Since TGFβ1 inhibits the proliferation of normal B-cells, its disturbed activity in B cell lymphomas is conceivable. We found high expression of TGFβ1 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 TGFβ1 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 TGFβ1 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 TGFβ and the retained sensitivity to anti-IgM indicate that c-myc and Ig receptor can operate independently of TGFβ in the regulation of lymphoid cell proliferation.
|Number of pages||4|
|Issue number||1 A|
|Publication status||Published - Jan 1 1994|
ASJC Scopus subject areas
- Cancer Research