Ecancermedicalscience. 2009;3:131. doi: 10.3332/ecancer.2009.131. Epub 2009 Jan 15.
ABSTRACT
Pancreatic cancer consists of an accumulation of genetic and epigenetic alterations. Recently, aberrant methylation of CpG islands of cancer-related genes has emerged as an important epigenetic mechanism of their transcriptional dysregulation during tumour development [1]. Therefore, new diagnostic methods, for early detection based on a better understanding of the molecular biology of pancreatic cancer, are required. We examined the methylation status of p(16INK4A), RASSF 1A and methylguanine methyltransferase (MGMT) genes considered to be inactivated by promoter methylation in several tumours.The p(16INK4A) is an important G1/S cell cycle regulator gene [2]. RASSF 1A gene is involved in apoptotic signalling, microtubule stabilization and cell cycle progression [3]. The MGMT gene removes mutagenic and cytotoxic alkyl-adducts from the O6-position of guanine in DNA. Hypermethylation of the gene leads to the inactivation of DNA repair and to microsatellite instability [4].To date, little is known about the exact role of hypermethylation of these genes in pancreatic adenocarcinoma, as the molecular mechanisms underlying these neoplasms remain poorly understood.
PMID:22276000 | PMC:PMC3223988 | DOI:10.3332/ecancer.2009.131
Pancreatic cancer consists of an accumulation of genetic and epigenetic alterations. Recently, aberrant methylation of CpG islands of cancer-related genes has emerged as an important epigenetic mechanism of their transcriptional dysregulation during tumour development [1]. Therefore, new diagnostic methods, for early detection based on a better understanding of the molecular biology of pancreatic cancer, are required. We examined the methylation status of p(16INK4A), RASSF 1A and methylguanine…
