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Abstract

Abstract

Inactivating mutations in the tumor-suppressor genes result in tissue overgrowth. This can occur because the mutant tissue either grows faster than wild-type tissue and/or continues to grow beyond a time when wild-type tissue stops growing. There are three general classes of tumor-suppressor genes that regulate the growth of imaginal disc epithelia. Mutations in the hyperplastic tumor-suppressor genes result in increased cell proliferation but do not disrupt normal tissue architecture. These genes include , and components of the pathway. Mutations in a second class of genes, the neoplastic tumor-suppressor genes, disrupt proteins that function either as scaffolds at cell-cell junctions () or as components of the endocytic pathway (, ESCRT components). For the third group, the nonautonomous tumor-suppressor genes, mutant cells stimulate the proliferation of adjacent wild-type cells. Understanding the interactions between these three classes of genes will improve our understanding of how cell and tissue growth are coordinated during organismal development and perturbed in disease states such as cancer.

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/content/journals/10.1146/annurev.genet.39.073003.100738
2006-12-01
2024-06-18
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  • Article Type: Review Article
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