ReviewGenes2025
Germline and Somatic Changes Associated with the Development of Inherited and De Novo Pediatric Acute Myeloid Leukemia.
Review in Genes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Gilteritinib and chemotherapy in children with relapsed/refractory FLT3-ITD AML: results from the phase 1/2 SKIPPER trial.Blood advances · 2026Trial
- Precision Pediatric Cancer Nanomedicine: Advancing Personalized Nano Therapies to Reduce Non-Communicable Diseases Through AI-Driven 3D-Printed Drugs.International journal of nanomedicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) accounts for only about 15-20% of pediatric leukemia and an overall incidence of 1.4 cases per 200,000 children under the age of 15 years. The majority of pediatric AML occurs de novo, often as the result of somatic first hits in utero. A minority of pediatric AML occurs in response to a predisposition syndrome, such as a bone marrow failure syndrome, or other inherited mutations and copy number changes. While the overall survival of pediatric patients with AML is approximately 70%, survival at the individual level is dependent on the abnormality detected either through cytogenomic analyses or sequencing for mutations in responsible genes. Indeed, de novo infant AML carries a more sobering prognosis than that of pediatric AML. This review describes many of the common genomic abnormalities associated with pediatric AML and characterizes their detection from a laboratory assessment perspective. Pediatric AML is primarily a disease of gene rearrangements rather than of gene mutations, and, as such, clinical cytogenetics takes a primary role.
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Registered trials
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.