A Matter of Dosage
- 25 October 2002
- journal article
- perspective
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 298 (5594) , 761-763
- https://doi.org/10.1126/science.1077707
Abstract
The canonical hypothesis of tumorigenesis is Knudson9s two-hit model, which stipulates that both alleles of a tumor suppressor gene must be inactivated for tumors to form. In their Perspective, Fodde and Smits discuss new work revealing that this model may not hold for a subgroup of tumor suppressor genes. Inactivation of only one allele of these tumor suppressor genes is sufficient, either on its own or in combination with other deleterious events, to cause tumor formation.Keywords
This publication has 16 references indexed in Scilit:
- BLM Heterozygosity and the Risk of Colorectal CancerScience, 2002
- Enhanced Tumor Formation in Mice Heterozygous for Blm MutationScience, 2002
- Mice heterozygous for mutation in Atm, the gene involved in ataxia-telangiectasia, have heightened susceptibility to cancerNature Genetics, 2002
- Biallelic Inactivation of BRCA2 in Fanconi AnemiaScience, 2002
- Neurofibromas in NF1: Schwann Cell Origin and Role of Tumor EnvironmentScience, 2002
- Low-penetrance susceptibility to breast cancer due to CHEK2*1100delC in noncarriers of BRCA1 or BRCA2 mutationsNature Genetics, 2002
- Dmp1 is haplo-insufficient for tumor suppression and modifies the frequencies of Arf and p53 mutations in Myc-induced lymphomasGenes & Development, 2001
- Evidence that haploinsufficiency ofPtch leads to medulloblastoma in miceGenes, Chromosomes and Cancer, 2000
- Retention of wild-type p53 in tumors from p53 heterozygous mice: reduction of p53 dosage can promote cancer formationThe EMBO Journal, 1998
- Mutation and Cancer: Statistical Study of RetinoblastomaProceedings of the National Academy of Sciences, 1971