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DOI: 10.1055/s-0031-1298149
© Georg Thieme Verlag KG Stuttgart · New York
Solasodine Rhamnosyl Glycosides Cause Apoptosis in Cancer Cells. Do They Also Prime the Immune System Resulting in Long-Term Protection against Cancer?
Publication History
received Nov. 9, 2011
revised Nov. 28, 2011
accepted Dec. 9, 2011
Publication Date:
13 January 2012 (online)

Abstract
Solasodine rhamnosyl glycosides (SRGs) induce apoptosis in a wide variety of cancer cells and are more effective than many well-established anticancer agents. Combination therapy of SRGs with cisplatin treats cisplatin–resistant cells such as lung cancer and breast cancer cells. Anticancer therapies with SRGs have been used intravenously, intraperitoneally, intralesionally, orally, and topically. Data is now presented that in addition to apoptosis and, perhaps as a consequence thereof, SRGs also have an effect of stimulating lasting immunity against cancer as shown with a mouse model and the terminal cancer Sarcoma 180. Mice were inoculated i. p. with Sarcoma 180. Groups of animals were administered SRGs half an hour after Sarcoma 180 inoculation. Mice treated with Sarcoma 180 but not with SRGs all died within 20 days. Four doses of SRGs caused total remission of Sarcoma 180 activity. Mice that went into remission were then reinoculated 20 days later with the cancer. Ten of twelve SRGs cured-animals were resistant to reinduction of terminal doses of the cancer. In comparison, twelve of twelve mice treated with SRGs without initial Sarcoma 180 activity but which were inoculated with Sarcoma 180 cells 20 days later, all died. In addition to apoptosis, SRGs stimulate lasting immunity against cancer. SRGs could play an important role in clinical management of diseases such a malignancy and also be used as a preventative therapy.
Key words
cancer - Solanum sodomaeum - Solanaceae - solamargine - solasonine - apoptosis - immunity
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Prof. Dr. Bill E. Cham
Australasian Medical Research
PO Box 7031
Port Vila
Republic of Vanuatu
South Pacific
Phone: +67 87 75 09 87
Email: bill.cham@gmail.com