Current theories proposed to interpret the pathogenesis of neoplastic disease can be grouped into two broad categories: those that are mainly cell-oriented and those that consider carcinogenesis as a tissuebased process. While the two views are not mutually exclusive, they do imply basically different approaches in the analysis of the long sequence of events leading to the emergence of the neoplastic phenotype. Cell-oriented hypotheses rest on the assumption that carcinogenesis is mainly, if not exclusively, a cell autonomous process; as such, it can be largely, if not entirely explained by a detailed characterization of genetic/molecular changes occurring inside the cell population undergoing neoplastic transformation. On the other hand, tissue-oriented hypotheses are based on a rather different paradigm: according to this perspective, carcinogenesis can be correctly interpreted and analysed only if it is considered as a true biological process taking place in a given tissue or organ: it follows that any conceptual framework attempting to describe or explain the natural history of neoplastic disease must incorporate the pathophysiology of the tissue microenvironment in which the process is occurring. While there is no doubt that cell-oriented (or cell-autonomous) hypotheses have dominated and shaped the field of cancer research for the past 30 – 40 years, the last decade has witnessed an ever increasing reappraisal of the fundamental concept that biological processes, including the biology of carcinogenesis, need to be placed into context if we are to gain meaningful information to be applied in the clinics. Thus, the role of the microenvironment has been re-emphasized both for its relevance to the pathogenesis of neoplastic disease and, most lately, as a possible target for preventive and/or therapeutic interventions.
Altered Morphology in the Pathogenesis of Neoplastic Disease
LACONI, EZIO
2013-01-01
Abstract
Current theories proposed to interpret the pathogenesis of neoplastic disease can be grouped into two broad categories: those that are mainly cell-oriented and those that consider carcinogenesis as a tissuebased process. While the two views are not mutually exclusive, they do imply basically different approaches in the analysis of the long sequence of events leading to the emergence of the neoplastic phenotype. Cell-oriented hypotheses rest on the assumption that carcinogenesis is mainly, if not exclusively, a cell autonomous process; as such, it can be largely, if not entirely explained by a detailed characterization of genetic/molecular changes occurring inside the cell population undergoing neoplastic transformation. On the other hand, tissue-oriented hypotheses are based on a rather different paradigm: according to this perspective, carcinogenesis can be correctly interpreted and analysed only if it is considered as a true biological process taking place in a given tissue or organ: it follows that any conceptual framework attempting to describe or explain the natural history of neoplastic disease must incorporate the pathophysiology of the tissue microenvironment in which the process is occurring. While there is no doubt that cell-oriented (or cell-autonomous) hypotheses have dominated and shaped the field of cancer research for the past 30 – 40 years, the last decade has witnessed an ever increasing reappraisal of the fundamental concept that biological processes, including the biology of carcinogenesis, need to be placed into context if we are to gain meaningful information to be applied in the clinics. Thus, the role of the microenvironment has been re-emphasized both for its relevance to the pathogenesis of neoplastic disease and, most lately, as a possible target for preventive and/or therapeutic interventions.
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