2015
DOI: 10.1007/s00535-015-1037-4
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The genetic classification of pancreatic neoplasia

Abstract: Cancer is caused by the accumulation of inherited and/or acquired alterations in specific genes. The recent decline in the cost of DNA sequencing has allowed tumor sequencing to be conducted on a large scale, which, in turn, has led to an unprecedented understanding of the genetic events that drive neoplasia. This understanding, when integrated with meticulous histologic analyses and with clinical findings, has direct clinical implications. The recent sequencing of all of the major types of cystic and noncysti… Show more

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Cited by 6 publications
(6 citation statements)
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References 149 publications
(184 reference statements)
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“…PDACs are the most commonly occurring form of PanC (90%), with mutated KRAS expressed in ≥95% of cases. Other frequently mutated genes present in ≥50% of PanC types are p16/CDKN2A , TP53 , and SMAD4 …”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…PDACs are the most commonly occurring form of PanC (90%), with mutated KRAS expressed in ≥95% of cases. Other frequently mutated genes present in ≥50% of PanC types are p16/CDKN2A , TP53 , and SMAD4 …”
Section: Introductionmentioning
confidence: 99%
“…Other frequently mutated genes present in ≥50% of PanC types are p16/CDKN2A, TP53, and SMAD4. 7 Other than genetic alterations, in recent years, cancer stem cells (CSCs) have been identified to play a major role in cancer progression and recurrence in pancreatic as well as other cancers. 8,9 PanC-CSCs were first identified in 2007 by Li et al,8 in established human PanC xenografts of NOD/SCID mice.…”
mentioning
confidence: 99%
“…The majority (ca 95%) are classified as ductal adenocarcinomas, and of the others, the majority are neuroendocrine in origin. Tumours are associated most strongly with k-RAS mutations in almost all patients 2 . Mutated P53 and mutations in several other oncogenes such as CDKN2 are frequently observed 1 .…”
mentioning
confidence: 99%
“…In mouse models, activating mutations of Kras seem essential for initiating the development of PanINs, and indeed, 90% of human PDACs have activating KRAS mutations, as do most of even the lowest grade of PanIN. 128,129 As noted, 128 targeting oncogenic Kras to various pancreatic cell types in GEMMs has shown the malignant potential of duct, endocrine and acinar cells; however, is this a reflection of the human situation? In humans, KRAS mutations are typically followed by loss of CDKN2/p16, while loss of TP53 and SMAD4 is usually only found in high-grade PanIN.…”
Section: Pancreasmentioning
confidence: 99%