Can chromosomal instability initiate tumorigenesis?

Franziska Michor, Yoh Iwasa, Bert Vogelstein, Christoph Lengauer, Martin A. Nowak

Research output: Contribution to journalReview articlepeer-review

147 Citations (Scopus)


Cancers result from the accumulation of inherited and somatic mutations in oncogenes and tumor suppressor genes. These genes encode proteins that function in growth regulatory and differentiation pathways. Mutations in those genes increase the net reproductive rate of cells. Chromosomal instability (CIN) is a feature of most human cancers. Mutations in CIN genes increase the rate at which whole chromosomes or large parts of chromosomes are lost or gained during cell division. CIN causes an imbalance in chromosome number (aneuploidy) and an enhanced rate of loss of heterozygosity, which is an important mechanism of inactivating tumor suppressor genes. A crucial question of cancer biology is whether CIN is an early event and thus a driving force of tumorigenesis. Here we discuss mathematical models of situations where inactivation of one or two tumor suppressor genes is required for tumorigenesis. If two tumor suppressor genes have to be inactivated in rate-limiting steps, then CIN is likely to emerge before the inactivation of the first tumor suppressor gene.

Original languageEnglish
Pages (from-to)43-49
Number of pages7
JournalSeminars in Cancer Biology
Issue number1
Publication statusPublished - Feb 2005

All Science Journal Classification (ASJC) codes

  • Cancer Research


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