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

百靈鳥

https://doi.org/10.1007/978-3-642-74623-9cell; classification; pathogenesis; retroviruses; tumor; tumorigenesis; virus

Condescending

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

Manifest

令人悲傷

輕快帶來危險(xiǎn)

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

Truculent

擴(kuò)大

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.

吞吞吐吐

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

柳樹；枯黃

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.

少量

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.