Abstract
I read with great interest the recent article by Maehara et al. [1]. Polysaccharide K (PSK) exerts remarkable anti-neoplastic effects against many systemic malignancies. For instance, the risk of early tumor recurrence is attenuated in gastric cancer patients who receive PSK in conjunction with regular chemotherapy. This is especially true in patients with pN3 lymph node metastasis [2]. Similarly, when administered with low-dose UFT, PSK promotes the regression and resolution of hepatic metastasis from gastric carcinomas [3]. Furthermore, patients with stage IB or II gastric cancer treated with 5-fluorouracil, mitomycin-C and PSK chemotherapy had higher 5-year overall survival rates than those treated with 5-fluorouracil and doxorubicinbased chemotherapy [4]. Increased apoptosis is seen in pro-myelomonocytic leukemia cells following the administration of PSK, which mediates these anti-neoplastic effects via modulation of the p38 mitogen-activated protein kinase pathway [5]. These effects are clearly seen in HL-60 cells. Similarly, PSK enhances apoptosis in Burkitt lymphomas [6] and treatment with beta-galactosidase enhances the apoptotic effects of PSK. Similarly, the progression of pre-lymphomas to lymphomas is attenuated by the administration of PSK. This is especially true when it is administered with RadLVspecific immunotoxin [7]. Selective activation of V beta 8 ? T cells accounts for the synergistic effect of this combination. In prostate carcinomas, PSK accentuates the anti-neoplastic effects of chemotherapeutic agents, such as docetaxel, and it also enhances the anti-tumor immune response against these neoplasms [8]. The above examples clearly illustrate the remarkable anti-tumor properties of PSK and the need for further studies to fully harness its anti-neoplastic effects. We trust that further large-scale randomized control studies in humans will be initiated very soon to investigate the effectiveness of PSK more extensively.
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