Data from a preclinical study suggest rethinking the "oncometabolite hypothesis," which calls for blocking the product of neomorphic IDH1/2 mutations to halt tumor progression. Instead, exploiting the vulnerability of IDH1/2-mutant tumor cells to PARP inhibition, as a result of defective DNA repair, appears to be a more effective strategy that will soon be tested in the clinic.
from Cancer via ola Kala on Inoreader http://ift.tt/2qMDBb0
via IFTTT
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου