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7 items found for " Keywords: AML"
Posts (1)
- 📰 GPCR Weekly News, September 11 to 17, 2023
study of sorafenib added to cladribine, high-dose cytarabine, G-CSF, and mitoxantrone in untreated AML
Other Pages (6)
- Activation of orphan receptor GPR132 induces cell differentiation in acute myeloid leukemia
Abstract Blocked cellular differentiation is a critical pathologic hallmark of acute myeloid leukemia (AML showed that genetic activation of the orphan GPCR GPR132 significantly induced cell differentiation of AML Notably, GPR132 activation by 8GL promoted differentiation and reduced colony formation in human AML We further showed that the combination of 8GL and an mTOR inhibitor synergistically elicited AML cell activation of orphan GPR132 represents a potential strategy for inducing myeloid differentiation in AML
- Spliceosome mutations are associated with clinical response in a phase 1b/2 study of the PLK1 inhibitor onvansertib in combination with decitabine in relapsed or refractory acute myeloid leukemia
leukemia Published date November 1, 2023 Abstract "PLK1 is overexpressed in acute myeloid leukemia (AML decitabine (DAC) demonstrated initial safety and efficacy in patients with relapsed/refractory (R/R) AML The current study aimed to identify molecular predictors of response to ONV + DAC in R/R AML patients A total of 44 R/R AML patients were treated with ONV + DAC and considered evaluable for efficacy. Maya Ridinger , Pamela S Becker , Tara L Lin , Sandra L Silberman , Eunice S Wang , Amer M Zeidan Tags AML
- Mutation Patterns Predict Drug Sensitivity in Acute Myeloid Leukemia
date June 14, 2024 Abstract " Purpose: The inherent genetic heterogeneity of acute myeloid leukemia (AML drug screening, and single-cell genomic profiling on leukemia cell samples derived from patients with AML at the individual cell level, highlighting the presence of distinct subclones within patients with AML highlights the importance of considering the gene mutation patterns for the prediction of drug response in AML It provides a framework for categorizing patients with AML by mutations that enable drug sensitivity