Chromosomal rearrangements are key events in cancer and evolution. These chromosomal rearrangements are dependent upon either legitimate, i.e. homologous, or illegitimate recombination of DNA. Recombination – legitimate or illegitimate – is often limited by the number of double-strand breaks (DSBs) in DNA. The number of DSBs in several biological systems is in turn limited by the activity of endogenous endonucleases. All mammalian cells harbor multiple endonucleases, including an important class that are normally kept quiescent but become activated during apoptosis (programmed cell death), either by removal of an inhibitory subunit or by migration out of mitochondria. Commitment to apoptosis need not be absolute; under certain conditions cells can ‘withdrawafter initiating the apoptosis program. We hypothesize that endogenous endonucleases, activated via ‘apoptosis interruptus (AI) in somatic tissue, initiate a portion of chromosomal rearrangements found in cancer. Chromosome rearrangements are also integral to speciation; AI in the germ line could generate gametes with chromosomal rearrangements. AI can be considered as the resolution of a dialectical conflict between individual survival of a cell and survival of the multicellular organism of which the cell is part.

Keywords:
Cancer, Evolution, Double-strand breaks, Apoptosis, DNase, DNA repair, Mutation, Mutagenesis, SOS
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© 2003 S. Karger AG, Basel
2002
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