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Janet Rowley

Researcher at University of Chicago

Publications -  46
Citations -  5527

Janet Rowley is an academic researcher from University of Chicago. The author has contributed to research in topics: Chromosomal translocation & Leukemia. The author has an hindex of 32, co-authored 46 publications receiving 5451 citations. Previous affiliations of Janet Rowley include Energy Research and Development Administration & United States Atomic Energy Commission.

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Clinical and cytogenetic correlations in 63 patients with therapy-related myelodysplastic syndromes and acute nonlymphocytic leukemia: further evidence for characteristic abnormalities of chromosomes no. 5 and 7.

TL;DR: Both t-MDS and t-ANLL are late complications of cytotoxic therapies that have distinctive clinical and histologic features and are associated with characteristic aberrations of chromosomes no. 5 and 7, and it seems likely that these two chromosomes contain genes involved in the pathogenesis of these hematopoietic neoplasms.
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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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Association of an inversion of chromosome 16 with abnormal marrow eosinophils in acute myelomonocytic leukemia. A unique cytogenetic-clinicopathological association

TL;DR: Patients with an inversion of chromosome 16 appear to represent a unique cytogenetic-clinicopathological subtype of acute nonlymphocytic leukemia with a favorable prognosis.
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The t(7;11)(p15;p15) translocation in acute myeloid leukaemia fuses the genes for nucleoporin NUP98 and class I homeoprotein HOXA9.

TL;DR: The t(7;11)(p15;p15) translocation is a recurrent chromosomal abnormality associated primarily with acute myeloid leukaemia (FAB M2 and M4) and the predicted NUP98–HOXA9 fusion protein may promote leukaemogenesis through inhibition of HOXA 9-mediated terminal differentiation and/or aberrant nucleocytoplasmic transport.
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Homozygous deletion of the alpha- and beta 1-interferon genes in human leukemia and derived cell lines

TL;DR: Evidence is presented of the homozygous deletion of the interferon genes in neoplastic hematopoietic cell lines and primary leukemia cells in the presence or absence of chromosomal deletions that are detectable at the level of the light microscope.