Sökning: "Microsatellite Instability"
Visar resultat 16 - 20 av 32 avhandlingar innehållade orden Microsatellite Instability.
16. Gut microbiota in colorectal cancer : The importance of Parvimonas micra
Sammanfattning : Colorectal cancer (CRC) is a heterogenous disease consisting of multiple molecular subtypes, each of which has diverse treatment responses and prognoses. The importance of the gut microbiota in CRC development and progression has undergone increasing recognition in recent years, with a structural segregation in terms of microbial composition between CRC patients and healthy controls. LÄS MER
17. Molecular genetics of hereditary non-polyposis colorectal cancer
Sammanfattning : 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. LÄS MER
18. Morphological Features and Mismatch Repair in Colorectal Tumors
Sammanfattning : 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. LÄS MER
19. Genetic and epidemiological studies of hereditary colorectal cancer
Sammanfattning : 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). LÄS MER
20. Targeting allelic loss in colorectal cancer
Sammanfattning : 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. LÄS MER