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Progression of Lymphomatoid Papulosis to Systemic Lymphoma Is Associated with Escape from Growth Inhibition by Transforming Growth Factor‐β and CD30 Ligand
Author(s) -
KADIN MARSHALL E.,
LEVI EDI,
KEMPF WERNER
Publication year - 2001
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2001.tb03711.x
Subject(s) - lymphomatoid papulosis , cd30 , lymphoma , transforming growth factor , cancer research , ligand (biochemistry) , antibody , cell growth , receptor , chemistry , medicine , immunology , biochemistry
A bstract : 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‐β) 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‐β failed to inhibit the growth of lymphoma cells from advanced disease due to mutations of the TGF‐β 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‐β and CD30 ligand.