A turning point in cancer research: sequencing the human genome.

been made by using model systems of limited complexity, such as cancer cells in vitro and oncogenic viruses. The use of cell cultures avoided the complexity of the whole animal but not the complexity of the animal genome. The use of oncogenic viruses seemed to circumvent this complexity by replacing it with the extraordinary simplicity of the viral genome. This simplicity made the study of viruses very productive. The persistence of the transformed state in a cell clone could be explained by the persistence of the viral genome in cells (1); genetic and molecular results showed that transformation is the consequence of the expression ofone or a few viral genes. Finally, the viral transforming genes, or "oncogenes," and the proteins they specify were identified. The crowning development was the demonstration that in retroviruses the onco-

[1]  P. Duesberg Activated proto-onc genes: sufficient or necessary for cancer? , 1985, Science.

[2]  N. Glaichenhaus,et al.  The roles of individual polyoma virus early proteins in oncogenic transformation , 1982, Nature.

[3]  H. Rubin Cancer as a dynamic developmental disorder. , 1985, Cancer research.

[4]  H. Schreiber,et al.  Identification of a unique tumor-specific antigen as a novel class I major histocompatibility molecule. , 1985, Proceedings of the National Academy of Sciences of the United States of America.

[5]  M. Bogart,et al.  Mechanism of T-cell lymphomagenesis: transformation of growth-factor-dependent T-lymphoblastoma cells to growth-factor-independent T-lymphoma cells. , 1984, Proceedings of the National Academy of Sciences of the United States of America.

[6]  Robert A. Weinberg,et al.  Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes , 1983, Nature.

[7]  H. Pfister Biology and biochemistry of papillomaviruses. , 1984, Reviews of physiology, biochemistry and pharmacology.

[8]  L. Foulds,et al.  The natural history of cancer. , 1958, Journal of chronic diseases.

[9]  E. H. Humphries,et al.  Formation of a transformed follicle is necessary but not sufficient for development of an avian leukosis virus-induced lymphoma. , 1985, Proceedings of the National Academy of Sciences of the United States of America.

[10]  P. Nowell The clonal evolution of tumor cell populations. , 1976, Science.

[11]  J. Bishop Cellular oncogenes and retroviruses. , 1983, Annual review of biochemistry.

[12]  H. Varmus,et al.  Proviral deletions and oncogene base-substitutions in insertionally mutagenized c-myc alleles may contribute to the progression of avian bursal tumors. , 1984, Proceedings of the National Academy of Sciences of the United States of America.

[13]  C. Gélinas,et al.  Tumorigenic activity of polyoma virus and SV40 DNAs in newborn rodents. , 1984, Virology.