Abandoning apoptosis in favor of selective differentiation has proven a fruitful strategy in the search for AML treatments.
Researchers uncover how the mutated NPM1 gene actually causes acute myeloid leukemia (AML). Their findings pave the way for targeted therapy for this largest subgroup of AMLs.
A clinical trial has demonstrated safety and preliminary evidence of efficacy for a new combination oral drug to treat sickle cell disease.
Cleveland Clinic Cancer Center researchers have identified a genetic alteration that plays a central role in the development of liver cancer and may lead to effective new treatments.
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Three clinical trials test combinations of tetrahydrouridine and decitabine for orally administered, non-cytotoxic, DNMT1-depleting treatment of TP53-mutated solid and liquid cancers.
Tetrahydrouridine renders decitabine orally bioavailable at nontoxic doses in first-in-human trial, safely increasing fetal hemoglobin (HbF) up to twofold in patients with sickle cell disease.
A new combination epigenetic therapy could enhance activity of immune checkpoint inhibitors in lung cancer. A proof-of-concept trial of oral tetrahydrouridine (THU)-decitabine, along with nivolumab, will begin soon at Cleveland Clinic.
Cleveland Clinic researchers are developing a non-toxic method to extend survival and response to 5-azacytidine, decitabine in treatment of myelodysplastic syndromes and acute myeloid leukemia.
Differentiation is the main physiologic control on cell growth and division in metazoa. Noncytotoxic differentiation treatment can spare normal stem cells and circumvent mutational apoptosis defects in cancer cells.
Using a non-cytotoxic concentration of the DNMT1-inhibitor decitabine to treat myelodysplastic syndrome, Cleveland Clinic researchers were able to increase exposure time for DNMT1 depletion to safely and effectively circumvent p53 mutational apoptotic defects, a cause of resistance to standard treatments. Patients had improved blood counts and extended transfusion-free periods.