Evolutionary malignant resistance of cells to damaging factors as common biological defence mechanism in neoplastic development. Review of conception.
Cells have some inborn resistance to harmful factors, which could be called physiological or natural resistance. The mechanisms of multixenobiotic resistance (MXR) and multidrug resistance (MDR) have common features in the formation of acquired resistance in microorganisms, carcinogenesis, tumour metastases and chemotherapy or irradiation. ATP-dependent membrane P-glycoprotein, as an MDR efflux pump, glutathione S-transferases and other products of evolutionary resistance-related genes arised for exportation and detoxification of cytotoxic xenobiotics and drugs are transmitted from bacteria to man. On the one hand, this evolutionary MXR as a common biological defence mechanism is a "driving" power to conserve homeostasis of cells, tissues and organs. On the other hand, mutation, selection and simplification of properties are the causes of functional and morphological changes in tumour cells which regress to a more primitive mode of existence (atavism) for adaptation to survival. In the present work are presented data on the forms of E. coli resistant to antibiotics and of sarcoma 45 resistant to alkylic preparations. They may be helpful in revealing the causes of resistance and acquired accelerated growth of cells. The development of tumours as fibromas 14-15 years following injection of a vital dye trypan blue into human skin supports our conception that neoplastic growth is a particular case of the evolutionary resistance of cells adapted to the damaging factors. So, tumour cells adopting the enhancement mechanisms of general biological persistent resistance, i. e. undergoing repeated cycles of malignancy enhancement, adapt themselves to survive under the changed unfavourable conditions.
Monceviciute-Eringiene
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Laboratory of Preventive Immunology, Lithuanian Oncological Centre, Vilnius.
D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1 / Q000378:metabolism; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001419:Bacteria / Q000187:drug effects*; D002273:Carcinogens / Q000633:toxicity*; D003674:Defense Mechanisms; D004352:Drug Resistance, Microbial; D018432:Drug Resistance, Multiple / Q000502:physiology*; D019008:Drug Resistance, Neoplasm / Q000502:physiology*; D005982:Glutathione Transferase / Q000378:metabolism; D006801:Humans; D007114:Immunization; D008954:Models, Biological; D009369:Neoplasms / Q000503:physiopathology*; D051381:Rats; D012509:Sarcoma / Q000503:physiopathology*; D014343:Trypan Blue / Q000494:pharmacology; D014407:Tumor Cells, Cultured / Q000187:drug effects; D015262:Xenobiotics / Q000494:pharmacology
D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1; D000900:Anti-Bacterial Agents; D002273:Carcinogens; D015262:Xenobiotics; D005982:Glutathione Transferase; D014343:Trypan Blue