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Mutational spectra: from model systems to cancer-related genes.

Both exogenous and endogenous DNA damage cause mutations. Mutagenic lesions are those that inhibit DNA replication or those that allow replication to proceed with diminished fidelity. As a consequence of their 'bypass' different types of mutations may be introduced: deletions, insertions and point mutations either transitions or transversions. Since the pioneering work of Benzer (1) and Miller [for a review see (2)] it is known that these permanent changes of the genome are the result of the direct interaction of the carcinogen with DNA. Carcinogens induce specific modifications of DNA, DNA-adducts, and their processing into mutations leads to what is known as a mutational spectrum, i.e. to a pattern of mutations that is often unique (in terms of type and sequence) of that specific carcinogen. This knowledge has suggested that the analysis of the site and nature of DNA changes in certain tumours might be useful in identifying the 'cause' of the tumour. However, mutational spectra are 'a many protein affair' (3) and therefore their interpretation is influenced and complicated by a series of factors. First, the analysis of mutations is always biased in some way since it is based on the window of observation of the selective mutation system used. If the detection system monitors the function of a protein mutation analysis will be confined to those genetic alterations that produce a functionally altered gene product. A mutagen will generally introduce a variety of lesions with different mutagenic potential. The primary sequence of the target gene will be one of the factors affecting the site-specificity of the lesion. The cell metabolism reflects another layer of complexity. Mutations will be affected by the efficiency of repair as well as by the replicative bypass efficiency and insertion preference. All these variables should be taken into account when we attempt to go 'from a gene to a carcinogen' (4).