Abstract
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Prostate cancer is the second leading cause of cancer death in men
We suggest that specific adenomatous polyposis coli (APC) mutations associated with beta-catenin functions cooperate toward chromosomal instability and aneuploidy in human sporadic colorectal adenomas
Cells in S-phase has doubled in number when they were kept on extracellular matrix (ECM)-gel or treated with heparan sulfate proteoglycan (HSPG) or fibronectin
Summary
Prostate cancer is the second leading cause of cancer death in men. A major prerequisite for tumor initiation and progression is the acquisition of chromosomal aberrations. Array-based comparative genomic hybridization (aCGH), which permits the screening of DNA samples for deletions and amplifications of chromosomal regions at a resolution 10–100 times greater than that of conventional CGH methodologies, will allow the rapid identification of the genes frequently amplified on these arms. The present study aims to analyse DNA copy number changes at 8q23-24 in colorectal cancer at high resolution in correlation to metastatic disease. We recently proposed a 800 kb region at 20q13.2 to harbor a putative oncogene relevant for gastric cancer, and gain of 20q appeared to be one of the major chromosomal changes involved in colorectal adenomato-carcinoma progression. Still several candidate oncogenes remain at 20q13, while areas outside this region frequently show gains To this end, we tested the presence of DNA copy number changes for multiple genes in a series of gastric and colorectal cancers, using multiplex ligation-dependent probe amplification (MLPA). MLPA is a quantitative multiplex PCR based approach that allows to determine the relative copy number of up to 40 genes in a single experiment, requiring only minimal amounts of DNA
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