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LCS101



RESEARCH


Integr Med Insights

Source:
Samuels N, Maimon Y, Zisk-Rony RY. Integr Med Insights. 2013; 8: 1–8. Published online 2013 January 22. doi: 10.4137/IMI.S10841

A randomized, placebo-controlled, double blinded trial found a significant reduction in chemotherapy-induced hematological toxicities in patients with breast cancer receiving adjunct treatment with LCS101. These patients developed significantly less severe anemia, leucopenia and neutropenia when compared to controls. Patients in the treatment group developed significantly less severe (grades 2-4) anemia (p < .01) and leukopenia (p < .03).



Onco Targets Ther

Source:
Rachmut IH, Samuels N, Melnick SJ, Ramachandran C, et al. Onco Targets Ther. 2013; 6: 437–445. doi: 10.2147/OTT.S42038

LCS101 was found to induce a dose-dependent upregulation of NK cell activation in the blood cells of healthy human subjects. NK cells are considered to be a central mediator in the “cross talk” between the adaptive and the innate immune systems, and play an important role in the inhibition and killing of tumor cells (Lee & Gasser, 2010). The LCS101 component Astragalus membranaceus has been shown to stimulate NK-cell activity in human peripheral lymphocytes, as well as restoring steroid-inhibited NK-cell activity (Mills & Bone, 2000). Polysaccharides of this herb were shown to enhance NK cell activity of normal subjects and patients with systemic lupus erythematosus. LCS101 was also shown to enhance cytokine production, increasing TNF-α secretion from murine macrophages 100fold when compared to untreated controls. TNF-α is a potent antitumor cytokine that enhances the activity of macrophages, NK cells, and cytotoxic T cells. Finally, LCS101 was observed to increase production of IFN-γ, correcting decreased levels following 5-FU treatment, and increasing unaltered levels of the cytokine following exposure to doxorubicin. IFN-γ production is induced by T cells, NK cells, and macrophages, and plays a role in the inhibition of tumor growth, promotion of Th1 immune responses, and differentiation of cytotoxic NK and T cells. Immune-competent mice who lack IFN-γ fail to normalize tissue homeostasis and clear low-level microbial infections, resulting in chronic inflammation with an increased incidence of hematological and solid-tissue cancers (Enzler et al, 2003).

 
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