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Anti-tumorigenic and Pro-apoptotic effects of CKBM on gastric cancer growth in nude mice.

Shin VY, So WH, Liu ES, Wu YJ, Pang SF, Cho CH - Int J Med Sci (2004)

Bottom Line: Results showed that higher doses of CKBM (0.4 or 0.8 ml/mouse/day) produced a dose-dependent inhibitory effect on gastric tumor growth after 28-day drug treatment.This was associated with a decrease of cellular proliferation by 30% with concomitant increase in apoptosis by 97% in gastric tumor cells when compared with the control group.In contrast, CKBM showed no effect on angiogenesis in gastric tumors.

View Article: PubMed Central - PubMed

Affiliation: 1 Department of Pharmacology, Faculty of Medicine, The University of Hong Kong, Hong Kong, HKSAR, China.

ABSTRACT
Natural botanical products can be integrated with western medicine to optimize the treatment outcome, increase immune function and minimize the side effects from western drug treatment. CKBM is a combination of herbs and yeasts formulated based on traditional Chinese medicinal principles. Previous study has demonstrated that CKBM is capable of improving immune responsiveness through the induction of cytokine mediators, such as TNF-alpha and IL-6. In this study, we aimed to investigate the effect of this immunomodulatory drug on gastric cancer growth using a human xenograft model. Gastric cancer tissues were implanted subcutaneously into athymic nude mice followed by a 14-day or 28-day of CKBM treatment. Results showed that higher doses of CKBM (0.4 or 0.8 ml/mouse/day) produced a dose-dependent inhibitory effect on gastric tumor growth after 28-day drug treatment. This was associated with a decrease of cellular proliferation by 30% with concomitant increase in apoptosis by 97% in gastric tumor cells when compared with the control group. In contrast, CKBM showed no effect on angiogenesis in gastric tumors. This study demonstrates the anti-tumorigenic action of CKBM on gastric cancer probably via inhibition of cell proliferation and induction of apoptosis, and provides future potential targets of this drug candidate on cancer therapy.

No MeSH data available.


Related in: MedlinePlus

Effect of CKBM treatment (0.2, 0.4 or 0.8 ml/mouse, given i.g. once daily) for (A) 14 days; (B) 28 days on number of apoptotic cells in gastric tumors (*P<0.01 when compared with the control group).. Values are means ± SEM of 4-13 mice per group.
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Figure 3: Effect of CKBM treatment (0.2, 0.4 or 0.8 ml/mouse, given i.g. once daily) for (A) 14 days; (B) 28 days on number of apoptotic cells in gastric tumors (*P<0.01 when compared with the control group).. Values are means ± SEM of 4-13 mice per group.

Mentions: There was no significant effect on the number of apoptotic cells in the gastric tumors after 14 days of drug treatment (Figure 3A). However, prolonged treatment of CKBM to 28 days dose-dependently exhibited an induction of apoptosis in gastric cancer cells. At doses of 0.4 and 0.8 ml/mouse of CKBM treatment, apoptosis was significantly increased by 76% and 97% respectively when compared with the corresponding control group (Figure 3B).


Anti-tumorigenic and Pro-apoptotic effects of CKBM on gastric cancer growth in nude mice.

Shin VY, So WH, Liu ES, Wu YJ, Pang SF, Cho CH - Int J Med Sci (2004)

Effect of CKBM treatment (0.2, 0.4 or 0.8 ml/mouse, given i.g. once daily) for (A) 14 days; (B) 28 days on number of apoptotic cells in gastric tumors (*P<0.01 when compared with the control group).. Values are means ± SEM of 4-13 mice per group.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC1074708&req=5

Figure 3: Effect of CKBM treatment (0.2, 0.4 or 0.8 ml/mouse, given i.g. once daily) for (A) 14 days; (B) 28 days on number of apoptotic cells in gastric tumors (*P<0.01 when compared with the control group).. Values are means ± SEM of 4-13 mice per group.
Mentions: There was no significant effect on the number of apoptotic cells in the gastric tumors after 14 days of drug treatment (Figure 3A). However, prolonged treatment of CKBM to 28 days dose-dependently exhibited an induction of apoptosis in gastric cancer cells. At doses of 0.4 and 0.8 ml/mouse of CKBM treatment, apoptosis was significantly increased by 76% and 97% respectively when compared with the corresponding control group (Figure 3B).

Bottom Line: Results showed that higher doses of CKBM (0.4 or 0.8 ml/mouse/day) produced a dose-dependent inhibitory effect on gastric tumor growth after 28-day drug treatment.This was associated with a decrease of cellular proliferation by 30% with concomitant increase in apoptosis by 97% in gastric tumor cells when compared with the control group.In contrast, CKBM showed no effect on angiogenesis in gastric tumors.

View Article: PubMed Central - PubMed

Affiliation: 1 Department of Pharmacology, Faculty of Medicine, The University of Hong Kong, Hong Kong, HKSAR, China.

ABSTRACT
Natural botanical products can be integrated with western medicine to optimize the treatment outcome, increase immune function and minimize the side effects from western drug treatment. CKBM is a combination of herbs and yeasts formulated based on traditional Chinese medicinal principles. Previous study has demonstrated that CKBM is capable of improving immune responsiveness through the induction of cytokine mediators, such as TNF-alpha and IL-6. In this study, we aimed to investigate the effect of this immunomodulatory drug on gastric cancer growth using a human xenograft model. Gastric cancer tissues were implanted subcutaneously into athymic nude mice followed by a 14-day or 28-day of CKBM treatment. Results showed that higher doses of CKBM (0.4 or 0.8 ml/mouse/day) produced a dose-dependent inhibitory effect on gastric tumor growth after 28-day drug treatment. This was associated with a decrease of cellular proliferation by 30% with concomitant increase in apoptosis by 97% in gastric tumor cells when compared with the control group. In contrast, CKBM showed no effect on angiogenesis in gastric tumors. This study demonstrates the anti-tumorigenic action of CKBM on gastric cancer probably via inhibition of cell proliferation and induction of apoptosis, and provides future potential targets of this drug candidate on cancer therapy.

No MeSH data available.


Related in: MedlinePlus