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Some cells may express erythroid or megakaryocytic antigens.
PCP-2 is expressed in megakaryocytic cell lines.
However, essential thrombocythemia resembles polycythemia vera in that cells of the megakaryocytic series are more sensitive to growth factors.
Megakaryocytic dysplasia.
Bone marrow biopsy showing hypercellularity with prominent erythroid, granulocytic, and megakaryocytic proliferation.
The receptor is normally located on myeloblast, mature neutrophil, but not on any erythroid or megakaryocytic lineage cells.
In patients with RA, the myeloid and megakaryocytic series in the bone marrow appear normal, but megaloblastoid erythroid hyperplasia is present.
M7: acute megakaryocytic leukemia (AMKL).
Increased megakaryocytes are often found in the marrow, and sometimes fragments of megakaryocytic nuclei are present in the blood, especially when the platelet count is very high.
Deletion of the miR-145 and miR-146 loci has been associated with elevated platelet count and megakaryocytic dysplasia associated with the 5q- syndrome.
For instance, PU.1 commits cells to the myeloid lineage whereas GATA-1 has an essential role in erythropoietic and megakaryocytic differentiation.
This down-modulation promotes erythropoiesis favoring translation of the key functional protein LMO2 resulting in reversible regulation of erythroid and megakaryocytic differentiation.
GATA-1 is essential for erythroid (red blood cell) and megakaryocytic (platelet producing cell) development and mice without GATA1 die as embryos.
The differential diagnosis for pure erythroid leukemia includes megaloblastic anemia secondary to vitamin B12 or folate deficiency, acute megakaryocytic leukemia, and ALL or lymphoma.
Certain cytokines such as IL-3, IL-6, IL-11, LIF, erythropoietin, and thrombopoietin all stimulate the maturation of megakaryocytic progenitor cells.
Rainis L, Bercovich D, Strehl S, et al.: Mutations in exon 2 of GATA1 are early events in megakaryocytic malignancies associated with trisomy 21.
Polycythemia vera (PCV), being a primary polycythemia, is caused by neoplastic proliferation and maturation of erythroid, megakaryocytic and granulocytic elements to produce what is referred to as panmyelosis.
Ge Y, Stout ML, Tatman DA, et al.: GATA1, cytidine deaminase, and the high cure rate of Down syndrome children with acute megakaryocytic leukemia.
Soda M, Willert K, Kaushansky K, Geddis A. Inhibition of GSK-3a promotes survival and proliferation of megakaryocytic cells through b-catenin-independent signaling.
Mercher T, Coniat MB, Monni R, et al.: Involvement of a human gene related to the Drosophila spen gene in the recurrent t(1;22) translocation of acute megakaryocytic leukemia.
Prominent myeloproliferative features, e.g. platelet count greater than 600 x 109 /L associated with megakaryocytic proliferation, or white blood cell count greater than 13.0 x 109 /L with or without splenomegaly.
First, the percentage of undifferentiated progenitor cells, blasts cells, is always less than 20% and there is considerably more dysplasia, defined as cytoplasmic and nuclear morphologic changes in erythroid, granulocytic and megakaryocytic precursors, than what is usually seen in cases of AML.