• Asian Pacific Journal of Cancer Prevention
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• 제14권4호
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• pp.2201-2205
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• 2013

Colorectal cancer (CRC) is one of the most common cancers in many parts of the world. Its development is a multi-step process involving three distinct stages, initiation that alters the molecular message of a normal cell, followed by promotion and progression that ultimately generates a phenotypically altered transformed malignant cell. Reports have suggested an association of the phosphoinositide-3-kinase (PI3K)/Akt pathway with colon tumorigenesis. Activation of Akt signaling and impaired expression of phosphatase and tensin homolog (PTEN) (a negative regulator of Akt) has been reported in 60-70% of human colon cancers and inhibitors of PI3K/Akt signaling have been suggested as potential therapeutic agents. Around 80% of human colon tumors possess mutations in the APC gene and half of the remainder feature ${\beta}$-catenin gene mutations which affect downstream signaling of the PI3K/Akt pathway. In recent years, there has been a great focus in targeting these signaling pathways, with natural and synthetic drugs reducing the tumor burden in different experiment models. In this review we survey the role of PI3K/Akt/mTOR and Wnt signaling in CRC.

• 약학회지
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• 제38권6호
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• pp.763-769
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• 1994

Bifidobacterium bifidum, one strain of medical preparation being on the market for human intestinal disorders, was sensitive to rifampicin and fluoroquinolones. If this preparation is taken with rifampicin and fluoroquinolones, its therapeutic effect can't be expected. Serial passage of B. bifidum RFR61, which was obtained by MNNG mutation method, on agar with 2-fold minimal inhibitory concentration of ofloxacin produced B. bifidum OFR9 with minimal inhibitory contentrations of fluoroquinolones up to $4{\sim}256-fold$ higher than that for the original strain. B. bifidum OFR9 produced almost the same amount of organic acid as parental strain. This strain showed growth inhibitory activity against E. coli NM522, Shigella dysenteriae ATCC9752 and E. coli 078. No inactivations of rifampicin and ofloxacin by this resistant mutant strain were found.