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Peer-reviewedCC BY 4.0Molecular Oncology

PANoptosis in the pathogenesis of myelodysplastic syndromes

  • Rohit Thalla1,2
  • Jyoti Lamichhane1,2
  • Cameron Lewis1,2
  • Peter Breslin1,2,3
  • Jiwang Zhang1,2
  1. 1Oncology Institute, Cardinal Bernardin Cancer Center Loyola University Chicago Medical Center Maywood IL USA
  2. 2Department of Cancer Biology Loyola University Chicago Medical Center Maywood IL USA
  3. 3Departments of Biology and Molecular/Cellular Physiology Loyola University Chicago Maywood IL USA
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Abstract

Myelodysplastic syndromes (MDS) are a heterogeneous group of pre‐leukemic diseases marked by ineffective bone marrow (BM) hematopoiesis, peripheral cytopenia, morphologic dysplasia, and an increased risk of leukemic transformation. Increased programmed cell death (PCD) of hematopoietic stem/progenitor cells (HSPCs) and its associated inflammatory BM microenvironment have been speculated to be one of the major causes of ineffective hematopoiesis. PANoptosis is a collective term for three types of PCD: pyroptosis, apoptosis, and necroptosis. All three are mediated by a very large protein complex called a PANoptosome, composed of the key mediators of the three types of PCD. We reported that the diseased cells in MDS with genetic abnormalities, especially spliceosome mutations, show aberrant hypersensitivity to PANoptotic stimuli. Our study suggests that increased PANoptosis of BM HSPCs is one of the reasons for the ineffective hematopoiesis in MDS patients, and targeting PANoptosis may be a novel treatment strategy for MDS. Here we summarize recent advances in research into PANoptosis and discuss the potential role of PANoptosis in the pathogenesis of MDS. We discuss the potential mechanisms for targeting PANoptotic pathways to treat MDS.

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Cite

BibTeXRIS
BibTeX
@article{thalla2026panoptosis,
  title = {{PANoptosis in the pathogenesis of myelodysplastic syndromes}},
  author = {Rohit Thalla and Jyoti Lamichhane and Cameron Lewis and Peter Breslin and Jiwang Zhang},
  journal = {Molecular Oncology},
  year = {2026},
  month = jul,
  doi = {10.1002/1878-0261.70309},
  url = {https://doi.org/10.1002/1878-0261.70309},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - PANoptosis in the pathogenesis of myelodysplastic syndromes
AU  - Rohit Thalla
AU  - Jyoti Lamichhane
AU  - Cameron Lewis
AU  - Peter Breslin
AU  - Jiwang Zhang
PY  - 2026
DA  - 2026/07/24
JO  - Molecular Oncology
DO  - 10.1002/1878-0261.70309
UR  - https://doi.org/10.1002/1878-0261.70309
AB  - Myelodysplastic syndromes (MDS) are a heterogeneous group of pre‐leukemic diseases marked by ineffective bone marrow (BM) hematopoiesis, peripheral cytopenia, morphologic dysplasia, and an increased risk of leukemic transformation. Increased programmed cell death (PCD) of hematopoietic stem/progenitor cells (HSPCs) and its associated inflammatory BM microenvironment have been speculated to be one of the major causes of ineffective hematopoiesis. PANoptosis is a collective term for three types of PCD: pyroptosis, apoptosis, and necroptosis. All three are mediated by a very large protein complex called a PANoptosome, composed of the key mediators of the three types of PCD. We reported that the diseased cells in MDS with genetic abnormalities, especially spliceosome mutations, show aberrant hypersensitivity to PANoptotic stimuli. Our study suggests that increased PANoptosis of BM HSPCs is one of the reasons for the ineffective hematopoiesis in MDS patients, and targeting PANoptosis may be a novel treatment strategy for MDS. Here we summarize recent advances in research into PANoptosis and discuss the potential role of PANoptosis in the pathogenesis of MDS. We discuss the potential mechanisms for targeting PANoptotic pathways to treat MDS.
SN  - 1574-7891
SN  - 1878-0261
ER  -