TY - JOUR
T1 - Increase of plasma transforming growth factor beta (TGFβ during immunotherapy with IL-2
AU - Puolakkainen, Pauli
AU - Twardzik, Dan
AU - Ranchalis, Jane
AU - Moroni, Mauro
AU - Mandeli, John
AU - Paciucci, Paolo Alberto
N1 - Funding Information:
This work was supported in part by National Cancer Institute Grant no. 5P30-CA23102, by the T. J. Martell Memorial Foundation for Leukemia and Cancer Research, and by the Jeffrey Forlenza Grant for Leukemia and Cancer Research.
PY - 1995
Y1 - 1995
N2 - Interleukin-2 (IL-2) is a lymphokine with pleiotropic activities on the immune system. When administered in vivo, besides inducing unrestricted tumor cytotoxicity, it is also responsible for the secondary release of other lymphokines, such as IL-1, TNF, and marrow growth factors, which may mediate some of the clinical toxicities (as well as therapeutic effects) seen during IL-2 immunotherapy. Among the clinical effects of IL-2, we previously reported thrombocytopenia and IL-2-induced in vitro inhibition of platelet aggregatiori accompanied by rapid secretion of alpha-granule components such as platelet factor 4 (PF4) and beta-thromboglobulin. Platelets coiistitute one of the largest storage forms of TGFβ Preliminary evaluation of this factor in patients receiving IL-2 had indicated that plasma TGFβ activity increased in cancer patients following IL-2 therapy. We report a more detailed study of the quantitation of TCFβ activity, in the plasma of 23 cancer patients treated with IL-2 immunotherapy. Of interest, we found that although elevation of the bioactive form of TGFβ occurred in most patients during IL-2 therapy, it was significantly higher in patients with clinical regression of tumor (p =,004). In the first 2 weeks of therapy increase of plasma TGFP activity appeared to correlate with a decrease of platelet counts, suggesting that the factor may derive from the storage form of TGFβ contained therein.
AB - Interleukin-2 (IL-2) is a lymphokine with pleiotropic activities on the immune system. When administered in vivo, besides inducing unrestricted tumor cytotoxicity, it is also responsible for the secondary release of other lymphokines, such as IL-1, TNF, and marrow growth factors, which may mediate some of the clinical toxicities (as well as therapeutic effects) seen during IL-2 immunotherapy. Among the clinical effects of IL-2, we previously reported thrombocytopenia and IL-2-induced in vitro inhibition of platelet aggregatiori accompanied by rapid secretion of alpha-granule components such as platelet factor 4 (PF4) and beta-thromboglobulin. Platelets coiistitute one of the largest storage forms of TGFβ Preliminary evaluation of this factor in patients receiving IL-2 had indicated that plasma TGFβ activity increased in cancer patients following IL-2 therapy. We report a more detailed study of the quantitation of TCFβ activity, in the plasma of 23 cancer patients treated with IL-2 immunotherapy. Of interest, we found that although elevation of the bioactive form of TGFβ occurred in most patients during IL-2 therapy, it was significantly higher in patients with clinical regression of tumor (p =,004). In the first 2 weeks of therapy increase of plasma TGFP activity appeared to correlate with a decrease of platelet counts, suggesting that the factor may derive from the storage form of TGFβ contained therein.
UR - http://www.scopus.com/inward/record.url?scp=0028887075&partnerID=8YFLogxK
U2 - 10.3109/07357909509024926
DO - 10.3109/07357909509024926
M3 - Article
C2 - 7583707
AN - SCOPUS:0028887075
SN - 0735-7907
VL - 13
SP - 583
EP - 589
JO - Cancer Investigation
JF - Cancer Investigation
IS - 6
ER -