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James R. Downing

Researcher at St. Jude Children's Research Hospital

Publications -  349
Citations -  82237

James R. Downing is an academic researcher from St. Jude Children's Research Hospital. The author has contributed to research in topics: Leukemia & Gene. The author has an hindex of 108, co-authored 345 publications receiving 74630 citations. Previous affiliations of James R. Downing include University of Tennessee & National Institutes of Health.

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Molecular classification of cancer: class discovery and class prediction by gene expression monitoring.

TL;DR: A generic approach to cancer classification based on gene expression monitoring by DNA microarrays is described and applied to human acute leukemias as a test case and suggests a general strategy for discovering and predicting cancer classes for other types of cancer, independent of previous biological knowledge.
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MicroRNA expression profiles classify human cancers

TL;DR: A new, bead-based flow cytometric miRNA expression profiling method is used to present a systematic expression analysis of 217 mammalian miRNAs from 334 samples, including multiple human cancers, and finds the miRNA profiles are surprisingly informative, reflecting the developmental lineage and differentiation state of the tumours.
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Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia

Timothy J. Ley, +138 more
TL;DR: It is found that a complex interplay of genetic events contributes to AML pathogenesis in individual patients and the databases from this study are widely available to serve as a foundation for further investigations of AMl pathogenesis, classification, and risk stratification.
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Classification, subtype discovery, and prediction of outcome in pediatric acute lymphoblastic leukemia by gene expression profiling.

TL;DR: Oligonucleotide microarrays used to analyze the pattern of genes expressed in leukemic blasts from 360 pediatric ALL patients identified each of the prognostically important leukemia subtypes, and within some genetic subgroups, expression profiles identified those patients that would eventually fail therapy.
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AML1, the Target of Multiple Chromosomal Translocations in Human Leukemia, Is Essential for Normal Fetal Liver Hematopoiesis

TL;DR: The results suggest that AML1-regulated target genes are essential for definitive hematopoiesis of all lineages, and that this defect was intrinsic to the stem cells in that AMl1-/-ES cells failed to contribute to hematocerosis in chimeric animals.