Angiogenesis and Anti-Angiogenesis in Hematological by Domenico Ribatti

By Domenico Ribatti

It has been often authorized that angiogenesis is all for 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 ailment burden, analysis and remedy consequence. Reciprocal optimistic and unfavorable 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 by means of 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 website wealthy in blood vessels the place endothelial cells and mural cells akin to pericytes and soft muscle cells create a microenvironment that is affecting the habit of numerous stem and progenitor cells, in hematological malignancies.

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1990). In both reactive lymph nodes and in lymph nodes with follicular lymphomas, MVD is higher in the paracortex than in the follicles and that there are no difference in MVD between reactive germinal centers and neoplastic follicles (Passalidou et al. 2003). Moreover, MVD in the paracortex in reactive lymph nodes is higher than in diffuse large large lymphomas (Passalidou et al. 2003). In FL, several studies have recognized an increase in MVD in reactive parts of affected lymph nodes outside the follicles, as compared to the neoplastic follicles (Koster et al.

1). Chronic lymphocytic leukemia is the most common leukemia in Western countries, and it account for approximately one-third of all leukemias in the United States. Approximately, 50 % of freshly isolated CLL cells expressed mRNA and protein for VEGF (Dias et al. 2000). Moreover, VEGF released by CLL cells stimulated endothelial cell proliferation in vitro in the Matrigel assay, conditioned media from cultured CLL cells stimulated angiogenesis in the CAM assay, and this was inhibited by a blocking anti-VEGF antibody (Kini et al.

2000), suggesting that these microvessels are involved in the pathogenesis of the disease. In fact, in vitro studies have demonstrated increased secretion of VEGF by tumor cells transfected with the bcr-abl construct (Mayerhofer et al. 2002) and the secretion can be inhibited by the bcr-abl specific tyrosine kinase inhibitor STI571 (imatinib mesylate) (Ebos et al. 2002). In myelodysplastic syndrome (MDS), MVD has been investigated and VEGF and VEGFR-2 have been detected in myeloblasts and their expression was higher and correlated with MVD in high risk as compared to low risk patients (Bellamy et al.

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