Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

alpha-L-Fucosidase (EC 3.2.1.51; FUS) activity and isoenzyme characteristics were analyzed in normal lymphocytes, normal granulocytes (PMNs) and myeloid and lymphoid leukemic cells, (AML, AMMoL, ALL, CLL and CML). CLL lymphocytes had a lower mean specific activity than normal lymphocytes (2.5 v 4.0, p less than 0.05). ALL blasts had a higher mean specific activity compared to normal lymphocytes (9.7 v 4.0; p less than 0.001), CLL lymphocytes (9.7 v 2.5; p less than 0.001) and AML blasts (9.7 v 7.6 p = NS). Normal PMNs had a higher mean specific activity than normal lymphocytes (7.0 v 4.0 p less than 0.05) but similar activity when compared to CML cells or AML blasts. Blasts from AMMoL patients had higher activity than normal PMNs (9.0 v 7.0; p less than 0.05). The isoenzyme patterns of normal and leukemic granulocytes and lymphocytes were obtained by automated chromatofocusing on PBE-94 microcolumns with normal and leukemic lymphocyte lysates. With normal and leukemic lymphoid lysates two major isoenzyme components (B and A) were isolated. The isoenzyme pattern of PMN, AML, CML and AMMoL revealed 3 major peaks (B, A, I), totally different from that seen in lymphoid cells. The patterns of AML, CML and PMN appeared to be similar to each other; however, the isoenzyme pattern obtained from AMMoL cells could be distinguished from the others by a prominent I peak. Thus the FUS isoenzyme profile distinguishes the blasts of AMMoL from AML, and AMMoL and AML from ALL.
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PMID:Distinct alpha-L-fucosidase isoenzyme profiles in human leukemic cells. 316 92

alpha-L-Fucosidase (EC 3.2.1.51; FUS) activity and isoenzyme characteristics were analyzed in normal lymphocytes, normal (polymorphonuclear leukocytes, PMNs), and myeloid and lymphoid leukemic cells. Chronic lymphocytic leukemia (CLL) lymphocytes had a lower mean specific activity than normal lymphocytes (2.5 vs. 4.0, p less than 0.05). Acute lymphoblastic leukemia (ALL) blasts had a higher mean specific activity compared to normal lymphocytes (9.7 vs. 4.0; p less than 0.001), CLL lymphocytes (9.7 vs. 2.5; p less than 0.001), and acute myeloid leukemic (AML) blasts (9.7 vs. 7.6; p = NS). Normal PMNs had a higher mean specific activity than normal lymphocytes (7.0 vs. 4.0; p less than 0.05) but similar activity when compared to CML cells or AML blasts. Blasts from acute myelomonocytic leukemia (AMMoL) patients had higher activity than normal PMNs (9.0 vs. 7.0; p greater than 0.05). The isoenzyme patterns of normal and leukemic granulocytes and lymphocytes were obtained by automated chromatofocusing on PBE-94 microcolumns with normal and leukemic lymphocyte lysates. With normal and leukemic lymphoid lysates two major isoenzyme components (B and A) were isolated. The isoenzyme patterns of PMN, AML, CML, and AMMoL revealed three major peaks (B, A, I), totally different from those seen in lymphoid cells. The patterns of AML, CML, and PMN appeared to be similar to each other; however, the isoenzyme pattern obtained from AMMoL cells could be distinguished from the others by a prominent I peak. Thus, the FUS isoenzyme profile distinguishes the blasts of AMMoL from AML; and AMMol and AML from ALL.
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PMID:Distinct alpha-L-fucosidase isoenzyme profiles in human leukemic cells. 360 77

Altered mRNA metabolism is a feature of many cancers including blast crisis chronic myelogenous leukemia. Indeed, loss of function of many tumor suppressors regulating cell proliferation, survival, and differentiation results from aberrant mRNA processing, nuclear export, and/or translation. Here, we summarize the effects of increased BCR/ABL oncogenic activity on the expression and function of RNA binding proteins (e.g., FUS, hnRNP A1, hnRNP E2, hnRNP K, and La/SSB) with posttranscriptional and translational regulatory activities and their importance for the phenotype of BCR/ABL-transformed hematopoietic progenitors. We also provide evidence that these studies not only advance our understanding on the molecular mechanisms contributing to tumor/leukemia emergence, maintenance, and/or progression but they also serve for the identification of novel molecular targets useful for the development of alternative therapies for imatinib-resistant and blast crisis chronic myelogenous leukemia and, perhaps, for other cancers characterized by similar alterations in the mRNA metabolism.
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PMID:From mRNA metabolism to cancer therapy: chronic myelogenous leukemia shows the way. 1736 15

H19 is a long non-coding RNA which was lowly expressed in chronic myeloid leukemia (CML). Here, we found that the overexpression of H19 significantly inhibited cell viability and colony formation and prolongs survival in CML cell lines and three xenografted mouse models. The H19 target proteins and microRNAs (miRNAs) were identified using a combination of computational prediction and RNA pull-down, including PCBP1, FUS protein, and miR-19a-3p and miR-106b-5p. Targeting PCBP1, FUS protein, miR-19a-3p, and miR-106b-5p significantly inhibits the cell growth and colony formation of CML cell lines. Co-overexpression of H19 and PCBP1, FUS, miR-19a-3p, and miR-106b-5p decreases the inhibitory effect of H19 in CML. These findings might provide a novel molecular insight into CML.
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PMID:The Identification of Long Non-coding RNA H19 Target and Its Function in Chronic Myeloid Leukemia. 3216 Jul 7