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Telomere Length in Colorectal Cancer
Tomášová, Kristýna ; Stiborová, Marie (advisor) ; Liška, Václav (referee)
Telomeres are non-coding nucleoprotein structures that make up the very end of each linear chromosome. They stabilize chromosome structure and thus prevent the ends from being recognized by DNA damage response machinery. Telomere shortening in the synthesis phase of the cell cycle is related to the loss of protective ability and the finite replicative potential of the cell. The environmental factors, impaired DNA repair pathways, and loss of telomeric DNA-binding proteins exert negative effects on telomere function. Telomere dysfunction instigates chromosomal rearrangements and together with telomere erosion precedes tumorigenesis. Extension of telomeric DNA is catalyzed by the enzyme telomerase, whose activity is repressed in most adult somatic cells, except for stem cells, lymphocytes, and some cancer cell types. Colorectal cancer comprises malignant tumors of the colon and rectum. It is the second most common cancer in both sexes in the Czech Republic, with over 81,000 cases diagnosed in 2013 and 55.2% overall survival at 5 years. This study focuses on the association of telomere length to clinico-pathological features of the colorectal cancer patients and investigates also the effect of cancer treatment on telomere length. Further, it compares two methods of telomere length measurement; the...
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The Role of DNA Repair in the Onset and Therapy of Ovarian Cancer
Tomášová, Kristýna ; Vodička, Pavel (advisor) ; Čáp, Michal (referee)
DNA repair and DNA damage response are very important biological systems, inevitable to maintain genomic stability and fidelity of the genetic information, for the onset of ovarian cancer. Further, DNA repair is also substantially involved in the response to the therapy, since many chemotherapeutics act as DNA damaging agents. This literary analysis is intended to survay the relevance of DNA repair to ovarian carcinogenesis. Special emphasis is placed on repair defects, as it is inextricably associated with the onset of cancer and treatment outcome. Apart from well-known alternations in ovarian cancer susceptibility genes, such as BRCA1 and BRCA2 involved in homologous recombination repair, ample space will be dedicated to less common gene mutations across different repair pathways. Research confirms that abnormalities in the proteins responsible for homologous recombination repair are the leading cause of ovarian cancer. The majority of authors also suggested that targeting DNA repair pathways, especially base excision repair, can improve chemotherapy efficiency in a synergic manner. The same applies to nucleotide excision repair, which repairs platinum-DNA adducts and thus contibutes to platinum drugs resistance emerging. By way of contrast, mismatch repair in ovarian cancer is rather poorly...
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