Tumor-specific lytic path "hyperploid progression mediated death": Resolving side effects through targeting retinoblastoma or p53 mutant.

ABSTRACT: A major advance was made to reduce the side effects of cancer therapy via the elucidation of the tumor-specific lytic path "hyperploid progression-mediated death" targeting retinoblastoma (Rb) or p53-mutants defective in G1 DNA damage checkpoint. The genetic basis of human cancers was uncovered through the cloning of the tumor suppressor Rb gene. It encodes a nuclear DNA-binding protein whose self-interaction is regulated by cyclin-dependent kinases. A 3D-structure of Rb dimer is shown, confirming its multimeric status. Rb assumes a central role in cell cycle regulation and the "Rb pathway" is universally inactivated in human cancers. Hyperploidy refers to a state in which cells contain one or more extra chromosomes. Hyperploid progression occurs due to continued cell-

SUBMITTER: Hong FU 

PROVIDER: S-EPMC7701912 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature