Publications by authors named "T S Nechiporuk"
Article Synopsis
- Emerging research highlights how factors in the leukemia microenvironment protect cancer cells from treatments and contribute to drug resistance, signaling the need for targeted therapies in acute myeloid leukemia (AML).
- A study involving around 300 AML patient samples found that higher levels of the cytokine CCL2 correlate with reduced effectiveness of MEK inhibitors, leading to further investigations into the mechanisms behind this resistance.
- The findings suggest that targeting both CCL2 and the MEK pathway can improve treatment responses in AML, proposing a combination therapy as a promising strategy to overcome drug resistance and enhance patient outcomes.
Article Synopsis
- Venetoclax, when combined with azacytidine, shows promise in treating acute myeloid leukemia (AML), but some patients develop resistance, which can limit the treatment's effectiveness.
- Researchers tested 25 different drug combinations with venetoclax on AML patient samples to discover which combinations might work better than the standard venetoclax + azacytidine approach.
- By analyzing tumor cell states and incorporating clinical features, the study identified new drug combinations that could be more effective for certain patient subtypes, paving the way for personalized treatment strategies in AML.
Article Synopsis
- * CG-806 (luxeptinib) is a promising dual BTK/SYK inhibitor that has shown effectiveness in preclinical trials, killing MCL cells and overcoming resistance seen with ibrutinib by suppressing anti-apoptotic proteins.
- * In studies, CG-806 improved survival rates in certain MCL models, revealing that understanding the Bcl-2 network and combining it with other treatments could enhance drug efficacy, making it a focus for future cancer therapy research. *
To understand mechanisms of response to BET inhibitors (BETi), we mined the Beat AML functional genomic dataset and performed genome-wide CRISPR screens on BETi- sensitive and BETi- resistant AML cells. Both strategies revealed regulators of monocytic differentiation, SPI1, JUNB, FOS, and aryl-hydrocarbon receptor signaling (AHR/ARNT), as determinants of BETi response. AHR activation synergized with BETi while inhibition antagonized BETi-mediated cytotoxicity.
View Article and Find Full Text PDFOur study details the stepwise evolution of gilteritinib resistance in FLT3-mutated acute myeloid leukemia (AML). Early resistance is mediated by the bone marrow microenvironment, which protects residual leukemia cells. Over time, leukemia cells evolve intrinsic mechanisms of resistance, or late resistance.
View Article and Find Full Text PDF