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Norah R. McCabe

Researcher at University of Chicago

Publications -  14
Citations -  1934

Norah R. McCabe is an academic researcher from University of Chicago. The author has contributed to research in topics: Chromosomal translocation & Breakpoint. The author has an hindex of 9, co-authored 14 publications receiving 1875 citations.

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Identification of a gene, MLL, that spans the breakpoint in 11q23 translocations associated with human leukemias

TL;DR: This gene MLL (myeloid/lymphoid, or mixed-lineage, leukemia) is named after a transcription unit that spans the breakpoint junctions of the 4;11, 9:11, and 11;19 translocations and two other transcripts that are upregulated in the RS4;11 cell line are described.
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Rearrangement of the MLL Gene in Acute Lymphoblastic and Acute Myeloid Leukemias with 11q23 Chromosomal Translocations

TL;DR: The ability to detect an MLL gene rearrangement rapidly and reliably, especially in patients with limited material for cytogenetic analysis, should make it possible to identify patients who have a poor prognosis and therefore require aggressive chemotherapy or marrow transplantation.
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Rearrangements of the MLL gene in therapy-related acute myeloid leukemia in patients previously treated with agents targeting DNA-topoisomerase II.

TL;DR: The association of exposure to topo II- reactive chemotherapy with 11q23 rearrangements involving the MLL gene in t-AML suggests thatTopo II may play a role in the aberrant recombination events that occur in this region both in AML de novo and in t -AML.
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Identification of the gene associated with the recurring chromosomal translocations t(3;14)(q27;q32) and t(3;22)(q27;q11) in B-cell lymphomas.

TL;DR: The name BCL6 is proposed for this gene, since it is likely to play a role in the pathogenesis of certain B-cell lymphomas and preliminary nucleotide sequencing shows no identity of the cDNA to gene sequences in available data banks.
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Formation of a hyperdiploid karyotype in childhood acute lymphoblastic leukemia.

TL;DR: The results suggest that the hyperdiploid karyotype usually arises by simultaneous gain of chromosomes from a diploidKaryotype during a single abnormal cell division, and occasionally by doubling of chromosomes of near-haploid leukemia in which the chromosomes doubled.