It was recently discovered in an Australian wild animal population that a rare f
ID: 163147 • Letter: I
Question
It was recently discovered in an Australian wild animal population that a rare form of oral/facial cancer was spreading through the population. This contagious cancer has been reducing the animal population. Design an experiment to determine if this contagious cancer is due to a virus or the result of a non-viral mutation. (You must consider that this could be a novel virus that ONLY grows in the wild animal tissues indicated (or of course, it might NOT be a virus at all. That is what you need to find out). And, you must consider that this is a situation where the tumor is contagious. Something is being passed from one animal to another. Also, think about early studies on viruses and cancer.)
Explanation / Answer
Models for devil facial tumor disease (DFTD) and canine transmissible venereal tumor (CTVT) immune evasion. (a) DFTD escapes immune detection because major histocompatibility complex (MHC) class I and class II lack functional diversity in Tasmanian devils. The tumor cells continue to proliferate as they are not recognized as foreign. (b) CTVT has distinct phases of growth, progressive and regressive. During the progressive phase, the tumor cells do not express MHC class I or class II, and the tumor secretes transforming growth factor-1 (TGF1), a cytokine that inhibits tumor-infiltrating lymphocyte (including natural killer cell) cytotoxicity. Tumor cells may also inhibit some types of antigen-presenting cells. Tumor-infiltrating lymphocytes are present in low numbers. During the regressive phase, tumor-infiltrating lymphocytes increase in number, and their secretion of IFN and interleukin-6 (IL6) counteracts the repressive effects of tumor-derived TGF1, and induces MHC class I and class II expression in tumor cells. MHC expression reveals CTVT as an allograft, and it is rejected by both antibody-dependent and -independent cytotoxic processes.
Tasmanian devil facial tumor disease (DFTD) and canine transmissible venereal tumor (CTVT) are the only known naturally occurring clonally transmissible cancers. These cancers are transmitted by the physical transfer of viable tumor cells that can be transplanted across histocompatibility barriers into unrelated hosts. Despite their common etiology, DFTD and CTVT have evolved independently and have unique life histories and host adaptations. DFTD is a recently emerged aggressive facial tumor that is threatening the Tasmanian devil with extinction. CTVT is a sexually transmitted tumor of dogs that has a worldwide distribution and that probably arose thousands of years ago. By contrasting the biology, molecular genetics and immunology of these two unusual cancers, I highlight the common and unique features of clonally transmissible cancers, and discuss the implications of clonally transmissible cancers for host-pathogen evolution.
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