Alternative lengthening of telomeres renders cancer cells hypersensitive to ATR inhibitors

Abstract

Cancer's alternative means to an end To stay alive and proliferating, tumor cells must maintain their telomeres: the DNA sequences at the ends of chromosomes. The majority accomplish this by activating the enzyme telomerase. However, certain tumor types favor a different mechanism called alternative lengthening of telomeres (ALT), which involves DNA recombination. Flynn et al. delineated the molecular events that occur at the telomeres of ALT-proficient tumor cells by studying the function of a protein that is altered by mutation in these tumors. The analysis revealed a specific protein kinase that is essential for ALT, which could in principle be targeted to halt tumor growth. Science , this issue p. 273