Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P39060 (endostatin)
 2,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased levels of tumor angiogenesis have been demonstrated in variety of solid tumors and hematological malignancies including acute myeloid leukemia (AML). The aim of the study was to evaluate serum level of endostatin in newly diagnosed patients with AML before chemotherapy and after achieving complete remission (CR). Serum samples from 68 adult patients (28 females and 40 males, median age 42 years, range 21-83 years) with AML had been taken before chemotherapy was administered. In addition 21 out of 68 patient were analyzed again after achieving CR. Endostatin levels were measured using ChemiKine sandwich ELISA kit (Chemicon International). Twelve samples from healthy volunteers (5 females and 7 males, median age 40 years; range 35-65 years) were evaluated as the control. Endostatin serum levels were significantly higher in untreated AML patients than in the normal controls. In AML patients baseline endostatin levels were significantly lower than in CR. We did not found any correlation between white cell count or percentage of blasts in the bone marrow and endostatin level. Moreover endostatin levels did not differ statistically among AML FAB subgroups. Increased endostatin plasma levels may reflect intensity of inhibition of angiogenesis and may by useful in prognosis of CR in AML. Chemotherapy can modulate the regulation of angiogenesis in AML patients.
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PMID:Endostatin serum level in acute myeloid leukemia. 1580 Jul 18

Angiogenesis is an important event in the survival and progression of solid tumors. The angiogenic status and the exact role of the angiogenic cytokines in lymphoid leukemia has not been fully elucidated. We have investigated the profile of the systemic components of angiogenic regulation in B-lineage acute lymphoblastic leukemia (B-ALL) and B-chronic lymphocytic leukemia (B-CLL), namely vascular endothelial growth factor (VEGF), tumor necrosis factor-alpha (TNF-alpha), endostatin and matrix metalloproteinase-9 (MMP-9) using enzyme-linked immunosorbent assay (ELISA). In B-ALL patients, sVEGF, and MMP-9 were significantly lower than control levels at diagnosis (p < 0.001) and increased to near control levels in remission (p>0.05). Both serum TNF-alpha and endostatin levels showed no significant difference at diagnosis (p>0.05) and in remission (p>0.05) compared to control levels. VEGF, TNF-alpha, MMP-9 and endostatin levels were not significantly correlated with peripheral white cell count or bone marrow blast cell count, but were positively correlated with platelet count. In B-CLL patients, serum VEGF, MMP-9 and TNF-alpha were significantly higher (p < 0.001 = 0.009, 0.007, respectively) and decreased to near control levels in remission (p>0.05 for all). Serum endostatin levels showed no significant difference at diagnosis and in remission compared to control levels (p>0.05). A significant positive correlation between VEGF, TNF-alpha, MMP-9 and peripheral white cell counts, bone marrow lymphocytic count and platelets count were found. In conclusion, our data suggest that the driving forces of angiogenic factors (VEGF, TNF-alpha and MMP-9) in adult B-ALL appears different from that in B-CLL patients.
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PMID:Angiogenesis factor pattern differs in acute lymphoblastic leukemia and chronic lymphocytic leukemia. 1765 59