G
Gerald M. Segal
Researcher at Oregon Health & Science University
Publications - 12
Citations - 3941
Gerald M. Segal is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Haematopoiesis & Granulocyte macrophage colony-stimulating factor. The author has an hindex of 10, co-authored 12 publications receiving 3839 citations. Previous affiliations of Gerald M. Segal include Genetics Institute, Inc..
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Journal ArticleDOI
Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells.
Brian J. Druker,Shu Tamura,Elisabeth Buchdunger,Sayuri Ohno,Gerald M. Segal,Shane Fanning,Jürg Zimmermann,Nicholas B. Lydon +7 more
TL;DR: A compound, designed to inhibit the Abl protein tyrosine kinase, was evaluated for its effects on cells containing the Bcr–Abl fusion protein and it was found that this compound may be useful in the treatment of bcr–abl–positive leukemias.
Journal Article
Interleukin 1 stimulates endothelial cells to release multilineage human colony-stimulating activity.
TL;DR: It is concluded that endothelial cells, in response to IL 1, produce one or more growth factors that probably act on multiple classes of progenitor cells.
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Transient Myeloproliferative Disorder of the Down Type in the Normal Newborn
Derry Ridgway,Gerda I. Benda,Ellen Magenis,L. Allen,Gerald M. Segal,Rita M. Braziel,Robert C. Neerhout +6 more
TL;DR: It is concluded that spontaneous remission of congenital leukemia is not confined to infants with partial or complete systemic trisomy 21 but can occur in genetically normal newborns whose leukemic cells contain a third chromosome 21.
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Analysis of murine megakaryocyte colony size and ploidy: effects of interleukin-3.
TL;DR: The size and ploidy characteristics of day‐5 murine megakaryocyte colonies are structured as continua and that IL‐3 stimulates an increase in mean colony size and numbers without affecting ploidization are concluded.
Journal ArticleDOI
Repression of Fanconi anemia gene (FACC) expression inhibits growth of hematopoietic progenitor cells.
Gerald M. Segal,R E Magenis,Michael G. Brown,Winnie W. Keeble,T D Smith,Michael Heinrich,Grover C. Bagby +6 more
TL;DR: It is concluded that, while the FACC gene product plays a role in defining cellular tolerance to cross-linking agents, it also functions to regulate growth, differentiation, and/or survival of normal hematopoietic progenitor cells.