A 64-year-old man presented with progressive asthenia and pancytopenia. Complete blood counts showed hemoglobin 7.5 g/dL, white blood cell count 1.2 × 109/L, and platelets 25 × 109/L. A bone marrow aspirate revealed 7% myeloblasts and 69% erythroblasts with dysplastic features including cytoplasmic vacuoles, nuclear budding, and multinucleated cells (panels A-D; in all panels, original magnification ×600; May-Grünwald stain). Evident mitotic figures were observed in the red cell compartment in all phases of division, and both normal (panels E-H) and abnormal (panels I-L) features were apparent. In addition, some erythroblasts presented several distinct micronuclei (panels M-P). Cytogenetic analysis revealed an abnormal clone: 43∼45,XY,-5,-7,-18,?add(19)(q13.3),+mar1,min[cp20]. The diagnosis of myelodysplastic syndrome (MDS) with excess blasts was confirmed.

Multiple micronucleation is an uncommon finding in MDS that has been associated with disturbances in mitosis. More recently, it has also been described in the so-called mitotic catastrophe phenomenon, an oncosupressive mechanism that culminates in the death or senescence of mitosis-abnormal and genomically unstable cells. Failure of activation of this mechanism leads to persistent genomic instability and aneuploidy. MDSs are a heterogeneous group of disorders characterized by myeloid dysplasia, increased apoptosis, and senescence. It is a question for future research whether mitotic catastrophe also participates in the physiopathology of MDS, as could be speculated from the mitotic figures observed in this case.

A 64-year-old man presented with progressive asthenia and pancytopenia. Complete blood counts showed hemoglobin 7.5 g/dL, white blood cell count 1.2 × 109/L, and platelets 25 × 109/L. A bone marrow aspirate revealed 7% myeloblasts and 69% erythroblasts with dysplastic features including cytoplasmic vacuoles, nuclear budding, and multinucleated cells (panels A-D; in all panels, original magnification ×600; May-Grünwald stain). Evident mitotic figures were observed in the red cell compartment in all phases of division, and both normal (panels E-H) and abnormal (panels I-L) features were apparent. In addition, some erythroblasts presented several distinct micronuclei (panels M-P). Cytogenetic analysis revealed an abnormal clone: 43∼45,XY,-5,-7,-18,?add(19)(q13.3),+mar1,min[cp20]. The diagnosis of myelodysplastic syndrome (MDS) with excess blasts was confirmed.

Multiple micronucleation is an uncommon finding in MDS that has been associated with disturbances in mitosis. More recently, it has also been described in the so-called mitotic catastrophe phenomenon, an oncosupressive mechanism that culminates in the death or senescence of mitosis-abnormal and genomically unstable cells. Failure of activation of this mechanism leads to persistent genomic instability and aneuploidy. MDSs are a heterogeneous group of disorders characterized by myeloid dysplasia, increased apoptosis, and senescence. It is a question for future research whether mitotic catastrophe also participates in the physiopathology of MDS, as could be speculated from the mitotic figures observed in this case.

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