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'Cancer viruses'have played a paradoxical role in the history of cancer research. Discovered in 1911 by Peyton Rous (1) at the Rockefeller Institute, they were largely ignored for several decades. Witness his eventual recognition for a Nobel Prize, but not until 1966-setting an all time record for latency, and testimony to one more advantage of longevity. In the 1950s, another Rockefeller Nobelist, Wendell Stanley, spearheaded a campaign to focus attention on viruses as etiological agents in cancer, his plat­ form having been the chemical characterization of the tobacco mosaic virus as a pure protein-correction, ribonucleoprotein-in 1935 (2). This doctrine was a centerpiece of the U.S. National Cancer Crusade of 1971: if human cancers were caused by viruses, the central task was to isolate them and prepare vaccines for immunization. At that point, many observers felt that perhaps too much attention was being devoted to cancer viruses. It was problematic whether viruses played an etiological role in more than a handful of human cancers.

Scientists often look askance at their colleagues whose research appears too strongly focused on a single gene or gene product. We are supposed to be interested in the “big picture” and excessive zeal in pursuit of a single pixel might seem to border on an obsession that is likely to yield only details. However as this volume of Current Topics in Microbiology and Immunology demonstrates, this is certainly not the case for myc. Intense study of this en- matic proto-oncogene over the last twenty years has only broadened our view of its functions and led to insights into mechanisms relating to transcriptional regulation as well as to cell growth, proliferation, differentiation, apoptosis and organismal development. The myc gene originally came to light as a retroviral oncogene (v-myc) associated with a wide range of acute neoplasms. It was later shown to be a virally transduced cellular gene (c-myc) which is a member of family of on- genes (c-myc,N-myc,L-myc). These family members are themselves subject to a bewildering assortment of genetic rearrangements associated with many different types of tumors derived from many different types of cells. These rearrangements (including chromosomal translocation, viral integration, and gene ampli?cation) act to uncouple expression of the myc family genes from their normal physiological regulators. The chapter by LIU and LEVENS - scribes the key pathways leading to regulation of myc expression, showing that such regulation occurs at several different levels and through multiple mechanisms.

Hedgehog-GLI Signaling in Human Disease represents the first compilation of up-to-date reviews by top-level scientists in this important field of research. The chapters cover a wide spectrum of related interests, from the molecular bases of morphogen function, to human genetics to cancer research. The aim of the book is to disseminate information on this exciting field, to allow students, scientists and the public in general to gain access current information from research leaders and to provide a book that encompasses different aspects of research showing the fusion of basic research in model systems and medicine. This is a timely primer on how a system of cell communication, Hedgehog-GLI signaling, plays a critical role in human disease and thus provides the background for the development of novel and rational therapies.