ArticleNature communications2021
A human fetal liver-derived infant MLL-AF4 acute lymphoblastic leukemia model reveals a distinct fetal gene expression program.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 49 citations in OpenAlex.
- Developmental timing distinguishes pediatric and adult cancers through retention and rewiring mechanisms.Nature communications · 2026Review
- Characterizing the impact of MLL fusion variants and fusion partners on leukemia plasticity using a human CRISPR-engineered MLL-rearranged leukemia model.Neoplasia (New York, N.Y.) · 2026Article
- A microRNA expression signature in infant t(4;11) KMT2A::AFF1+ BCP-ALL uncovers novel therapeutic targets.HemaSphere · 2026Article
- CSF1R marks a subset of foetal haematopoietic multipotent progenitor cells with acute myeloid leukaemia propagation properties.Leukemia · 2026Article
- SKIDA1 sustains MLL::ENL-expressing hematopoietic progenitors during neonatal stages and promotes B-lineage priming.Blood neoplasia · 2026Article
- Article
- Pediatric leukemia: origins, pathogenesis, the role of microenvironment and immunological modulation.Frontiers in immunology · 2026Review
- Article
- Fetal context conveys heritable protection against MLL-rearranged AML that depends on MLL3.Blood · 2026Article
- Enhancer heterogeneity in acute lymphoblastic leukemia drives differential gene expression in patients.Blood · 2025Article
- PROM1/CD133 marks a proliferative stem cell-like population of blasts in KMT2A rearranged infant ALL.Blood advances · 2025Article
- Ontogeny-specific induction of the KMT2A::AFF1-fusion drives development of a distinct CD24 positive pre-leukemic state.Leukemia · 2025Article
- Transcriptomic characterisation of acute myeloid leukemia cell lines bearing the same t(9;11) driver mutation reveals different molecular signatures.BMC genomics · 2025Article
- Prenatal and Perinatal Factors Associated with Infant Acute Lymphoblastic Leukaemia: A Scoping Review.Cancers · 2025Review
- Developmental interplay between transcriptional alterations and a targetable cytokine signaling dependency in pediatric ETO2::GLIS2 leukemia.Molecular cancer · 2024Article
- Chromatin and aberrant enhancer activity in KMT2A rearranged acute lymphoblastic leukemia.Current opinion in genetics & development · 2024Review
- Functional relevance of circRNA aberrant expression in pediatric acute leukemia with KMT2A::AFF1 fusion.Blood advances · 2024Article
- Genome editing-induced t(4;11) chromosomal translocations model B cell precursor acute lymphoblastic leukemias with KMT2A-AFF1 fusion.The Journal of clinical investigation · 2024Article
- Review
- The human leukemic oncogene MLL-AF4 promotes hyperplastic growth of hematopoietic tissues iniScience · 2023Article
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Authors and funding
20 authors at 3 institutions in 1 country.
Funding
Abstract
Although 90% of children with acute lymphoblastic leukemia (ALL) are now cured, the prognosis for infant-ALL remains dismal. Infant-ALL is usually caused by a single genetic hit that arises in utero: an MLL/KMT2A gene rearrangement (MLL-r). This is sufficient to induce a uniquely aggressive and treatment-refractory leukemia compared to older children. The reasons for disparate outcomes in patients of different ages with identical driver mutations are unknown. Using the most common MLL-r in infant-ALL, MLL-AF4, as a disease model, we show that fetal-specific gene expression programs are maintained in MLL-AF4 infant-ALL but not in MLL-AF4 childhood-ALL. We use CRISPR-Cas9 gene editing of primary human fetal liver hematopoietic cells to produce a t(4;11)/MLL-AF4 translocation, which replicates the clinical features of infant-ALL and drives infant-ALL-specific and fetal-specific gene expression programs. These data support the hypothesis that fetal-specific gene expression programs cooperate with MLL-AF4 to initiate and maintain the distinct biology of infant-ALL.
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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.