Co‐operation between viral oncogenes in avian erythroid and myeloid leukaemia

One of the most striking characteristics of tumours is their uncontrolled growth, suggesting that generation of neoplasms must be intimately linked with control of cell proliferation. During the last ten years, significant progress has been made towards an understanding of the mechanism of tumourigenesis, particularly through the discovery of genes that are involved in the generation of tumours, the so-called oncogenes. Oncogenes were first discovered in the genome of tumourinducing retroviruses known to efficiently cause various types of tumours in animals. These genes, referred to as ‘viral oncogenes’ or ‘u-onc’ genes are, however, not related to genes of non-oncogenic retroviruses, but have been captured from the cellular genome during evolution of these viruses. Oncogene capture can be easily explained through the life cycle of retroviruses, during which the viral genome is integrated into the DNA of the host cell, leading to potential capture and packaging of cellular genetic material into progeny virus by recombination. Certain human tumours (in general these are not caused by retroviruses) also contain oncogenes, which can be transferred to normal cells by transfixtion where they cause uncontrolled growth. Many of the human oncogenes turned out to be identical to oncogenes that had already been known from retroviruses (for reviews see [1,2,3,4]). Thus, one can assume that the mechanisms of tumourigenesis by viral and non-viral oncogenes are rather similar. The 40 to 50 oncogenes known to date are all derived from normal cellular genes, referred to as protooncogenes or ‘c-onc’ genes. Thus genes that can give rise to tumour-inducing oncogenes might constitute only a minute fraction of the c. 1OOOOO genes repre-