Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: UNIPROT:P02794 (
ferritin
)
17,525
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Previous ultrastructural investigations have shown that the erythroblastic island is composed of erythroblasts at different stages of maturation which are intimately associated with a central macrophage. However, it is still unclear at which stage of erythroid differentiation this interaction occurs, mainly because of the lack of purified populations of normal erythroid progenitors [erythroid colony-forming units (CFU-E) and erythroid burst-forming units (BFU-E)] and early precursor cells (proerythroblasts) and because of our limited knowledge of their ultrastructural characteristics. In the present work we analyzed the ultrastructure of CFU-E enriched from normal human bone marrow by avidin-biotin immune rosetting and leukemic blasts of erythroid origin from two patients. Normal and leukemic CFU-Es were defined as glycophorin A (GPA)-negative blasts, devoid of rhopheocytosis, containing some
ferritin
molecules, either free in the cytoplasm or associated with theta-granules (theta-Gr) in the Golgi zone. Peroxidase activity was detected in the endoplasmic reticulum of these blasts. A preproerythroblast stage was identified, which corresponded to an intermediate phenotype with few GPA sites and rhopheocytosis. In contrast to hemoglobin synthesis, which was absolutely dependent on the presence of erythropoietin (Epo) during culture for 24 hours,
ferritin
molecules accumulated in the absence of Epo. Interestingly, leukemic CFU-
E-like
blasts were always in contact with bone marrow macrophages and adhesion between these cell types resisted mechanical dissociation. This result suggests that erythroid progenitors may be part of the erythroblastic island. The mechanisms involved in erythroblast-macrophage binding are still unknown, but the expression by macrophages and erythroid progenitors of receptors for fibronectin and thrombospondin (TSP), as well as their respective ligands in the case of macrophages, suggests that these molecules could be involved in the formation of the erythroblastic island.
...
PMID:Association between leukemic erythroid progenitors and bone marrow macrophages. 201 49
Diagnosis of megakaryoblastic and early erythroid leukemia requires the use of differentiation markers that in most cases permit their precise diagnosis. In some cases, their use can be misleading. Here we report and discuss some examples. A platelet peroxidase (PPO) activity is detected in most cases of early erythroid leukemias as well as in the CFU-
E-like
cells of normal marrow, thus providing evidence that PPO activity must be studied along with other (immunologic or ultrastructural) markers to permit a reliable diagnosis of megakaryoblastic leukemia. Ferritin molecules an erythroid marker, could be detected as a cluster at ultrastructural level in leukemic platelets and in micromegakaryocytes of one patient. However, in blasts of the erythroid lineage,
ferritin
molecules are also either dispersed in the cytoplasm or localized in theta granules. Immunologic markers have also their own limit. Indeed, in one patient, GB IIb and IIIa were detected on erythroid blasts, resulting in a phenotype very similar to HEL cells. Carbonic anhydrase (CA) I, an early erythroid marker, was detected in the platelets of four leukemic patients and was present along with an increased expression of CA II. This study emphasizes the fact that precise diagnosis of leukemia cannot be performed with a single marker of differentiation, but requires the simultaneous use of several lineage restricted markers.
...
PMID:Limits of phenotypic markers for the diagnosis of megakaryoblastic leukemia. 264 84