Transcriptional deregulation in hereditary disorders and cancer: the 12th annual CABM symposium, October 21-22, 1998, Piscataway, NJ.
As can be seen from the above descriptions, the presentations at the CABM symposium provided an extraordinarily rich and diverse panorama of some of the most exciting science in current molecular biology. The presentations provided both a general overview and a detailed analysis of multiple biological systems, which despite their specific differences, also generated insights into important common themes. The success of any meeting is most appropriately measured by the kinds of questions that are provoked for future study, not merely by the recitation of past discoveries. In fact, the different presentations often raised highly similar questions for future study. At the most fundamental levels of transcriptional regulation, what are the signals that provide specificity of gene expression? What is the structural basis of specific protein-protein interactions, such as those between homeodomain proteins and beta-catenin-Lef1 interactions, and how are these determinants altered in transcriptional regulation in oncogenesis and in genetic diseases? How is specificity achieved in transcriptional repression, given that the fundamental biochemical reactions often involve modifications of relatively ubiquitous components such as histones? To what extent do changes in specificity of gene activation and repression or in chromosomal architecture mediate the kinds of developmental and oncogenic signals mediated through transcriptional regulators such as Myc, BCL6 and other basic helix-loop-helix proteins and the HMGI proteins? How do altered signaling pathways affect diseases of development and differentiation such as cardiovascular disorders and aging itself? What are the pathways that integrate extracellular signals and transcription during the process of organogenesis? How do fundamental cellular structures such as adhesion junctions, and the interactions of a cell with other cells and extracellular matrix impact on normal and abnormal development and on malignancy, and how do these levels of structure and function alter nuclear regulation of transcription and cell division? These are some of the recurrent questions raised in talk after talk at this symposium, questions that undoubtedly will provide the impetus for important discoveries that will be presented at future CABM symposia.
Rabson
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AB
Center for Advanced Biotechnology and Medicine, Cancer Institute of New Jersey, UMDNJ-Robert Wood Johnson Medical School, Piscataway 08854, USA. rabson@mbcl.rutgers.edu
D000375:Aging / Q000235:genetics; D000818:Animals; D002843:Chromatin / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics; D005786:Gene Expression Regulation; D016259:Genes, myc; D030342:Genetic Diseases, Inborn / Q000235:genetics*; D006128:Growth / Q000235:genetics; D006331:Heart Diseases / Q000235:genetics; D018398:Homeodomain Proteins / Q000235:genetics; D006801:Humans; D009369:Neoplasms / Q000235:genetics*; D000075062:Pre-B-Cell Leukemia Transcription Factor 1; D011518:Proto-Oncogene Proteins / Q000235:genetics; D013698:Templates, Genetic; D014157:Transcription Factors / Q000235:genetics; D014158:Transcription, Genetic; D015533:Transcriptional Activation
D002843:Chromatin; D004268:DNA-Binding Proteins; D018398:Homeodomain Proteins; D000075062:Pre-B-Cell Leukemia Transcription Factor 1; D011518:Proto-Oncogene Proteins; D014157:Transcription Factors; C083400:PBX1 protein, human