C Myc In B Cell Neoplasia

The papers in this book were presented at the 14th Mechanisms in B-cell Neoplasia meeting that was held in Bethesda, Maryland October 21-23, 1996. In 1995 the organizers decided that the format of the meeting would be changed and that specific topics relevant to B-cell neoplasia would be discussed. This year's topic is on the c-myc oncogene in B-cell neoplasia which has been discussed in virtually every previous meeting. Some of the presentations announced for the first time dramatic advances in our understanding of c-myc and because this subject has become highly complex it was thought that devoting the whole meeting to this theme would be appropriate. The book, therefore, repre sents a review of many aspects of the myc problem but by no means is truly comprehensive. In a recent Medline search there were 8,505 references to myc, fully illustrating the magnitude of the interest and depth of this field. The organizers of the meeting have each contributed review chapters that summarize different aspects of the meeting. We thank the National Cancer Institute for sponsoring this workshop and the staff of Cygnus, Inc. , for their outstanding organizational assistance. The organizers are most grateful to Vickie Rogers for assembling the book and dealing with the edi torialization of the manuscripts. MICHAEL POlTER FRITZ MELCHERS Table of Contents M. POlTER and K. B. MARCU The c-myc Story: Where We've Been, Where We Seem to be Going. With 2 Figures . . . . . . . . . . . . . . . . . . . . . . . . I F.

The papers in this book were presented at the 6th Workshop on Mechanisms in B-Cell Neoplasia, held in Bethesda, March 23-25, 1988. On alternate years this meeting is sponsored by the . ;. Basel Institute of Immunology in Basel, Switzerland and by the National Cancer Institute in Bethesda, and is attended by 100 to 150 parti cipants. This 6th workshop, like the preceding five, was characterized by intense and enthusiastic discussion which reflects, we think, the exciting growth and development of this field. It is quite clear, however, that despite many general advances an understanding of the precise underlying mechanisms in B-cell tumor development is not yet defined. Probably, there is no single mechanism for all the various forms of B-cell neo plastic development. Many different forms of B-cell neoplasms are known, and these are distinguished by several characteristics: 1) the stage of development attained by the tumor stem cells; 2) mode of growth (slow or fast); 3) association with natural or inductive etiologic agents and 4) specific and consistent mutational mechanisms such as retroviral insertion, chromosomal rearrangement. Those charac teristic forms which arise naturally in relatively high frequency or those tumors with hallmark properties which can be induced consistently are the models most frequently studied, e. g. , endemic Burkitt's lymphoma, follicular lymphoma, acute and chronic lymphocytic leukemia and mUltiple myeloma in man; bursal lymphoma in chickens; Abelson virus induced pre B cell lymphomas and plasmacytomas in mice and immunocytomas in rats. Each model system, has special problems and advantages.

The eighth workshop in this series on Mechanisms in B-Cell Neoplasia 1990 was held in Wilson Hall at the National Institutes of Health, Bethesda, Maryland on March 28-30. Five major topics formed the basis for the discussions: 1) progress in experimental models of B-cell tumorigenesis, 2) the role of IL-6 in plasma cell tumor formation with particular emphasis on human myeloma, 3) immortaliza tion and regulation of mitosis in B-cells, 4) the mYQ gene in B-cell neoplasia, and 5) the role of EBV and other oncogenes in transforma tion of human B-Iymphocytes. A meeting on the Epidemiology of Myeloma was held at the N. I. H. on the preceding day, and many of those interested in the clinical aspects of myeloma were also participants at the workshop. Experimental Models of B-Cell Tumor Development We have seen in the last eight years the steady growth of model experimental systems, many of which have been designed to be counter parts of the major forms of human B cell tumors, e. g. , follicular lymphomas, Burkitt's lymphomas, acute B-cell leukemia and multiple myeloma. A variety of novel ways of inducing these tumors has been described. Advantage has been taken of the "experiments in nature" to identify critical genes that playa role in tumor pathogenesis. These genes have been identified by being near to viral insertion and chromosomal translocation sites, or by having been incorporated or transduced into a defective transforming retrovirus.

The 12th Workshop on "Mechanisms in B-Cell Neoplasia" continues this series of meetings on intriguing new developments in human and experimental B-cell tumors. The integration of knowledge from basic B-cell biology to the clinical problems of multiple myelomas, follicular lymphoma, mantle cell lymphoma and B-CLL present the challenges that were discussed in the meeting. The discussion focusses on: - Cellular components of the "myeloma clone" - Genomic instability in B-cells and B-cell tumors - The CD5 antigen and B1 cells - Regulation of cell cycle and apoptosis - Role of IL-6, BCL-2, BCL-1, myc in B-cell development.

Normal and Malignant B-Cell is a collection of harmonious chapters contributed by different authors. This book sets out to describe the B-cell during different stages of ontogeny and the molecular mechanisms of its antigen receptor diversity. It also discusses the main clinical and etiopathogenic aspects when it is transformed into a malignant cell. The book will be interesting and useful for clinicians, biologists, researchers, teachers, and graduate students of both doctoral and master's degrees in the field of immunology.