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Titlebook: Mechanisms in Myeloid Tumorigenesis 1988; Workshop at the Nati Grace L. C. Shen-Ong,Michael Potter,Neal G. Copela Conference proceedings 19

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https://doi.org/10.1007/978-3-642-74623-9cell; classification; pathogenesis; retroviruses; tumor; tumorigenesis; virus
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icial to a broad spectrum of readers ranging from pure and applied mathematicians in electromagnetic field theory to researchers and engineers who are familiar with mathematics. Further, it is also useful as a 978-981-19-0586-5978-981-19-0584-1Series ISSN 0342-4111 Series E-ISSN 1556-1534
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Michael R. Eccles,William R. Baumbach,Gregory D. Schuler,Michael D. Coler teaching the societal, ethical and political implications of digital technologies, particularly from a qualitative perspective. It also has relevance for a wider readership concerned about the influence of so978-981-19-1944-2978-981-19-1942-8
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The Pathology of Murine Myelogenous Leukemiasenesis of phenotype of the particular subtype to which the translocation is associated. The identification and characterization of genes significantly altered by the subtype-specific translocation should yield insight into both 1eukemogenesis and the control of normal differentiation.
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Radiation Induced Deletion of Chromosome 2 in Myeloid Leukemogenesisst to thymic lymphoma incidence being increased by fractionated irradiation. Partial body irradiation (300r) of the upper body (shielding the pelvis and lower extremities) reduced leukemia incidence (11% versus 38% in whole body exposed RF mice) (Upton ., 1958; Upton ., 1966). Males were found to be
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Mechanisms in the Transformation of IL3-Dependent Hematopoietic Stem Cellsgenic stimulation (Lee, and Ihle, 1981b). As a consequence of this immune response there is a dramatic increase in the cells proliferating in response to IL3 . (Lee, and Ihle, 1981) which has been hypothesized to constitute an increased pool of progenitors for transformation.
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Studies of Secondary Transforming Events in Murine , Retrovirus-Induced Monocyte Tumors87). In this tumor an endogenous ecotropic virus has integrated just upstream of the CSF-1 gene, thus activating production of CSF-1. This tumor now grows by an autocrine mechanism. Indeed all of the tumors have aquired a degree of autonomy, and so do not require CSF-1 for growth.
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