2012
DOI: 10.1097/ppo.0b013e31827459b6
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Pathology and Molecular Genetics of Pancreatic Neoplasms

Abstract: Cancer is fundamentally a genetic disease caused by the ac cumulation of somatic mutations in oncogenes and tumor suppressor genes. In the last decade, rapid advances in sequencing and bioinformatic technology led to an explosion in sequencing studies of cancer genomes, greatly expanding our knowledge of the genetic changes underlying a variety of tumor types. Several of these studies of cancer genomes have focused on pancreatic neoplasms, and cancers from the pancreas are some of the best characterized tumors… Show more

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Cited by 131 publications
(111 citation statements)
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References 103 publications
(112 reference statements)
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“…These findings help establish that PanIN lesions can indeed be precursors to invasive PDA. Supporting this conclusion, is the observation in genetically engineered mouse models that activation of Kras in the pancreas produces mouse PanIN lesions [33].…”
Section: Pancreatic Ductal Adenocarcinomasupporting
confidence: 56%
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“…These findings help establish that PanIN lesions can indeed be precursors to invasive PDA. Supporting this conclusion, is the observation in genetically engineered mouse models that activation of Kras in the pancreas produces mouse PanIN lesions [33].…”
Section: Pancreatic Ductal Adenocarcinomasupporting
confidence: 56%
“…Grossly, most SCAs appear as multilocular or unilocular microcystic lesions. They sometimes have a characteristic central star-shaped scar with calcifications [33]. Microscopically, the well-demarcated cysts have a single layer of cuboidal glycogen-rich epithelium.…”
Section: Serous Cystadenomasmentioning
confidence: 99%
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“…Cancer cell-specific mutations were additionally used to estimate the fraction of pancreatic cancer cells. Mutation allele frequencies of 55 cancer-related genes including KRAS, which is known to be mutated in approximately 90% of pancreatic cancers [20,[29][30][31], were analyzed by targeted deep sequencing. In the 19 tumor samples with a KRAS mutation (7 IPMNs, 12 pancreatic cancers), substantial levels of methylation of the fraction marker genes (methylation level ≥10%) were also observed in all of them (online suppl.…”
Section: Methylation Levels In Pancreatic Surgical Specimensmentioning
confidence: 99%
“…Similarly, numerous molecular alterations are also required for pancreatic intraepithelial neoplasias (PanIN) lesions to develop into PDAC. Previous studies have established that PDAC is characterized by four signature mutations including mutations in GTPase KRas (KRAS) oncogene and in cyclin-dependent kinase inhibitor 2A (CDKN2A), tumor protein p53 (TP53), and SMAD family member 4 (SMAD4) tumor suppressor genes (2,3). Approximately 90% of pancreatic neoplasms express mutant KRAS, which has been hypothesized to be the initiator of PDAC.…”
Section: Introductionmentioning
confidence: 99%