Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
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Target Concepts:
Gene/Protein
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Query: UMLS:C0023473 (
chronic myeloid leukemia
)
18,916
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Early
chronic myeloid leukemia
(
CML
) and leukemoid reaction (LR) sometimes show similar histological pictures. In order to assess the efficacy of immunohistochemistry in the discrimination of the two forms, twenty bone marrow (BM) trephines of patient with
CML
and twenty with LR were immunostained and studied. A wide spectrum of antibodies effective on paraffin-embedded tissues (NP 57 anti-neutrophil elastase, Leu M1, MAC 387, KP1, Y2/51, LCA, UCHL1, L26, BerH2 and
Glycophorin A
) and directed against granulopoietic, erythropoietic, megakaryocytic, monocytic and lymphoid cells was tested by means of the alkaline phosphatase anti-alkaline phosphatase (APAAP) method. Expression of neutrophil elastase in
CML
and LR showed a different pattern of reactivity in normal and neoplastic granulocytic cells and Y2/51 put in evidence significant discrepancies of megakaryocytes in the two groups. Moreover, a greater number of histiocytic, lymphoid and erythropoietic cells were detected in LR after immunostaining with KP1, LCA, UCHL1, L26 and
Glycophorin A
. The different immunophenotypical pictures observed, suggest the value of immunohistochemistry as a supplementary diagnostic tool for the differential diagnosis between early
CML
and LR.
...
PMID:[Immunophenotyping of early-phase chronic myeloid leukemia and leukemoid reaction]. 770 38
We compare the effects of Imatinib mesylate (Glivec) on
chronic myeloid leukemia
derived cell lines K562 and JURL-MK1. In both cell lines, the cell cycle arrests in G(1)/G(0) phase within 24 h after the addition of 1 microM Imatinib. This is followed by a decrease of Ki-67 expression and the induction of apoptosis. In JURL-MK1 cells, the apoptosis is faster in comparison with K562 cells: the caspase-3 activity reaches the peak value (20 to 30 fold of the control) after about 40 h and the apoptosis proceeds to its culmination point, the DNA fragmentation, within 48 h following 1 microM Imatinib addition. Unlike K562 cells, JURL-MK1 cells possess a probably functional p53 protein inducible by TPA (tetradecanoyl phorbol acetate) or UV-B irradiation. However, no increase in p53 expression was observed in Imatinib-treated JURL-MK1 cells indicating that the difference in the apoptosis rate between the two cell lines is not due to the lack of p53 in K562 cells. Imatinib also triggers erythroid differentiation both in JURL-MK1 and K562 cells.
Glycophorin A
expression occurred simultaneously with the apoptosis, even at the single cell level. In K562 cells, but not in JURL-MK1 cells, the differentiation process involved increased hemoglobin synthesis. However, during spontaneous evolution of JURL-MK1 cells in culture, the effects produced by Imatinib progressively changed from the fast apoptosis to the more complete erythroid differentiation. We suggest that the apoptosis and the erythroid differentiation are parallel effects of Imatinib and their relative contributions, kinetics and completeness are related to the differentiation stage of the treated cells.
...
PMID:Fast apoptosis and erythroid differentiation induced by imatinib mesylate in JURL-MK1 cells. 1577 Jun 64