Sökning: "LOH"
Visar resultat 16 - 20 av 56 avhandlingar innehållade ordet LOH.
16. Molecular progression and clonality or urinary bladder cancer
Sammanfattning : The general aim of this work was to investigate the clonality of multifocal bladder tumours, chromosomal deletions and model the initiation-progression of bladder tumours at a molecular level using microsatellite analysis. In a population-based study, we found correlation between stage and grade and the prevalence of loss of heterozygosity (LOH) at all observed chromosome 13 loci and stage and grade, respectively. LÄS MER
17. Genetic changes in childhood acute lymphoblastic leukaemia and other lymphoid malignancies
Sammanfattning : Malignant transformation of normal cells is the result of defects in cell growth control, differentiation and programmed cell death. It has been convincingly shown that malignant cells carry mutations in the genes controlling these cellular processes. LÄS MER
18. Delection mapping of human 3p in major epithelial types of cancer and fine localization of candidate tumor suppressor genes
Sammanfattning : Allele loss and deletion mapping using microsatellite markers and the detection of homozygous deletions represented until now the most powerful method to localize potential TSGs. Loss of heterozygosity (LOH) involving several chromosome 3p regions accompanied by chromosome 3p deletions are detected in almost 100% of renal cell carcinoma (RCC), small (SCLCs) and more than 90% of non-small (NSCLC) cell lung cancers. LÄS MER
19. Molecular genetic analysis of human breast cancer
Sammanfattning : Breast cancer accounts for approximately 20% of all female malignancies with hereditary breast cancer being implicated in 5-10% of these cases. Two highly penetrant hereditary breast cancer genes are known; BRCA1 (17q) and BRCA2 (13q), which also confer an increased risk of cancer at other sites. 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