles G MullighanDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA. Electronic address: charles.mullighan@stjude.org.
St. Jude Children's Research Hospital · US

Funding

CPML - Project 3: Genome-wide Studies of Adverse EffectsP50GM115279 · NIGMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI RELLING, MARY V · 2015 to 2019
$15.1M
Translating genomic discoveries to improved outcomes for high risk acute leukemiaR35CA197695 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Charles G Mullighan · 2017 to 2026
$11.4M
Childhood Hematological Malignancies Training ProgramT32CA236748 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Charles G Mullighan · 2019 to 2026
$2.0M
Role of WT1 in mixed phenotype acute leukemiaF32CA254140 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI MONTEFIORI, LINDSEY · 2020 to 2022
$152k
NCI NIH HHS F32 CA254140NCI NIH HHS R35 CA197695NCI NIH HHS T32 CA236748NIGMS NIH HHS P50 GM115279
6 · The paper itself

Abstract

Acute leukemias of ambiguous lineage (ALAL), including mixed phenotype acute leukemia (MPAL) and related entities such as early T-cell precursor acute leukemia (ETP-ALL), remain diagnostic and clinical challenges due to limited understanding of pathogenesis, reliance of immunophenotyping to classify disease, and the lack of a rational approach to guide selection of appropriate therapy. Recent studies utilizing genomic sequencing and complementary approaches have provided key insights that are changing the way in which such leukemias are classified, and potentially, treated. Several recurrent genomic alterations define leukemias that straddle immunophenotypic entities, such as ZNF384-rearranged childhood B-ALL and B/myeloid MPAL, and BCL11B-rearranged T/myeloid MPAL, ETP-ALL and AML. In contrast, some cases of MPAL represent canonical ALL/AML entities exhibiting lineage aberrancy. For many cases of ALAL, experimental approaches indicate lineage aberrancy arises from acquisition of a founding genetic alteration into a hematopoietic stem or progenitor cell. Determination of optimal therapeutic approach requires genomic characterization of uniformly treated ALAL patients in prospective studies, but several approaches, including kinase inhibitors and BH3 mimetics may be efficacious in subsets of ALAL.

Indexed as

GenomicsPrecursor Cell Lymphoblastic Leukemia-LymphomaChildHumansImmunophenotypingProspective StudiesRepressor ProteinsTumor Suppressor ProteinsBCL11B protein, humanRepressor ProteinsTumor Suppressor Proteins14q32ALALBCL11BEnhancer hijackingLineage ambiguousMixed phenotype acute leukemia

Identifiers

PMID34865701
PMCPMC8649174
OpenAlexW3209184978

What OpenQuestion holds

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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.