Functional analysis demonstrates that DHX15R222G cooperates with AML1-ETO fusion protein to enhance AML leukemia stem cell (LSC) activity and promote resistance to standard chemotherapy, and underscores the pivotal role of oncogenic DHX15 mutations in regulating AML LSC activity.
Acute myeloid leukemia (AML) is defined by epigenetic heterogeneity, and recurrent mutations in chromatin remodelers are associated with a poor prognosis. Whether these mutations drive treatment resistance through remodeling of the tumor immune microenvironment remains unclear. ARID1B, a recurrently mutated SWI/SNF sub...
Wan-Xiu Mao, Jia-Yi Cui, Hanqi Su et al.· International Immunopharmaco...· 0 citations
Chromosomal translocations produce oncogenic fusion proteins such as AML1-ETO, which predominantly occupy gene promoters to induce transcriptional reprogramming in leukemia stem cells (LSCs), consequently driving the pathogenesis of t(8;21) acute myeloid leukemia (AML). However, whether AML1-ETO is recruited to additio...
Shuyi Li, Shu-Jiao He, Yongwei Su et al.· Proceedings of the National...· 0 citations
PTBP1 is established as a critical regulator of AML cell fitness and a clinically actionable therapeutic combination that exploits AML dependency on PTBP1-CDC42 signaling to enhance the efficacy of venetoclax-based regimens is identified.
Acute myeloid leukemia (AML) cells rely heavily on mitochondrial oxidative phosphorylation (OXPHOS) for energy, making mitochondrial function a promising therapeutic target. TCF12, a transcription factor belonging to the basic helix-loop-helix (bHLH) family, has been implicated in various cancers and is highly expresse...
The data support the development of the MYC/GSPT1 degrader GT19630 as a therapeutic strategy of MYC-driven hematologic malignancies as a therapeutic strategy of therapy-resistant hematologic malignancies.
Yuki Nishida, Valeria Impedovo, Edward Ayoub et al.· Blood· 0 citations