One decade of comparative molecular carcinogenesis.
The field of comparative carcinogenesis has expanded greatly during the last decade. During this decade, the advent of molecular biology techniques allowed the isolation and identification of several oncogenes and tumor suppressor genes. Analysis of genetic alterations in these genes enabled the first dissection and comparison of carcinogenesis pathways in humans and rodents at the molecular level. The results showed that most of the oncogenes-/tumor suppressor genes found to be altered in humans were also altered in rodents. Even the molecular pathways involved in carcinogenesis appear to be similar in some organs. Unfortunately, there are still many unknown steps in the process of carcinogenesis. However, overall, the results still indicate that in spite of the differences between rodents and humans, the use and comparison of rodent models with human tumorigenesis is one of the best ways to 1) examine the mechanisms of carcinogenesis, 2) to identify potential carcinogenic compounds, and 3) to help determine potential carcinogenic risk for humans. The potential validity of the comparative carcinogenesis approach should become even more valuable as it becomes more fine-tuned due to the application of new approaches and the identification of new genes for study. The rapid pace of genomic mapping, the use of loss of heterozygosity studies, and the use of genetically susceptible populations (rodents and humans) has and will continue to allow the localization, isolation, and identification of new cancer genes. As each gene is analyzed in human and rodent tumors, the molecular pathway comparisons will become more accurate and detailed. This combined with molecular epidemiological and transgenic approaches will assure that the field of comparative carcinogenesis will continue to grow and be important in the next decade.
Goodrow
T L
TL
Department of Pathology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
D000818:Animals; D003043:Cocarcinogenesis; D004198:Disease Susceptibility; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D009369:Neoplasms / Q000209:etiology / Q000235:genetics*; D009374:Neoplasms, Experimental / Q000209:etiology / Q000235:genetics; D009857:Oncogenes; D051381:Rats; D013045:Species Specificity