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- W4246994048 abstract "Retinoblastoma is the most common ocular cancer of children. Several years ago, Knudson noted that the incidence of retinoblastoma followed a statistical pattern of inheritance suggesting the acquisition of two mutations [1]. He proposed the ‘‘twohit’’ mutation hypothesis as a mechanism of at least initially developing this form of cancer. Comings elaborated on this model shortly thereafter and proposed that the two mutations were actually affecting the two alleles of the same gene [2]. This theory lead to the concept of tumor suppressor proteins and ultimately to the cloning of the retinoblastoma susceptibility gene (Rb1) and the characterization of its protein product (pRB) [3-5]. Mutations in both alleles of the Rb1 gene that lead to protein dysfunction, improper expression, or loss of heterozygosity have been identified in all human retinoblastomas to date." @default.
- W4246994048 created "2022-05-12" @default.
- W4246994048 date "2003-08-26" @default.
- W4246994048 modified "2023-10-14" @default.
- W4246994048 title "p53 and the Molecular Regulation of Cell Fate in Retinoblastoma" @default.
- W4246994048 doi "https://doi.org/10.1201/b14820-13" @default.
- W4246994048 hasPublicationYear "2003" @default.
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