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Telomere Dysfunction and Evolution of Instestinal Carcinoma in Mice and Humans

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This research is one of many scientific attempts to better understand the specifics of telomere function and its effects on the cell growth. By understanding this relationship it becomes possible to understand the behavior of telomeres in the uncontrollable cell growth, which could be a step further in the understanding and the treatment of cancers. Some prior experiments revealed that some carcinogenesis (development of cancer) such as colorectal carcinogenesis are followed by the robust telomerase activity, which suggested the necessity of telomere lengthening for the progression of cancer. However, knocking out the telomerase gene and bringing thus the telomeres to their dysfunctional state, researchers discovered some very interesting trends in the growth of tumors. This research looks at the impact of such dysfunctional telomeres on the behavior of tumor cells.

They monitored the effects of different levels of telomere dysfunction on the growth and behavior of carcinomas in the Apc(Adenomatous Polyopsis Coli - tumor suppressor gene) min mice (knocked out one Apc allele, which thus decreases the Apc gene's activity in half). They generated Terc-/-(knocked out telomerase gene)Apc-min mice which they then crossed and created four generations. These mice had no telomerase activity that is needed to lengthen the telomeres of the parental chromosomes in the germ line so that the offspring of each consecutive generation would inherit the shorter version of chromosomes than the prior generation. This kind of manipulation provides a situation where each generation has shorter telomeres, which means greater telomere dysfunction, and thus greater chromosomal instability. If chromosomes are unstable, that means that they are more prone to chromosomal aberrations and promotion of the Apc-min allele deletion. In fact, Apc-min is the key assay in tracking down the effects of telomeres. Intestinal carcinomas will have greater success if there is no Apc allele to perform suppression. Apc allele can get deleted if the whole chromosome 18, on which the Apc allele is, gets lost, and it is the chromosomal instability (caused by the telomere dysfunction) that can lead to this kind of loss.

The results showed that the survival rate of the control mouse (Terc+/+Apc-min) and the first generation (G1) mouse (Terc-/-Apc-min) had a much greater survival rate than the G2 and G3. This makes sense, because the shorter the telomeres are, the greater the chromosomal instability is and thus there's a greater loss of the Apc suppressor allele. However, in the G4 where the telomeres were the shortest there was an increase in survival. This indicated that the telomere dysfunction has different influences on the emergence and growth of cancer. In accord to this was another interesting set of results. They counted the number of microadenomas (smaller tumor cells) versus the number of macroadenomas (larger tumor cells-also indicators of a more progressive tumor growth) in each generation (adenoma phenotype is quantitative). There was a significant increase in the number of microadenomas and significan decrease of macroadenomas in G3 and G4 in relation to the number of previous G1 and G2 generations. In fact the number of macroadenomas peaked in the G2 and one of the G3 and 5 out of 6 in G4 mice showed almost no



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