TY - JOUR
T1 - Biological mechanism and clinical effect of protein-bound polysaccharide K (KRESTIN®)
T2 - Review of development and future perspectives
AU - Maehara, Yoshihiko
AU - Tsujitani, Shunichi
AU - Saeki, Hiroshi
AU - Oki, Eiji
AU - Yoshinaga, Keiji
AU - Emi, Yasunori
AU - Morita, Masaru
AU - Kohnoe, Shunji
AU - Kakeji, Yoshihiro
AU - Yano, Tokujiro
AU - Baba, Hideo
N1 - Funding Information:
Y.M. has received honoraria and research funding from Daiichi Sankyo Co. Ltd. and Kureha Corp. H.B. has received research funding from Daiichi Sankyo Co. Ltd. All other authors declare no conflicts of interest.
PY - 2012/1
Y1 - 2012/1
N2 - The mechanism of action of protein-bound polysaccharide K (PSK; KRESTIN®) involves the following actions: (1) recovery from immunosuppression induced by humoral factors such as transforming growth factor (TGF)-β or as a result of surgery and chemotherapy; (2) activation of antitumor immune responses including maturation of dendritic cells, correction of Th1/Th2 imbalance, and promotion of interleukin-15 production by monocytes; and (3) enhancement of the antitumor effect of chemotherapy by induction of apoptosis and inhibition of metastasis through direct actions on tumor cells. The clinical effectiveness of PSK has been demonstrated for various cancers. In patients with gastric or colorectal cancer, combined use of PSK with postoperative adjuvant chemotherapy prolongs survival, and this effect has been confirmed in multiple meta-analyses. For small-cell lung carcinoma, PSK in conjunction with chemotherapy prolongs the remission period. In addition, PSK has been shown to be effective against various other cancers, reduce the adverse effects of chemotherapy, and improve quality of life. Future studies should examine the effects of PSK under different host immune conditions and tumor properties, elucidate the mechanism of action exhibited in each situation, and identify biomarkers.
AB - The mechanism of action of protein-bound polysaccharide K (PSK; KRESTIN®) involves the following actions: (1) recovery from immunosuppression induced by humoral factors such as transforming growth factor (TGF)-β or as a result of surgery and chemotherapy; (2) activation of antitumor immune responses including maturation of dendritic cells, correction of Th1/Th2 imbalance, and promotion of interleukin-15 production by monocytes; and (3) enhancement of the antitumor effect of chemotherapy by induction of apoptosis and inhibition of metastasis through direct actions on tumor cells. The clinical effectiveness of PSK has been demonstrated for various cancers. In patients with gastric or colorectal cancer, combined use of PSK with postoperative adjuvant chemotherapy prolongs survival, and this effect has been confirmed in multiple meta-analyses. For small-cell lung carcinoma, PSK in conjunction with chemotherapy prolongs the remission period. In addition, PSK has been shown to be effective against various other cancers, reduce the adverse effects of chemotherapy, and improve quality of life. Future studies should examine the effects of PSK under different host immune conditions and tumor properties, elucidate the mechanism of action exhibited in each situation, and identify biomarkers.
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U2 - 10.1007/s00595-011-0075-7
DO - 10.1007/s00595-011-0075-7
M3 - Review article
C2 - 22139128
AN - SCOPUS:84857795063
SN - 0941-1291
VL - 42
SP - 8
EP - 28
JO - Surgery today
JF - Surgery today
IS - 1
ER -
