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May 8, 2026Translational OncologyOpen Access

Mitochondrial RNA helicase DDX28 promotes cell cycle and DNA repair programs and shapes an immunosuppressive microenvironment in acute myeloid leukemia

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Authors

ZWZi WangYLYunli LiuXGXinzhu Guan

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Overview

Randomized trial uncovers DDX28's role in DNA repair and immune suppression in acute myeloid leukemia, suggesting new therapeutic avenues.

Key Points

  • This research aims to evaluate DDX28 as a prognostic biomarker and its role in cell cycle and immune evasion mechanisms in acute myeloid leukemia.
  • Profiled DDX28 expression across AML cohorts using integrated multi-omics resources.
  • Applied functional annotation and pathway analysis to explore the mechanistic role of DDX28.
  • Conducted single-cell RNA-seq to analyze DDX28 distribution in malignant blasts and T cells.
  • High DDX28 expression correlates with inferior survival and increased blast burden.
  • Elevated DDX28 levels are linked to promoter hypomethylation and greater enrichment in cell cycle and DNA repair programs.
  • DDX28 knockdown in HEL cells decreased proliferation and impaired migration and invasion capabilities.

Cite This Study

Wang et al. (2026) studied this question.

synapsesocial.com/papers/69fd7ddcbfa21ec5bbf060d7https://doi.org/10.1016/j.tranon.2026.102766
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