ArticleOncogene2008
Identification of the novel AML1 fusion partner gene, LAF4, a fusion partner of MLL, in childhood T-cell acute lymphoblastic leukemia with t(2;21)(q11;q22) by bubble PCR method for cDNA.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 33 citations in OpenAlex.
- Disruption of the novel nested geneeLife · 2025Article
- RUNX1 interacts with lncRNA SMANTIS to regulate monocytic cell functions.Communications biology · 2024Article
- Molecular heterogeneity in the novel fusion geneOncology letters · 2017Article
- RUNX1 truncation resulting from a cryptic and novel t(6;21)(q25;q22) chromosome translocation in acute myeloid leukemia: A case report.Oncology reports · 2016Article
- Article
- Laf4/Aff3, a gene involved in intellectual disability, is required for cellular migration in the mouse cerebral cortex.PloS one · 2014Article
- Monosomy 13 in metaphase spreads is a predictor of poor long-term outcome after bortezomib plus dexamethasone treatment for relapsed/refractory multiple myeloma.International journal of hematology · 2012Article
- Deregulated transcription factors in leukemia.International journal of hematology · 2011Review
- Possible involvement of RasGRP4 in leukemogenesis.International journal of hematology · 2009Article
- Signatures of selection in fusion transcripts resulting from chromosomal translocations in human cancer.PloS one · 2009Article
- A novel fusion 5'AFF3/3'BCL2 originated from a t(2;18)(q11.2;q21.33) translocation in follicular lymphoma.Oncogene · 2008Article
- Complementing mutations in core binding factor leukemias: from mouse models to clinical applications.Oncogene · 2008Review
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AML1 gene is frequently rearranged by chromosomal translocations in acute leukemia. We identified that the LAF4 gene on 2q11.2-12 was fused to the AML1 gene on 21q22 in a pediatric patient having T-cell acute lymphoblastic leukemia (T-ALL) with t(2;21)(q11;q22) using the bubble PCR method for cDNA. The genomic break points were within intron 7 of AML1 and of LAF4, resulting in the in-frame fusion of exon 7 of AML1 and exon 8 of LAF4. The LAF4 gene is a member of the AF4/FMR2 family and was previously identified as a fusion partner of MLL in B-precursor ALL with t(2;11)(q11;q23), although AML1-LAF4 was in T-ALL. LAF4 is the first gene fused with both AML1 and MLL in acute leukemia. Almost all AML1 translocations except for TEL-AML1 are associated with myeloid leukemia; however, AML1-LAF4 was associated with T-ALL as well as AML1-FGA7 in t(4;21)(q28;q22). These findings provide new insight into the common mechanism of AML1 and MLL fusion proteins in the pathogenesis of ALL. Furthermore, we successfully applied bubble PCR to clone the novel AML1-LAF4 fusion transcript. Bubble PCR is a powerful tool for detecting unknown fusion transcripts as well as genomic fusion points.
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