Publications by authors named "Kevin C Gantz"
We discovered that the survival and growth of many primary acute myeloid leukemia (AML) samples and cell lines, but not normal CD34+ cells, are dependent on SIRT5, a lysine deacylase implicated in regulating multiple metabolic pathways. Dependence on SIRT5 is genotype-agnostic and extends to RAS- and p53-mutated AML. Results were comparable between SIRT5 knockdown and SIRT5 inhibition using NRD167, a potent and selective SIRT5 inhibitor.
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- Myelofibrosis is a serious blood disorder linked to mutations in the JAK/STAT signaling pathway, leading to symptoms that JAK inhibitors can alleviate but do not cure.
- Researchers conducted a study to explore the role of nuclear-cytoplasmic transport (NCT) in myelofibrosis, identifying a potential new therapeutic target using cell lines and mouse models.
- The study found that inhibiting NCT significantly reduced cell viability in myelofibrosis and improved the effects of ruxolitinib, suggesting that NCT could enhance treatment outcomes for patients.
Article Synopsis
- Researchers are investigating how some chronic myeloid leukemia (CML) patients develop resistance to tyrosine kinase inhibitors (TKIs) without mutations in the BCR-ABL1 gene, which is typically associated with this resistance.
- They used a lentiviral shRNA library to target around 5000 cell signaling genes in a CML cell line known for its resistance, identifying key genes that when knocked down, significantly affected cell growth.
- Their findings highlight RAN and XPO1 as important factors in overcoming TKI resistance, suggesting they could be potential targets for enhancing treatment effectiveness in CML patients with BCR-ABL1 kinase-independent resistance.