Increased Serum Activin A Levels in Mycosis Fungoides and Sézary Syndrome

This is the authors' abstract. We don't add key points for this paper.

Activins, members of the transforming growth factor β superfamily, were originally discovered as reproductive hormones, which stimulate FSH release, and were identified in many tissues. Activins are homoor heterodimers composed of βA and βB subunits. Among 3 isoforms of activins: activin A (βA/βA), activin B (βB/βB), and activin AB (βA/βB); activin A is the most abundant and best-characterized variant. Activin A has various functions, such as regulating cell differentiation, proliferation, and apoptosis. It has been shown that activin A plays important roles in the development and progression of solid tumors including breast carcinoma (1), ovarian carcinoma (2), and colorectal carcinoma (3). In addition, a recent study has revealed that activin overexpression is an early event in murine and human skin tumorigenesis via attracting tumor-associated macrophages (4). Tumorassociated macrophages are thought to have important roles in progression of not only skin solid tumors but also cutaneous T-cell lymphoma, based on the reports which describe that the depletion of tumor-associated macrophages delays tumor formation of cutaneous T-cell lymphoma cells in skin (5) and that cutaneous T-cell lymphoma patients with an increased number of tumor-associated macrophages had worse prognosis (6). To elucidate activin A involvement in the progression of mycosis fungoides (MF) and Sézary syndrome (SS), we measured serum activin A levels in patients with MF/SS.