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[Cancer Research 60, 1683-1689, March 15, 2000]
© 2000 American Association for Cancer Research

Molecular Biology and Genetics

Chromosomal Fragile Site FRA16D and DNA Instability in Cancer1

Marie Mangelsdorf2, Karin Ried2, Erica Woollatt2, Sonia Dayan, Helen Eyre, Merran Finnis, Lynne Hobson, Julie Nancarrow, Deon Venter, Elizabeth Baker and Robert I. Richards3

Department of Cytogenetics and Molecular Genetics, Women’s and Children’s Hospital, Adelaide, South Australia 5006, Australia [M. M., K. R., E. W., S. D., H. E., M. F., L. H., J. N., E. B., R. I. R.]; Peter MacCallum Cancer Institute, East Melbourne, Victoria, Australia [D. V.]; and Department of Genetics, The University of Adelaide, South Australia 5000, Australia [R. I. R.]

It has been proposed that common aphidicolin-inducible fragile sites, in general, predispose to specific chromosomal breakage associated with deletion, amplification, and/or translocation in certain forms of cancer. Although this appears to be the case for the fragile site FRA3B and may be the case for FRA7G, it is not yet clear whether this association is a general property of this class of fragile site. The major aim of the present study was to determine whether the FRA16D chromosomal fragile site locus has a role to play in predisposing DNA sequences within and adjacent to the fragile site to DNA instability (such as deletion or translocation), which could lead to or be associated with neoplasia. We report the localization of FRA16D within a contig of cloned DNA and demonstrate that this fragile site coincides with a region of homozygous deletion in a gastric adenocarcinoma cell line and is bracketed by translocation breakpoints in multiple myeloma, as reported previously (Chesi, M., et al., Blood, 91: 4457–4463, 1998). Therefore, given similar findings at the FRA3B and FRA7G fragile sites, it is likely that common aphidicolin-inducible fragile sites exhibit the general property of localized DNA instability in cancer cells.




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