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Comparative oncology is a branch of comparative pathology that is relatively new …


Biology Articles » Evolutionary Biology » Comparative Oncology and Comparative Tumor Immunology » Comparative oncology

Comparative oncology
- Comparative Oncology and Comparative Tumor Immunology

One of the tasks of comparative oncology is the identification of carcinogenic factors and mechanisms of their influence on the cells of different, phylogenetically distant multicellular organisms, as well as of differences in sensitivity of these cells to carcinogenic factors. Even though there are no reliable data regarding the incidence of tumors in different groups of multicellular organisms, some studies indicate the possibility that tumor incidence might be growing along with the growing complexity of observed species and their place on the evolutionary scale. [1,2,3,4]

The rationale behind such phenomenon could be the stability of genome and the reliability of mechanisms controlling the cell-cycle. For example, simple multicellular organisms, such as yeasts, may have simpler and more reliable machinery and more effective repair mechanisms for damaged DNA sequences. Unlike these, higher multicellular organisms, like vertebrates, have a more complex but less stable genome, as well as more complex surveillance mechanisms, which could be taken into account for a higher tumor incidence in vertebrates in comparison with the lower multicellular organisms. Yet, there are data that significant differences regarding tumor incidence might be present across different classes of vertebrates.

Thus, Effron et al. [5] presented the rate of neoplasia at necropsy of captive wild animals of the Zoological Society of San Diego collection. Neoplasia was present at necropsy in 2.75% of 3,127 mammals, 1.89% of 5,957 birds, and 2.19% of 1,233 reptiles. Interestingly, neoplasms were not detected during 198 necropsies of amphibians. The same authors argue that the most common types of tumors differ greatly across vertebrate classes as well [5]. Notably, lymphosarcoma was the most common tumor registered in birds and reptiles while various types of tumors, such as adenomas, hepatoma and different lines of carcinomas were registered in mammals.

Unfortunately, the research did not include tumor incidence in cartilaginous fish and bony fish, though there are data indicating a very low tumor incidence in the former and particularly in the latter. Namely, Hendricks et al. [6] failed to prove the presence of tumors on 144 necropsies in brown bullheads (Ictalurus nebulosus), but tumor incidence in the same type of fish taken from polluted waters ranged 30% on the sample of 532 [6].

Neoplasms do appear in all non-mammalian vertebrates and this is important in and of itself since these animals can serve as models to understand the behaviour and trajectory of such tumors in mammals and humans. Thus, an inter-disciplinary effort must begin among collectors, zookeepers, veterinarians, comparative pathologists in order to obtain comprehensive documentation that would help us to understand neoplasms more thoroughly not only in non-mammals, but also in mammals and humans. There are many reasons to believe that the phenomenon of carcinogenesis follows the same or similar postulates across all vertebrate classes. A large number of studies also indicate the possibility that the biological fundaments of carcinogenesis in vertebrates are observable in invertebrates, as well. It is clearly, therefore, that one of the primary steps leading towards carcinogenesis in all vertebrates is the destabilization of the genome and loss of cells' ability to repair DNA damage. Genome destabilization ending in carcinogenesis is, basically, the consequence of a series of mutations or translocations, and comes largely as a result of the influence of chemical agents, viral infections, radiation and chronic inflammations including auto-immune processes. What makes an altered cell malignant is the activation of individual genes or group of genes, otherwise normally functional during embryogenesis. An incomplete and inadequate ontogenic regression in terms of both time and space results in the loss of sociability of the altered cell, destruction of its environment and the host. The described mechanism of cell alteration has been verified in all classes of vertebrates, except for cartilaginous fish where few cases of tumors have been registered. Some of the reasons for considerable variations regarding tumor incidence across vertebrate classes, may be contained within genome stability, as well as various possibilities for repairment of the DNA damage [7,8].

Although some neoplasms are directly hereditary, genetic predisposition is only one of factors affecting the occurrence of all neoplasms. The tendency of certain species to develop particular types of tumors is a well-known aspect of comparative oncology [9]. Apart from a great similarity in cell organization across vertebrates, there is an opinion that DNA and mechanisms regulating the cell-cycle in lower vertebrates are more stable and more resistant to the influence of various carcinogens [10]. This explanation is quite acceptable from the aspect of control mechanisms of the cell-cycle and DNA stability as being "the first line of defence" from malignant cell alteration. The immune system could represent "the second line" of anti-tumor defence. Due to the possible significance of the immune system in anti-tumor protection, differences in anti-tumor efficacy among different groups of multicellular organisms could also be of great influence for the incidence of manifesting tumors [4]. However, it is very difficult to make a viable conclusion as to how much the failure of the "first", particularly "the second" line of defence really contribute to even greater differences in tumor incidence across various groups of multicellular organisms. This dilemma may be solved by future research in the field of comparative oncology, particularly by developing disciplines such as comparative tumor genetics and comparative tumor immunology.


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