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Through numerous discussions with colleagues it became apparent that the time was right to begin a series of workshop-like meetings on myeloid tumorigenesis. Myeloid tumors are the nonlymphocytic tumors of the hematopoietic system which include tumors of the neutrophilic, monocytic, erythrocytic, basophilic (mast cell) and megakaryocytic lineages. Pioneering studies in myeloid tumorigenesis were initially made in chickens with the discovery of retroviruses that induce various kinds of myeloid tumors acutely (myelocytomatosis, myeloblastosis, and erythroblastosis). These avian retroviruses were subsequently shown to contain the oncogenes v-myb, v-~, v-~, v-erbA, or v-erbB. There have been dramatic advances in studying the pathogenesis of hematopoietic tumors in genetically defined mammalian systems. Many of the well developed model systems in inbred mice, have focused on T- and B-1ymphoma development. Although myeloid tumors have been found in mice, they have not been studied as intensively as lymphoid tumors. Possibly this is because myeloid tumors are less common than lymphoid tumors. Recently, there has been renewed interest in murine myeloid tumor systems. This focus has resulted from 1) the discovery of inbred strains of mice (e. g. BXH-2, AKXD- 23, SJL/J) that are highly susceptible to spontaneous or induced myeloid tumorigenesis; 2) establishment of transplantable murine myeloid tumors (e.
List of contents
I. Classification of myeloid tumors.- The Pathology of Murine Myelogenous Leukemias.- II. Specific Chromosomal Abnormalities in Human and Murine Myeloid Hematologic Malignancies.- Chromosomal Abnormalities in Myeloid Hematologic Malignancies.- Radiation Induced Deletion of Chromosome 2 in Myeloid Leukemogenesis.- III. Disruption of "Oncogenes" by Virus Insertion in Murine Myeloid Tumorigenesis.- Recombinant Inbred Mouse Strains: Models for Studying the Molecular Genetic Basis of Myeloid Tumorigenesis.- Mechanisms in the Transformation of IL3-Dependent Hematopoietic Stem Cells.- Alternate Forms of MYB: Consequences of virus insertion in myeloid tumorigenesis and alternative splicing in normal development.- IV. Myeloid Leukemogensis Induced by Acute Transforming Virus Constructs in In Vitro and In Vivo Model Systems.- Retrovirus-induced Tumors Whose Developemnt is Facilitiated by a Chronic Immune Response: A Comparison of Two Tumors Committed to the Monocytic Lineage.- Studies of Secondary Transforming Events in Murine c-myc Retrovirus-Induced Monocyte Tumors.- Analysis of the Leukaemogenic Properties of the bcr-v-abl and GM-CSF Genes Using a New Retroviral Vector.- Biological effects of retroviral transfection of the murine Interleukin-3 gene into FDCP-Mix cells.- Conversion of Factor-Dependent Myeloid Cells to Factor Independence: Autocrine Stimulation is Not Coincident with Tumorigenicity.- V. Specific Genes Involved in Myeloid Tumorigenesis.- Biosynthesis of Macrophage Colony-Stimulating Factor (CSF-1): Differential Processing of CSF-1 Precursors Suggests Alternative Mechanisms for Stimulating CSF-1 Receptors.- The ets Family of Genes: Molecular Biology & Functional Implications.- VI. Proposed Mechanisms in Myeloid Tumorigenesis.- Adhesive Defects in ChronicMyeloid Leukaemia.- Induction of Leukemia by Avian Myeloblastosis Virus: A Mechanistic Hypothesis.- Role of Biologic Response Modifiers in the Growth and Differentiation of Myeloid Leukemic Cells.
About the author
Michael Potter is Reader in the Philosophy of Mathematics at Cambridge University. He is the author of Sets (OUP, 1990), Reason's Nearest Kin (OUP, 2000), Set Theory and its Philosophy (OUP, 2004), and Mathematical Knowledge (edited with Mary Leng and Alexander Paseau, OUP, 2007).
