Carcinogenesis remains an unchartered territory, whatever our progress in understanding the malignant process may be. The multistage, orderly hypothesis of initiation, promotion and progression was based on empirical observations in models ? and has remained a hypothesis for many decades. Even the success of molecular biology is not able to mimic ?real-life? carcinogenesis and does not provide an answer to the essential questions: does clinical cancer arise from one or more cells, is it dependent solely on genes or on an environmental event or events or both? And more recently, how big or small is the role of epigenetic factors, such as the modulated gap-junctional intercellular communication?
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