Pathogenesis

The recent advances in our understanding of the nature and pathogenesis of CIMF have recently been reviewed.26 The characteristic extracellular matrix is composed of a variety of interstitial and basement membrane glycoproteins, including collagen types I, III, IV, V, and VI, fibronectin, vitronectin, laminin, and tenascin, as well as a marked neovascularization. In contrast to the clonal hematopoiesis, the increased stromal tissue is a reactive, or secondary phenomenon, resulting from the inappropriate release of megakaryocyte or platelet-derived growth factors, including PDGF, TGF-P, bFGF, and calmodulin, and monocytic cytokines. Circulating hematopoietic precursors, including pluripotent (CFU-GM) and lineage-restricted progenitor cells (CFU-GEMM, CFU-MK, and BFU-E), are increased up to 160 times their concentrations in control blood. Cytogenetic studies have highlighted three chromosomal abnormalities, namely del(13q), del(20q), and partial trisomy 1q, which account for 70 percent of all abnormalities at diagnosis, and suggest that in many patients gene loss and/or inactiva-tion may be an important pathogenetic mechanism.

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