By Domenico Ribatti
It has been in general accredited that angiogenesis is desirous about the pathogenesis of hematological malignancies, like acute and persistent leukemia, lymphoma, myelodysplastic syndromes, myeloproliferative neoplasms and a number of myeloma. the level of angiogenesis within the bone marrow has been correlated with illness burden, diagnosis and remedy end result. Reciprocal confident and adverse interactions among tumor cells and bone marrow stromal cells, particularly hematopoietic stem cells, fibroblasts, osteoblasts/osteoclasts, endothelial cells, endothelial progenitor cells, T cells, macrophages and mast cells, mediated via an array of cytokines, receptors and adhesion molecules, modulate the angiogenic reaction in hematological tumors. extra lately, it's been emphasised the pro-angiogenic function of the so known as “vascular niche”, indicating a domain wealthy in blood vessels the place endothelial cells and mural cells reminiscent of pericytes and soft muscle cells create a microenvironment that has effects on the habit of a number of stem and progenitor cells, in hematological malignancies.
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2002). In primary diffuse central nervous system lymphomas (PCNSL), VEGF expression is correlated to MVD and VEGF expression is associated with a longer survival and blood-brain barrier alteration (Takeuchi et al. 2007). In 24 human diffuse large B-cell PCNSL studied by means of immunocytochemistry and confocal laser microscopy has been demonstrated that: (a) Aquaporin 4 (AQP4) expression was directly correlated with Ki-67 index, while AQP4 expression was low in tumor areas with a low Ki-67 index.
2000; Chen et al. 2000). Intracellular FGF-2 levels in lymphocytes of B-CLL patients correlated with stage of disease (Menzel et al. 1996; König et al. 1997), and a positive correlation was identified between serum FGF-2 levels and Bcl-2 expression (König et al. 1997; Bairey et al. 2000), resulting in increased leukemia cell survival and increased cellular FGF-2 in high-risk CLL was associated with fludarabine resistance (Menzel et al. 1996). Baban et al. (1996) first reported the elevated expression of VEGF in CLL patients, measured in both serum and leukemic cells (Kini et al.
2000). The pro-survival signaling mechanism protect AML cells from chemotherapy-induced apoptosis through upregulation of anti-apoptotic proteins (Dias et al. 2000). In pediatric AML various isoforms of VEGF, including VEGF121, VEGF165, and VEGF189, are expressed in AML cells (Kruizinga et al. 2011). 1) (Ferretti et al. 2010), expressed Ang-1, Ang-2, and their receptor, Tie-2 (Wakabayashi et al. 2004; Hatfiled et al. 2008), and blocking Angs interactions with Tie-2 decreased AML cell proliferation (Reikvam et al.