Progression of lymphomatoid papulosis to systemic lymphoma is associated with escape from growth inhibition by transforming growth factor-beta and CD30 ligand.

Abstract	Our objective is to understand the mechanism of progression of lymphomatoid papulosis (LyP) to CD30+ systemic lymphoma. LyP lesions appear in recurrent crops that regress, only to reappear at a later date in the same or different locations. About 10% of patients develop systemic lymphoma. Because transforming growth factor-beta (TGF-beta) and CD30 ligand inhibit the growth of normal lymphocytes and can be detected in regressing lesions of LyP, we tested the effect of these cytokines on cell lines clonally derived from LyP in the progression to systemic lymphoma. TGF-beta failed to inhibit the growth of lymphoma cells from advanced disease due to mutations of the TGF-beta receptor complex that prevented binding of the ligand to tumor cells. A CD30 ligand agonist antibody caused proliferation of tumor cells from one patient and had no effect on tumor cells of another. In contrast, a Fas agonist antibody caused significant growth inhibition of all cell lines. The results suggest that progression of LyP to lymphoma is associated with escape of lymphoma cells from growth regulation by TGF-beta and CD30 ligand.
Authors	M E Kadin, E Levi, W Kempf
Journal	Annals of the New York Academy of Sciences (Ann N Y Acad Sci) Vol. 941 Pg. 59-68 (Sep 2001) ISSN: 0077-8923 [Print] United States
PMID	11594583 (Publication Type: Journal Article)
Chemical References	Antibodies CD30 Ligand Ki-1 Antigen Membrane Glycoproteins Receptors, Transforming Growth Factor beta TGFB1 protein, human TNFSF8 protein, human Transforming Growth Factor beta Transforming Growth Factor beta1 DNA
Topics	Antibodies (immunology) CD30 Ligand Cell Division DNA (analysis) Disease Progression Female Humans Ki-1 Antigen (genetics, metabolism) Lymphoma, T-Cell, Cutaneous (etiology, genetics, pathology) Lymphomatoid Papulosis (complications, metabolism) Membrane Glycoproteins (genetics, physiology) Models, Biological Mutation Receptors, Transforming Growth Factor beta (genetics) Skin Neoplasms (etiology, genetics, pathology) Transforming Growth Factor beta (immunology, physiology) Transforming Growth Factor beta1 Tumor Cells, Cultured

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