Background: Despite advances in our understanding of the molecular pathogenesis of acute myeloid leukemia (AML), the prognosis remains poor, mainly due to high relapse rates. Therefore, novel treatment strategies are needed to improve therapeutic outcomes for AML patients.
Background: Isocitrate dehydrogenase (IDH) is an essential enzyme in the TCA cycle. Recurrent mutations in IDH1 or IDH2 are prevalent in several cancers, including glioma and acute myeloid leukemia (AML). IDH mutations reduce cellular levels of α-ketoglutarate (α-KG), resulting in accumulation of 2-hydroxyglutarate (2-HG), an α-KG antagonist.
Background: Although virtually all patients (pts) with AML or MDS harbor at least one somatic mutation, a minority of pts possess genetic mutations considered directly targetable by a drug. Moreover, in pts with multiple gene mutations, single-gene/single-drug matching often produces conflicting drug recommendations.
Programmed death-ligand 1 (PD-L1) expression is correlated with objective response rates to PD-1 and PD-L1 immunotherapies.
60% of myelodysplastic syndromes (MDS) patients fail to achieve clinical improvement with hypomethylating agents (HMAs).
Hypomethylating agents (HMAs) (azacitidine (aza), decitabine (dec)) and lenalidomide (len) are approved agents and used to treat patients with myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML).
Cancer networks were used to create predictive computational simulation models of head and neck squamous cell carcinoma (HNSCC) cell lines SCC4, SCC15, and SCC25.
Human β-defensin 3 (HBD3) is present in high concentrations in the oral cavity of individuals with head and neck squamous cell carcinomas (HNSCC).