Outlines of a general framework of cancer initiation in the cell

According to the central dogma of molecular biology, informationflows in the living cell from DNA through RNA to proteins. Therefore mostinvestigations of cancer initiation try to explain these effects bycarcinogen binding to, or radiation hits on, DNA which lead to the firststeps of the malignant transformations. On the other hand, recent detailedtheoretical investigations have shown that proteins are good disorderedhopping conductors (their conductivity is in the order of good conductingamorphous glasses). Their conductivity can be substantially influenced bybinding of chemicals or by the effects of radiation if they causeconformational changes (as recent calculations have shown). These effectscan also destroy bonds or generate new bonds in proteins. If the affectedproteins are regulatory proteins, they can be inactivated in both ways.Namely, on the basis of Warburg's experiments, one can postulate thatif the hindrance of oxygen metabolism leads to fermentation, and with it tothe malignant transformation, this means also the hindrance of electronflow in the Szent‐Györgyi–Krebs cycle. In other words thehindrance of electron transport in this cycle most probably has the sameeffect as the lack of oxygen, which in this way most probably leads againto a malignant transformation. Finally the inactivation of regulatoryenzymes can influence also the regulation of the expression of oncogenes.If in this way oncogenes become overactivated (or antioncogenes becomeinactive), the changes started by the inactivation of regulatory enzymesbecome hereditary. It seems that if we look at the cell as a complicatedself‐regulatory system, primary changes both at their DNA or regulatoryprotein molecules caused by external agents can disturb its self‐regulationand transform it in this way into another stationary, possiblyprecancerous, state. © 1997 John Wiley & Sons, Inc. Int JQuant Chem 64 : 379–385, 1997