Since TGF beta 1 inhibits the proliferation of normal B-cells, its disturbed activity in B cell lymphomas is conceivable. We found high expression of TGF beta 1 mRNA in three human B cell non-Hodgkin lymphoma xenografts; also, the gene product (in latent form) was detectable in all lymphoma cells. However, on exposing the cells to exogenously activated TGF beta 1, the incorporation of tritiated thymidine decreased in normal (murine thymocytes, human peripheral mononuclear cells), but not in lymphoma cells. These observations suggest the malfunction of TGF beta 1 mediated regulatory pathway (e.g. insufficient activation or receptor expression) which can contribute to the unlimited expansion of a lymphoid clone. The opposite expression of c-myc to TGF beta and the retained sensitivity to anti-IgM indicate that c-myc and Ig receptor can operate independently of TGF beta in the regulation of lymphoid cell proliferation.