Evidence map›Paper›PMID 26463423›Full record

ReviewBlood2015

Revisiting the biology of infant t(4;11)/MLL-AF4+ B-cell acute lymphoblastic leukemia.

Alejandra Sanjuan-Pla, Clara Bueno, Cristina Prieto, Pamela Acha, Ronald W Stam, Rolf Marschalek, Pablo Menéndez

Open access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
11.6field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 123 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Concurrent MLL-AF4Frontiers in pediatrics · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Updates inBiomedicines · 2023
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. The Social Norm of Hematopoietic Stem Cells and Dysregulation in Leukemia.International journal of molecular sciences · 2022
    Review
  20. Article

6 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 3 countries.

Alejandra Sanjuan-PlaJosep Carreras Leukemia Research Institute and School of Medicine, University of Barcelona, Barcelona, Spain;
Clara BuenoJosep Carreras Leukemia Research Institute and School of Medicine, University of Barcelona, Barcelona, Spain;
Cristina PrietoJosep Carreras Leukemia Research Institute and School of Medicine, University of Barcelona, Barcelona, Spain;
Pamela AchaJosep Carreras Leukemia Research Institute and School of Medicine, University of Barcelona, Barcelona, Spain;
Ronald W StamDepartment of Pediatric Oncology/Hematology, Erasmus Medical Center-Sophia Children's Hospital, Rotterdam, The Netherlands;
Rolf MarschalekInstitute of Pharmaceutical Biology, Goethe-University, Frankfurt/Main, Germany; and.
Pablo MenéndezJosep Carreras Leukemia Research Institute and School of Medicine, University of Barcelona, Barcelona, Spain; Institució Catalana de Recerca i Estudis Avançats, Barcelona, Spain.
Universitat de Barcelona · ESErasmus MC - Sophia Children’s Hospital · NLGoethe University Frankfurt · DEJosep Carreras Leukaemia Research Institute · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infant B-cell acute lymphoblastic leukemia (B-ALL) accounts for 10% of childhood ALL. The genetic hallmark of most infant B-ALL is chromosomal rearrangements of the mixed-lineage leukemia (MLL) gene. Despite improvement in the clinical management and survival (∼85-90%) of childhood B-ALL, the outcome of infants with MLL-rearranged (MLL-r) B-ALL remains dismal, with overall survival <35%. Among MLL-r infant B-ALL, t(4;11)+ patients harboring the fusion MLL-AF4 (MA4) display a particularly poor prognosis and a pro-B/mixed phenotype. Studies in monozygotic twins and archived blood spots have provided compelling evidence of a single cell of prenatal origin as the target for MA4 fusion, explaining the brief leukemia latency. Despite its aggressiveness and short latency, current progress on its etiology, pathogenesis, and cellular origin is limited as evidenced by the lack of mouse/human models recapitulating the disease phenotype/latency. We propose this is because infant cancer is from an etiologic and pathogenesis standpoint distinct from adult cancer and should be seen as a developmental disease. This is supported by whole-genome sequencing studies suggesting that opposite to the view of cancer as a "multiple-and-sequential-hit" model, t(4;11) alone might be sufficient to spawn leukemia. The stable genome of these patients suggests that, in infant developmental cancer, one "big-hit" might be sufficient for overt disease and supports a key contribution of epigenetics and a prenatal cell of origin during a critical developmental window of stem cell vulnerability in the leukemia pathogenesis. Here, we revisit the biology of t(4;11)+ infant B-ALL with an emphasis on its origin, genetics, and disease models.

Indexed as

AnimalsDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseHumansInfantMyeloid-Lymphoid Leukemia ProteinNuclear ProteinsOncogene Proteins, FusionPrecursor B-Cell Lymphoblastic Leukemia-LymphomaTranscriptional Elongation FactorsTranslocation, GeneticAFF1 protein, humanDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinNuclear ProteinsOncogene Proteins, FusionTranscriptional Elongation Factors

Identifiers

PMID26463423
PMCPMC4683329
OpenAlexW2302369664

What OpenQuestion holds

Textmetadata
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.