Ubiquitous somatic mutations in simple repeated sequences reveal a new mechanism for colonic carcinogenesis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1993-06

AUTHORS

Yurij Ionov, Miguel A. Peinado, Sergei Malkhosyan, Darryl Shibata, Manuel Perucho

ABSTRACT

SPONTANEOUS errors in DNA replication have been suggested to play a significant role in neoplastic transformation and to explain the chromosomal alterations seen in cancer cells1. A defective replication factor could increase the mutation rate in clonal variants arising during tumour progression, but despite intensive efforts, increases in tumour cell mutation rates have not been unambiguously shown2. Here we use an unbiased genomic fingerprinting technique3 to show that 12 per cent of colorectal carcinomas carry somatic deletions in poly(dA . dT) sequences and other simple repeats. We estimate that cells from these tumours can carry more than 100,000 such mutations. Only tumours with affected poly(dA . dT) sequences carry mutations in the other simple repeats examined, and such mutations can be found in all neoplastic regions of multiple tumours from the same patient, including adenomas. Tumours with these mutations show distinctive genotypic and phenotypic features. We conclude that these mutations reflect a previously undescribed form of carcinogenesis in the colon (predisposition to which may be inherited) mediated by a mutation in a DNA replication factor resulting in reduced fidelity for replication or repair (a 'mutator mutation'). More... »

PAGES

558-561

References to SciGraph publications

Journal

TITLE

Nature

ISSUE

6429

VOLUME

363

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/363558a0

    DOI

    http://dx.doi.org/10.1038/363558a0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1043263395

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/8505985


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