Abstract
Active hexose correlated compound (AHCC) is known as a dietary supplement derived from an extract of a basidiomycete mushroom. The present study was conducted to evaluate the role of AHCC in alleviating the side effects, particularly hematological toxicity, in non-tumor-bearing mice receiving monotherapy with gemcitabine (GEM). The results from the GEM treatment groups with and without AHCC administration were compared to control group that received vehicle alone. The GEM alone treatment reduced peripheral leukocytes and hemoglobin, and bone marrow cell viability in spite of no influence on body weight, food consumption, and renal and hepatic parameters. Supplementation with AHCC significantly alleviated these side effects. The colony forming assay of bone marrow cells revealed that AHCC improved reduction of colony forming unit-granulocyte macrophage (CFU-GM) and burst forming unit-erythroid (BFU-E) related to GEM administration. However, when mRNA expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) and erythropoietin (EPO) was examined using a quantitative reverse transcription polymerase chain reaction (RT-PCR), AHCC showed no effect for the mRNA levels of their hematopoietic growth factors. These results support the concept that AHCC can be beneficial for cancer patients with GEM treatment through alleviating the hematotoxicity.
Highlights
Gemcitabine (2’,2’-difluoro-2’-deoxycytidine, GEM), a pyrimidine based nucleoside analog, [1] is metabolized to gemcitabine diphosphate and triphosphate inside the cell by nucleoside kinases [2]
The colony forming assay of bone marrow cells revealed that Active hexose correlated compound (AHCC) improved reduction of colony forming unit-granulocyte macrophage (CFU-GM) and burst forming unit-erythroid (BFU-E) related to GEM administration
We investigated the influence of AHCC on some of the side effects associated with GEM as an initial study in preparation for a human clinical trail
Summary
Gemcitabine (2’,2’-difluoro-2’-deoxycytidine, GEM), a pyrimidine based nucleoside analog, [1] is metabolized to gemcitabine diphosphate and triphosphate inside the cell by nucleoside kinases [2]. Hematological toxicity and flu-like symptoms caused by GEM are the most common side effect, they are mild and shortlived [10]. These toxicities related to GEM can lower the quality of life in cancer patients and often trigger reductions in the dosage, frequency and duration of chemotherapy, decreasing potential for optimal therapeutic outcomes. The role of AHCC in attenuating various side effects was explored in non-tumor-bearing mice receiving monotherapy with paclitaxel, or multidrug chemotherapy including cisplatin plus paclitaxel, cisplatin plus 5-fluorouracil, 5-fluorouracil plus irinotecan, cyclophosphamide plus doxorubicin, and 6-mercaptopurine plus methotrexate [19,20]. We focused on GEM-induced hematotoxicity including bone marrow suppression, which is a dose-limiting toxicity
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