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. 2000 Nov 15;88(4):620-5.
doi: 10.1002/1097-0215(20001115)88:4<620::aid-ijc16>3.0.co;2-z.

Molecular analysis of PTEN and MXI1 in primary bladder carcinoma

D S Wang  1 , K Rieger-Christ, J M Latini, A Moinzadeh, J Stoffel, J A Pezza, K Saini, J A Libertino, I C Summerhayes
Affiliations

Molecular analysis of PTEN and MXI1 in primary bladder carcinoma

D S Wang et al. Int J Cancer. .

Abstract

Loss of heterozygosity (LOH) on 10q is associated with late-stage events in urothelial neoplastic progression. The tumor suppressor gene PTEN, which is mutated or homozygously deleted in numerous cancers, maps to a region of 10q within the reported region of minimal loss in bladder tumors. In two recent studies alterations in the PTEN gene occur at a low frequency in bladder tumors displaying 10q LOH. We have screened 35 late-stage bladder tumors for mutations in PTEN and MXI1, both genes mapping to chromosome 10q. Using single-strand conformation polymorphism analysis, we identified 6 tumors harboring mutations in PTEN and 2 additional tumors displaying homozygous deletion at this locus. No MXI1 mutations were identified within the same tumor panel. Of 16 bladder tumor cell lines analyzed, 2 showed homozygous deletion of PTEN and 3 harbored point mutations resulting in an amino acid change. Two cell lines harbored missense mutations in MXI1. We report a significantly higher frequency of PTEN alterations in bladder carcinoma (23%) than was previously recorded, with no accompanying mutations in the MXI1 gene.

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