Search for dissertations about: "Microsatellite Instability"
Showing result 16 - 20 of 32 swedish dissertations containing the words Microsatellite Instability.
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16. Gastroesophageal reflux disease - complications and prognostic aspects
Abstract : This thesis investigates several aspects on gastroesophageal reflux disease (GERD) and associated complications as Barrett’s esophagus and esophageal adenocarcinoma. I. To clarify the natural course of GERD, a pH-metry verified cohort was re-evaluated after 20 years. The course of GERD may well be progressive. READ MORE
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17. Molecular genetics of hereditary non-polyposis colorectal cancer
Abstract : Colorectal cancer (CRC) is one of the most prevalent malignancies in the Western World and one of the most predominant causes of death by cancer. There is a subgroup of syndromes with a high incidence of CRC which is transmitted in an autosomal dominant fashion. READ MORE
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18. Morphological Features and Mismatch Repair in Colorectal Tumors
Abstract : Corlorectal cancer affects 5% of individuals in the Western world and heredity is estimated to cause at least 10% of the tumors. Defective mismatch repair (MMR) is a tumorigenic mechanism through which about 15% of colorectal cancer develops and this feature characterizes tumors associated with Hereditary Nonpolyposis Colorectal Cancer (HNPCC) or Lynch syndrome. READ MORE
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19. Genetic and epidemiological studies of hereditary colorectal cancer
Abstract : Lynch syndrome (Hereditary Nonpolyposis Colorectal Cancer, HNPCC) is the most common hereditary syndrome predisposing to colorectal cancer, accounting for 1-3% of all colorectal cancer. This multi-organ cancer predisposition syndrome is caused by mutations in the mismatch repair (MMR) genes, especially MLH1 and MSH2, and to lesser extents MSH6 and PMS2, which lead to widespread genetic instability and thus microsatellite instability (MSI). READ MORE
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20. Targeting allelic loss in colorectal cancer
Abstract : Targeted cancer therapy exploits molecular differences between tumor and normal cells to selectively kill cancer cells. Whereas targeting of activated oncogenes has proved clinically useful, few current therapies exploit loss-of-function mutations in tumor suppressor genes or in the genome at large. READ MORE