Comment on: Genomics of primary chemoresistance and remission induction failure in paediatric and adult acute myeloid leukaemia

Induction of a Timed Metabolic Collapse to Overcome Cancer Chemoresistance

“…Clonal evolution has been studied particularly well in acute myeloid leukemia (AML), a highly lethal hematopoietic cancer where residual clones persist through therapy and ultimately cause relapse (Ding et al, 2012a). Yet, genetic analysis has provided only limited insight into chemo-therapy resistance commonly observed in AML, and driver mutations are frequently not amenable to targeted therapies (Magee, 2017). We and others have shown that AML cells have distinctive metabolic dependencies compared with their normal counterparts, often irrespective of the driving mutations (Chen et al, 2016;German et al, 2016;Jacque et al, 2015;Lagadinou et al, 2013;Ni et al, 2019;Sykes et al, 2016;Wang et al, 2014).…”

Induction of a Timed Metabolic Collapse to Overcome Cancer Chemoresistance

“…Clonal evolution has been studied particularly well in acute myeloid leukemia (AML), a highly lethal hematopoietic cancer where residual clones persist through therapy and ultimately cause relapse (Ding et al, 2012a). Yet, genetic analysis has provided only limited insight into chemotherapy resistance commonly observed in AML, and driver mutations are frequently not amenable to targeted therapies (Magee, 2017). We and others have shown that AML cells have…”

Induction of a Timed Metabolic Collapse to Overcome Cancer Chemoresistance

“…Clonal evolution has been studied particularly well in acute myeloid leukemia (AML), a highly lethal hematopoietic cancer where residual clones persist through therapy and ultimately cause relapse (Ding et al, 2012a). Yet, genetic analysis has provided only limited insight into chemo-therapy resistance commonly observed in AML, and driver mutations are frequently not amenable to targeted therapies (Magee, 2017). We and others have shown that AML cells have distinctive metabolic dependencies compared with their normal counterparts, often irrespective of the driving mutations (Chen et al, 2016;German et al, 2016;Jacque et al, 2015;Lagadinou et al, 2013;Ni et al, 2019;Sykes et al, 2016;Wang et al, 2014).…”