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Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation
Published on: November 26, 2018
Angiogenesis factor pattern differs in acute lymphoblastic leukemia and chronic lymphocytic leukemia
Salah Aref1, O Salama, S Shamaa
1Hematology Unit, Clinical Pathology Department, Mansoura Faculty of Medicine, Mansoura, Egypt. salaharef@yahoo.com
Abstract:
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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