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Carcinogenesis, Vol. 23, No. 5, 727-734, May 2002
© 2002 Oxford University Press

CANCER BIOLOGY

Unbalanced overexpression of the mutant allele in murine Patched mutants

Julia Calzada-Wack1,2,*, Roland Kappler1,2,5,*, Udo Schnitzbauer1,2, Thomas Richter1, Michaela Nathrath1, Michael Rosemann2, Stephan N. Wagner3, Rüdiger Hein4 and Heidi Hahn1,2,5,6

1 Institute of Pathology, Technical University Munich, Munich,
2 Institute of Pathology, GSF-National Research Center of Environment and Health, Neuherberg,
3 Department of Dermatology, University of Essen, Essen and
4 Department of Dermatology, Technical University of Munich, Munich, Federal Republic of Germany

Inherited mutations of Patched (PTCH) in the nevoid basal cell carcinoma syndrome (NBCCS) lead to several developmental defects and contribute to tumor formation in a variety of tissues. PTCH mutations have been also identified in sporadic tumors associated with NBCCS including basal cell carcinoma (BCC) and medulloblastoma. Mice heterozygous for Ptch recapitulate the typical developmental symptoms of NBCCS and develop rhabdomyosarcoma (RMS) and medulloblastoma. PTCH is assumed to act as a tumor suppressor gene although inactivation of both alleles has been demonstrated only in a fraction of tumors. We have investigated the status of Ptch in RMS of heterozygous Ptch neo67/+ mice. Although the wild-type Ptch allele was retained in tumor tissue, the high levels of Ptch mRNA in these tumors result from overexpression of the mutant Ptch transcript. Our results suggest that the wild-type Ptch allele might be selectively silenced in RMS tissue or, alternatively, that haploinsufficiency of Ptch is sufficient to promote RMS formation in mice.


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