An Mll-AF9 fusion gene made by homologous recombination causes acute leukemia in chimeric mice: a method to create fusion oncogenes.
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Summary
This novel use of homologous recombination in embryonal stem cells has been used to produce a fusion oncogene and formally proves that chromosomal translocations contribute to malignancy and provides a general strategy to create fusion oncogenes for studying their role in tumorigenesis.
- Type
- article
- Published
- 1996-06-14
- Cited by
- 555
- References
- 27
- Access
- Open access
- OpenAlex
- https://openalex.org/W1976631985
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:8561019
Keywords
Biology, Fusion gene, Homologous recombination, Chromosomal translocation, Chimeric gene
References
- Isolation of monoclonal antibodies specific for human c-myc proto-oncogene product
- Rescue of the En-1 mutant phenotype by replacement of En-1 with En-2.
- A serine/proline-rich protein is fused to HRX in t(4;11) acute leukemias.
- MLLT3 gene on 9p22 involved in t(9;11) leukemia encodes a serine/proline rich protein homologous to MLLT1 on 19p13.
- Southern blot analysis of ALL-1 rearrangements at chromosome 11q23 in acute leukemia.
- Production of chimeras and genetically defined offspring from targeted ES cells.
- Acute leukemias of different lineages have similar MLL gene fusions encoding related chimeric proteins resulting from chromosomal translocation.
- Rearrangement of the MLL gene in acute lymphoblastic and acute myeloid leukemias with 11q23 chromosomal translocations.
- Transgenic models of tumor development.
- The t(4;11) chromosome translocation of human acute leukemias fuses the ALL-1 gene, related to Drosophila trithorax, to the AF-4 gene.
- Disruption of the proto-oncogene int-2 in mouse embryo-derived stem cells: a general strategy for targeting mutations to non-selectable genes
- Site-directed mutagenesis by gene targeting in mouse embryo-derived stem cells.
- Chromosomal translocations in human cancer
- A site–directed chromosomal translocation induced in embryonic stem cells by Cre-loxP recombination
- Cre-mediated site-specific translocation between nonhomologous mouse chromosomes.
- Introduction of a lacZ reporter gene into the mouse int-2 locus by homologous recombination.
- The oncogenic cysteine-rich LIM domain protein rbtn2 is essential for erythroid development.
- Genes on chromosomes 4, 9, and 19 involved in 11q23 abnormalities in acute leukemia share sequence homology and/or common motifs.
- Molecular basis of IIq23 rearrangements in hematopoietic malignant proliferations
- Analysis of the murine All-1 gene reveals conserved domains with human ALL-1 and identifies a motif shared with DNA methyltransferases.
Cited by
- Expression of a knocked-in AML1-ETO leukemia gene inhibits the establishment of normal definitive hematopoiesis and directly generates dysplastic hematopoietic progenitors.
- dELL, a drosophila homologue of transcription elongation factor ELL (eleven‐nineteen lysine rich leukemia), is required for early development
- Lymphoma‐ and leukemia‐associated chromosomal translocations in healthy individuals
- Myeloproliferative stem cell disorders by deregulated Rap1 activation in SPA-1-deficient mice.
- Transformation of myeloid progenitors by MLL oncoproteins is dependent on Hoxa7 and Hoxa9.
- A murine Mll-AF4 knock-in model results in lymphoid and myeloid deregulation and hematologic malignancy.
- Mouse Chromosome Engineering for Modeling Human Disease
- The relative fitness of hematopoietic progenitors influences leukemia progression
- The AF4.MLL fusion protein is capable of inducing ALL in mice without requirement of MLL.AF4.
- Activation, Regulation and Transcription of the Human and Murine Globin Loci.
- myeloid leukemia Biologic and clinical significance of the FLT3 transcript level in acute
- Novel SH3 protein encoded by the AF3p21 gene is fused to the mixed lineage leukemia protein in a therapy-related leukemia with t(3;11) (p21;q23).
- Growth disturbance in fetal liver hematopoiesis of Mll-mutant mice.
- Mechanisms of MLL Fusion Protein-Mediated Leukemic Transformation
- A new cytokine-dependent monoblastic cell line with t(9;11)(p22;q23) differentiates to macrophages with macrophage colony-stimulating factor (M-CSF) and to osteoclast-like cells with M-CSF and interleukin-4.
- The impact of biology on the treatment of secondary AML.
- Association of germline p53 mutation with MLL segmental jumping translocation in treatment-related leukemia.
- Studying the role of the fusion protein MLL-AF4 in leukemogenesis with the help of siRNAs
- A model to investigate the oncogenic activity of MLL-fusions in Acute Myeloid Leukaemia
- Cell Memory and Cancer – The Story of the Trithorax and Polycomb Group Genes
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