Article
Tyrosine kinase inhibitor-induced defects in DNA repair sensitize FLT3(ITD)-positive leukemia cells to PARP1 inhibitors.
Blood - 5 Jul 2018
Maifrede Silvia, Nieborowska-Skorska Margaret, Sullivan-Reed Katherine, Dasgupta Yashodhara, Podszywalow-Bartnicka Paulina, Le Bac Viet, Solecka Martyna, Lian Zhaorui, Belyaeva Elizaveta A, Nersesyan Alina, Machnicki Marcin M, Toma Monika, Chatain Nicolas, Rydzanicz Malgorzata, Zhao Huaqing, Jelinek Jaroslav, Piwocka Katarzyna, Sliwinski Tomasz, Stoklosa Tomasz, Ploski Rafal, Fischer Thomas, Sykes Stephen M, Koschmieder Steffen, Bullinger Lars, Valent Peter, Wasik Mariusz A, Huang Jian, Skorski Tomasz
Abstract excerpt
Mutations in FMS-like tyrosine kinase 3 (FLT3), such as internal tandem duplications (ITDs), can be found in up to 23% of patients with acute myeloid leukemia (AML) and confer a poor prognosis. Current treatment options for FLT3(ITD)-positive AMLs include genotoxic therapy and FLT3 inhibitors (FLT3i's), which are rarely curative. PARP1 inhibitors (PARP1i's) have been successfully applied to induce synthetic...
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