We conclude that besides morphology of megakaryocytes and other features, JAK2V617F allelic burden can help differentiate CMML from PMF with monocytosis.
Of note, 2 cases of JAK2 V617F+ primary myelofibrosis with SRSF2 mutation initially were diagnosed as CMML based on significant peripheral blood monocytosis.
Unexpectedly, the IL-6-/-/IL-10-/- mice manifested more pronounced gut inflammation and earlier disease onset than IL-10-/- mice, both locally (colon and small bowel) and systemically (splenomegaly, ulcerative dermatitis, leukocytosis, neutrophilia, and monocytosis).
Monocyte subset screening (CD14/CD16 expression) was performed on 68 blood and 25 bone marrow specimens with a monocytosis and/or flagged as possible CMML.
The HematoFlow™ solution, able to quantify CD16 negative monocytes, could be a useful tool to manage monocytosis which remains a common issue in routine laboratories.
Monocyte subset screening (CD14/CD16 expression) was performed on 68 blood and 25 bone marrow specimens with a monocytosis and/or flagged as possible CMML.
Monocyte subset screening (CD14/CD16 expression) was performed on 68 blood and 25 bone marrow specimens with a monocytosis and/or flagged as possible CMML.
The HematoFlow™ solution, able to quantify CD16 negative monocytes, could be a useful tool to manage monocytosis which remains a common issue in routine laboratories.
Defined by a persistent peripheral blood monocytosis ≥1 × 10<sup>9</sup>/L and monocytes accounting for ≥10% of the white blood cells, this aging-associated disease combines cell proliferation as a consequence of myeloid progenitor hypersensitivity to granulocyte-macrophage colony-stimulating factor with myeloid cell dysplasia and ineffective hematopoiesis.
We also measured cell-surface levels of the common β subunit of the IL-3/GM-CSF receptor (IL-3Rβ) which has been linked to defective cholesterol homeostasis and may promote monocytosis.
Of note, 2 cases of JAK2 V617F+ primary myelofibrosis with SRSF2 mutation initially were diagnosed as CMML based on significant peripheral blood monocytosis.
The striking association between TET2 gene alterations and monocytosis, already observed in patients with systemic mastocytosis, could indicate a negative role of TET2 in the control of monocytic lineage determination.
Monocytosis characterized by a shift to anti-inflammatory monocytes is associated with survival prolongation in the hosts of IL-10 transduced liver allografts.