Yi Lisa Lyu

TL;DR: It is shown that dexrazoxane specifically abolished the DNA damage signal gamma-H2AX induced by doxorubicin, but not camptothecin or hydrogen peroxide, in H9C2 cardiomyocytes, and this results suggest that dex Razoxane antagonizesDoxorubsicin-induced DNA damage through its interference with Top2beta, which could implicate Top2 beta indoxorUBicin cardiotoxicity.

TL;DR: It is shown here that VP-16-induced carcinogenesis involves mainly the β rather than the α isozyme of Top2, suggesting the importance of developing Top2α-specific anticancer drugs for effective chemotherapy without the development of treatment-related secondary malignancies.

TL;DR: The results suggest that many cancer therapeutics induce elevated tumor antigen presentation through MHC I, which could represent a common mechanism for enhanced antitumor immune response through T cell cytotoxicity during metronomic chemotherapy, as well as increased efficacy of combined chemo- (or radio-)/immuno-therapy.

TL;DR: It was shown that VP-16-induced DNA damage signals were attenuated upon proteasome inhibition, suggesting the involvement of proteasomes in the repair/processing of both TopIIα-DNA and TopIIβ-DNA adducts.

TL;DR: The finding of a type IA DNA topoisomerase in mitochondria further supports the notion of a key role of such enzymes in DNA transactions.