Human sebaceous tumors harbor inactivating mutations in LEF1
Copyright policy )Human sebaceous tumors harbor inactivating mutations in LEF1
We found that one-third of human sebaceous tumors examined had double-nucleotide substitutions in the same LEF1 allele, irrespective of DNA mismatch repair status. The mutations impaired both LEF1 binding to beta-catenin and transcriptional activation, and are the first tumor-associated mutations that inactivate Wnt signaling. Mutant LEF1 not only inhibited expression of beta-catenin target genes but also stimulated expression of sebocyte markers, suggesting that it may determine the differentiated characteristics of sebaceous tumors.
- University of Massachusetts Medical School United States
- The University of Texas MD Anderson Cancer Center United States
- Cancer Research UK United Kingdom
- Städtisches Klinikum Dessau Germany
- Yamagata University Japan
Adenoma, Genetic Markers, Base Sequence, Sequence Homology, Amino Acid, Transcription, Genetic, Lymphoid Enhancer-Binding Factor 1, Molecular Sequence Data, DNA, Sequence Analysis, DNA, Cell Line, Gene Expression Regulation, Neoplastic, Amino Acid Substitution, Genes, Reporter, Humans, Amino Acid Sequence, Sebaceous Gland Neoplasms, Luciferases, Alleles, Conserved Sequence, Signal Transduction
Adenoma, Genetic Markers, Base Sequence, Sequence Homology, Amino Acid, Transcription, Genetic, Lymphoid Enhancer-Binding Factor 1, Molecular Sequence Data, DNA, Sequence Analysis, DNA, Cell Line, Gene Expression Regulation, Neoplastic, Amino Acid Substitution, Genes, Reporter, Humans, Amino Acid Sequence, Sebaceous Gland Neoplasms, Luciferases, Alleles, Conserved Sequence, Signal Transduction
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