In<unk> , megakaryocytes are more sensitive to growth factors. Platelets derived from the abnormal megakaryocytes are activated, which, along with the elevated platelet count, contributes to the likelihood of forming blood clots. The increased possibility of bleeding when the platelet count is over 1 million is due to von Willebrand factor (vWF) sequestration by the increased mass of platelets, leaving insufficient vWF for platelet adhesion. A mutation in the JAK2 kinase (V617F) is present in 40–50% of cases and is diagnostic if present. JAK2 is a member of the Janus kinase family. In 2013, two groups detected calreticulin mutations in a majority of JAK2-negative/MPL-negative patients with<unk>  and primary myelofibrosis, which makes CALR mutations the second most common in myeloproliferative neoplasms. All mutations (insertions or deletions) affected the last exon, generating a reading frame shift of the resulting protein, that creates a novel terminal peptide and causes a loss of endoplasmic reticulum KDEL retention signal.
Essential thrombocythemia
Refractory cytopenia of childhood
Polycythemia vera
Transient erythroblastopenia of childhood
Primary myelofibrosis
Chronic neutrophilic leukemia
Drug-induced thrombocytopenic purpura
Aplastic anemia