Abstract
Carcinogenesis is a multistage process, resulting from the accumulation of genetic alterations. Proliferation of normal cells is thought to be regulated by growth-promoting proto-oncogenes counterbalanced by growth-constraining tumour suppressor genes (TSG) (Weinberg 1991). During tumour initiation and progression, proto-oncogenes may be activated by amplification, rearrangement or point mutation, whilst loss of function of TSG may be caused by deletion or mutation. Precisely how many genetic alterations are required for tumourigenesis is unclear; statistical analysis based on age-specific data suggests that five or six steps are generally necessary (Renan 1993). In a molecular model specific for colorectal tumourigenesis, it has been proposed that mutations in at least four to five genes are required for the formation of a malignant tumour (Fearon and Vogelstein 1990). In the case of head and neck cancer, however, it has been suggested that a greater number of genetic lesions are required (Renan 1993), and it is evident from allelotype analysis that the process is complex (Field et al. 1995b).
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Current topics in pathology. Ergebnisse der Pathologie
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
