Vidatox 30 CH has tumor activating effect in hepatocellular carcinoma.
Complementary and alternative medicine (CAM) is the term used to describe many kinds of products, practices, and systems that are not part of conventional medicine. Cancer patients usually do everything they can to combat the disease, manage its symptoms, and cope with the side effects of treatment. Unfortunately, patients who use CAM underestimate the risk of interaction with cancer therapy or worse they omit conventional therapy thus reducing the possibility of cancer remission. Herein we analyzed the effects of Vidatox 30 CH (venom extracted from the Junceus Rhopalurus scorpion) on hepatocellular carcinoma (HCC), the second leading cause of cancer-related deaths. We found out that Vidatox increases HCC proliferation and invasion whereas it does not seem to interact with sorafenib, the orally active multikinase inhibitor approved for the treatment of advanced hepatocellular carcinoma. Our results suggest that the concentration of Vidatox used in the present study has not anti-neoplastic effects and care must be taken in hiring Vidatox in patients with HCC.
Center for Applied Biomedical Research (CRBA), S. Orsola-Malpighi University Hospital, Bologna, Italy.|Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy.
Catia
C
Giovannini
Center for Applied Biomedical Research (CRBA), S. Orsola-Malpighi University Hospital, Bologna, Italy.
Michele
M
Baglioni
Department of Veterinary Medical Sciences, University of Bologna, Ozzano dell'Emilia, Bologna, Italy.
Marco
M
Baron Toaldo
Department of Medical and Surgical Sciences, S. Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy.
Matteo
M
Cescon
Center for Applied Biomedical Research (CRBA), S. Orsola-Malpighi University Hospital, Bologna, Italy.|Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy.
Luigi
L
Bolondi
Center for Applied Biomedical Research (CRBA), S. Orsola-Malpighi University Hospital, Bologna, Italy.
Laura
L
Gramantieri
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D006528:Carcinoma, Hepatocellular / Q000139:chemically induced* / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004052:Diethylnitrosamine; D015972:Gene Expression Regulation, Neoplastic; D056945:Hep G2 Cells; D022781:Hepatocytes / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008113:Liver Neoplasms / Q000139:chemically induced* / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D008297:Male; D009536:Niacinamide / Q000031:analogs & derivatives* / Q000494:pharmacology; D010671:Phenylurea Compounds / Q000494:pharmacology*; D017208:Rats, Wistar; D012605:Scorpions / Q000737:chemistry / Q000472:pathogenicity / Q000502:physiology; D015398:Signal Transduction; D000077157:Sorafenib; D013111:Spider Venoms / Q000037:antagonists & inhibitors / Q000302:isolation & purification / Q000633:toxicity*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000235:genetics / Q000378:metabolism
D000970:Antineoplastic Agents; D018797:Cell Cycle Proteins; D016207:Cytokines; D010671:Phenylurea Compounds; D013111:Spider Venoms; D016159:Tumor Suppressor Protein p53; D009536:Niacinamide; D004052:Diethylnitrosamine; D000077157:Sorafenib; C000602029:Kdr protein, rat; D040301:Vascular Endothelial Growth Factor Receptor-2