Molecular mechanisms of the cross-impact of pathological processes in combined diabetes and cancer. Research and clinical aspects.
The mechanisms of interaction and cross-impact of metabolic processes in a combined diabetes and cancer condition are discussed. A hypothesis is proposed whereby the processes responsible for destruction of the organism in the case of diabetes--long-term hyperglycemia and generation of methylglyoxal--may substantially impact tumor development. The hypothesis is based on the fact that both diabetes and carcinogenesis cause dysfunction of the vital cellular signal system regulated by the protein kinase C (PKC) family. Normalization of the PKC functional activity in the case of diabetes restrains development of diabetic complications and inhibits the processes of tumor growth and metastasizing in carcinogenesis. On this basis, an attempt is made to interpret both the detrimental and beneficial effects of diabetes on cancer. The resultant effect is determined by the type of tumor and the duration and level of hyperglycemia. The mechanisms of the impact of diabetes mellitus on cancer are analyzed to develop recommendations for combined cancer therapy options.
Aleksandrovski
Ya A
YA
Kantorforschungsgruppe, 76530 Baden-Baden, Germany. Yakov.Alexandrovski@t-online.de
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D003920:Diabetes Mellitus / Q000276:immunology / Q000473:pathology* / Q000628:therapy; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism; D009369:Neoplasms / Q000276:immunology / Q000473:pathology* / Q000628:therapy; D009504:Neutrophils / Q000473:pathology; D011493:Protein Kinase C / Q000378:metabolism; D011765:Pyruvaldehyde / Q000494:pharmacology; D014407:Tumor Cells, Cultured
D011765:Pyruvaldehyde; D011493:Protein Kinase C