Comparison of cytogenetics, Southern blotting, and fluorescence in situ hybridization as methods for detecting MLL gene rearrangements in children with acute leukemia and with 11q23 abnormalities

No abstract is available for this paper.

• Publication year

  1999

• Venue

  Leukemia

• Publication date

  1999-11-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1038/sj.leu.2401512PMID 10557043
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Detection of genomic changes in cancer byin situ hybridization

  2004cited by this paper
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  1999cited by this paper
• No evidence for MLL/AF4 expression in normal cord blood samples.

  1999cited by this paper
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  1998cited by this paper
• The t(6;11)(q27;q23) translocation in acute leukemia: a laboratory and clinical study of 30 cases

  1998cited by this paper
• The translocations, t(11;19)(q23;p13.1) and t(11;19)(q23;p13.3): a cytogenetic and clinical profile of 53 patients

  1998cited by this paper
• Partial tandem duplications of the MLL gene are detectable in peripheral blood and bone marrow of nearly all healthy donors.

  1998cited by this paper
• t(11;22)(q23;q11.2) In acute myeloid leukemia of infant twins fuses MLL with hCDCrel, a cell division cycle gene in the genomic region of deletion in DiGeorge and velocardiofacial syndromes.

  1998cited by this paper
• Hematological malignancies with a deletion of 11q23: cytogenetic and clinical aspects

  1998cited by this paper
• Rearrangement of ALL1 (MLL) in acute myeloid leukemia with normal cytogenetics.

  1998cited by this paper
• The t(10;11)(p12;q23) translocation in acute leukaemia: a cytogenetic and clinical study of 20 patients

  1998cited by this paper
• What significance should we attribute to the detection of MLL fusion transcripts?

  1998cited by this paper
• 2 ) in acute myeloid leukemia of infant twins fuses MLL with hCDC rel , a cell division cycle gene in the genomic region of deletion in DiGeorge and velocardiofacial syndromes

  1998cited by this paper
• Ten novel 11q23 chromosomal partner sites. European 11q23 Workshop participants.

  1998cited by this paper
• MLL is fused to CBP, a histone acetyltransferase, in therapy-related acute myeloid leukemia with a t(11;16)(q23;p13.3).

  1997cited by this paper
• Partial duplication of the MLL gene in acute myelogenous leukemia without karyotypic aberration.

  1997cited by this paper
• EEN encodes for a member of a new family of proteins containing an Src homology 3 domain and is the third gene located on chromosome 19p13 that fuses to MLL in human leukemia.

  1997cited by this paper
• AF6q21, a novel partner of the MLL gene in t(6;11)(q21;q23), defines a forkhead transcriptional factor subfamily.

  1997cited by this paper
• The t(11;16)(q23;p13) translocation in myelodysplastic syndrome fuses the MLL gene to the CBP gene.

  1997cited by this paper
• Genetic studies of childhood acute lymphoblastic leukemia with emphasis on p16, MLL, and ETV6 gene abnormalities: results of St Jude Total Therapy Study XII

  1997cited by this paper
• Incidence and characterization of MLL gene (11q23) rearrangements in acute myeloid leukemia M1 and M5.

  1996cited by this paper
• Catalog of Chromosome Aberrations in Cancer

  1996cited by this paper
• Molecular rearrangement of the MLL gene in adult acute myeloid leukemia without cytogenetic evidence of 11q23 aberration.

  1996cited by this paper
• Prognostic factors in the acute lymphoid and myeloid leukemias of infants.

  1996cited by this paper
• Infant leukaemia biology, aetiology and treatment.

  1996cited by this paper
• Rearrangement of the MLL gene confers a poor prognosis in childhood acute lymphoblastic leukemia, regardless of presenting age.

  1996cited by this paper
• Acute lymphoblastic leukemias with deletion of 11q23 or a novel inversion (11)(p13q23) lack MLL gene rearrangements and have favorable clinical features.

  1995cited by this paper
• Detection of 11q23/MLL rearrangements in infant leukemias with fluorescence in situ hybridization and molecular analysis.

  1995cited by this paper
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  1995cited by this paper
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  1995cited by this paper
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  1995cited by this paper
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  1995cited by this paper
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  1995cited by this paper
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  1994cited by this paper
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  1994cited by this paper
• ALL-1 partial duplication in acute leukemia.

  1994cited by this paper
• Cloning of ELL, a gene that fuses to MLL in a t(11;19)(q23;p13.1) in acute myeloid leukemia.

  1994cited by this paper
• Prevalence and clinical correlations of MLL gene rearrangements in AML-M4/5.

  1994cited by this paper
• ALL-1 tandem duplication in acute myeloid leukemia with a normal karyotype involves homologous recombination between Alu elements.

  1994cited by this paper
• A novel gene, AF-1p, fused to HRX in t(1;11)(p32;q23), is not related to AF-4, AF-9 nor ENL.

  1994cited by this paper
• Molecular rearrangement of the ALL-1 gene in acute myeloid leukemia without cytogenetic evidence of 11q23 chromosomal translocations.

  1994cited by this paper
• A reverse transcriptase-polymerase chain reaction detects heterogeneous chimeric mRNAs in leukemias with 11q23 abnormalities.

  1994cited by this paper
• Cytogenetic features of infants less than 12 months of age at diagnosis of acute lymphoblastic leukemia: impact of the 11q23 breakpoint on outcome: a report of the Childrens Cancer Group.

  1994cited by this paper
• ENL, the gene fused with HRX in t(11;19) leukemias, encodes a nuclear protein with transcriptional activation potential in lymphoid and myeloid cells.

  1994cited by this paper
• 11q23/MLL rearrangement confers a poor prognosis in infants with acute lymphoblastic leukemia.

  1994cited by this paper
• Molecular rearrangements of the MLL gene are present in most cases of infant acute myeloid leukemia and are strongly correlated with monocytic or myelomonocytic phenotypes.

  1994cited by this paper
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  1993cited by this paper
• Current status of cytogenetic research in childhood acute lymphoblastic leukemia.

  1993cited by this paper
• Molecular rearrangements on chromosome 11q23 predominate in infant acute lymphoblastic leukemia and are associated with specific biologic variables and poor outcome.

  1993cited by this paper
• A novel translocation, t(9;11)(q33;q23) involving the HRX gene in an acute monocytic leukemia.

  1993cited by this paper
• ALL-1 gene at chromosome 11q23 is consistently altered in acute leukemia of early infancy.

  1993cited by this paper
• Rearrangement of the MLL gene in acute lymphoblastic and acute myeloid leukemias with 11q23 chromosomal translocations.

  1993cited by this paper
• Genes on chromosomes 4, 9, and 19 involved in 11q23 abnormalities in acute leukemia share sequence homology and/or common motifs.

  1993cited by this paper
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  1993cited by this paper
• Acute leukemias of different lineages have similar MLL gene fusions encoding related chimeric proteins resulting from chromosomal translocation.

  1993cited by this paper
• Characterization of two 11q23.3–11q24 deletions and mapping of associated anonymous DNA markers

  1993cited by this paper
• Heterogeneity of breakpoints of 11q23 rearrangements in hematologic malignancies identified with fluorescence in situ hybridization.

  1993cited by this paper
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  1993cited by this paper
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  1993cited by this paper
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  1993cited by this paper
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  1992cited by this paper
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  1992cited by this paper
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  1991cited by this paper
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  1991cited by this paper
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  1990cited by this paper
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  1990cited by this paper
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  1988cited by this paper
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  1987cited by this paper
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  1985cited by this paper
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  1984cited by this paper
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  1982cited by this paper

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  2007cites this paper
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  2007cites this paper
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  2005cites this paper
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