BCL-XL drives fibrotic and leukemic progression in myeloproliferative neoplasms - Takeaways - MDSpire

BCL-XL drives fibrotic and leukemic progression in myeloproliferative neoplasms

  • By

  • Chunyan Wu

  • Yiting Wang

  • Quanchao Zhang

  • Chan Li

  • Yuanzhong Chen

  • Yong Wu

  • June 2, 2026

  • 0 min

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  • 1

    BCL-XL is significantly upregulated in myeloproliferative neoplasms (MPNs), contributing to apoptosis resistance and fibrotic progression.

  • 2

    Bone marrow mesenchymal stromal cells from MPN patients exhibit a myofibroblast-like phenotype, promoting fibrosis through increased α-SMA and fibronectin expression.

  • 3

    Inhibition of BCL-XL with ABT-263 selectively induces apoptosis in PMF-derived MSCs and reduces their profibrotic characteristics.

  • 4

    Combined targeting of BCL-XL and JAK2 results in synergistic antifibrotic and pro-apoptotic effects in MPN and acute myeloid leukemia cells.

  • 5

    These findings suggest that BCL-XL is a key mediator of MPN-associated fibrosis and therapeutic resistance, highlighting its potential as a treatment target.

Original Source(s)

BCL-XL drives fibrotic and leukemic progression in myeloproliferative neoplasms

  • by Chunyan Wu, Yiting Wang, Quanchao Zhang, Chan Li, Yuanzhong Chen, Yong Wu

  • June 2, 2026

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