Associations of AML MRD levels with posttransplant clinical outcomes
Patients with no detectable FLT3 mutations had the best outcomes after an allogenic hematopoietic cell transplant.
List view / Grid view
Patients with no detectable FLT3 mutations had the best outcomes after an allogenic hematopoietic cell transplant.
It was discovered that targeting RAS proteins prevent cancer cells from using different signalling pathways to escape cell death.
Pharmacological concomitant therapies or further genetic improvement of CAR T-cells can increase their effectiveness against TP53-mutant AML cells.
Researchers have created dual-targeted CARs, which performed better than single-targeted CARs in both in vivo and in vitro experiments.
Researchers conducted a proteogenomic characterisation and found that drug exposure changes drug sensitivity.
PLK4 inhibition could be a novel therapeutic for an acute myeloid leukaemia subtype carrying the TP53 mutation.
RBM5 removal from cells meant that HOXA9 mRNA levels were greatly reduced, which could lead to therapies targeting HOXA9-driven leukaemia.
Using shRNA screening enabled researchers to investigate the roles of individual specific factors in maintaining the network found in AML.
Discovery about the NPM1c variant could lead to new drugs targeting the cell growth of acute myeloid leukaemia.
Discovery about the DNA of leukaemia cells suggests promising target for gene therapy in paediatric oncology.
Spanish scientists have developed a new method to identify between cancerous and healthy cells for cases of acute myeloid leukaemia (AML).
US researchers find combination of chloroquine and venetoclax promotes cancer cell death in mouse models with acute myeloid leukaemia (AML).
Here, Dr Michael Leek describes the benefits of gamma-delta T cells for cancer therapy, exploring why they present a potential alternative to other immuno-oncology platforms.
Researchers from the US have identified several new small molecules that can induce mitophagy in leukaemia cells.
Researchers have developed a novel method for enhancing CAR T therapy through a drug combination and cellular engineering that improves the strength and durability of the tumour-killing effect of a CAR T directed against AML.