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U. Impola, M.A. Cuccuru, M.V. Masala, L. Jeskanen, F. Cottoni, U. Saarialho‐Kere, Preliminary communication: matrix metalloproteinases in Kaposi's sarcoma, British Journal of Dermatology, Volume 149, Issue 4, 1 October 2003, Pages 905–907, https://doi.org/10.1046/j.1365-2133.2003.05561.x
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Sir, Kaposi's sarcoma (KS) is an angioproliferative disease characterized by angiogenesis, proliferation of spindle cells and an inflammatory infiltrate.1 Viral oncogenesis by human herpesvirus‐8 and cytokine‐induced growth together with some state of immunocompromise represent important conditions for the pathogenesis of all forms of KS. The classic form is often indolent, whereas AIDS‐associated KS can be widely disseminated.
Several matrix metalloproteinases (MMPs) such as collagenase‐1 (MMP‐1), stromelysin‐1 (MMP‐3), 72‐kDa gelatinase (MMP‐2), 92‐kDa gelatinase (MMP‐9), matrilysin‐1 (MMP‐7), membrane type 1 MMP and MMP‐19 have been reported in endothelial cells.2 Based on in vitro data on gelatinases in KS cells and the association of many MMPs with neoangiogenesis, it has been proposed that in KS inhibition of MMP activity using their synthetic inhibitors can effectively reduce tumour growth and migration.2 MMP‐2 mRNA has previously been described in fibroblasts, spindle cells and perivascular cells of AIDS‐associated KS lesions,3 while stromelysin‐3 was not found. Furthermore, production of MMP‐1, 3 and 9 has been demonstrated in KS cell cultures in vitro.4 However, some MMPs, such as MMP‐3, 7, 9 and 12, can promote the production of angiostatin and endostatin and may inhibit angiogenesis and tumour growth.5 Thus, information on which MMPs to target in different types of tumours is essential.