Comparing venetoclax in combination with hypomethylating agents to hypomethylating agent-based therapies for treatment naive TP53-mutated acute myeloid leukemia: results from the Consortium on Myeloid Malignancies and Neoplastic Diseases (COMMAND)
Talha Badar, Ahmad Nanaa, Ehab Atallah, Rory M. Shallis, Sacchi de Camargo Correia Guilherme, Aaron D. Goldberg, Antoine N. Saliba, Anand Patel, Jan Philipp Bewersdorf, Adam DuVall, Danielle Bradshaw, Yasmin Abaza, Guru Subramanian Guru Murthy, Neil Palmisiano, Amer M. Zeidan, Vamsi Kota, Mark R. Litzow
Abstract
TP53 is a tumor suppressor gene located on the short arm of chromosome 17(p13), known to be involved in multiple cellular processes and regulate cell proliferation by responding to various stress [ 1 , 2 ]. TP53 is a frequently mutated (m) gene found across diverse types of cancers, strongly linked to large structural and complex chromosomal abnormalities [ 3 , 4 ]. It is reported in 5–10% of patients diagnosed with acute myeloid leukemia (AML), more prevalent among the elderly and those with therapy-related AML and/or complex cytogenetics (CG). AML with TP53 mutations is associated with poor prognosis and inferior responses to traditional therapies [ 3 , 4 ].