2020
DOI: 10.1016/j.hpb.2020.01.017
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Carcinosarcoma of the pancreas: comprehensive clinicopathological and molecular characterization

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Cited by 11 publications
(16 citation statements)
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“…From the clinical point of view, compared to conventional PDAC, UC usually show a worse prognosis, whereas UCOGC is generally associated to a better prognosis, when not associated with a PDAC component [3,5,6]. Some studies have demonstrated that UC and UCOGC have a molecular landscape very similar to PDAC, based on alterations that affect the classic PDAC drivers, including the oncogene KRAS and the tumor suppressor genes TP53, SMAD4, and CDKN2A [5,7,8]. As such, somatic mutations are unlikely to explain the unique phenotype of UC and UCOGC.…”
Section: Introductionmentioning
confidence: 99%
“…From the clinical point of view, compared to conventional PDAC, UC usually show a worse prognosis, whereas UCOGC is generally associated to a better prognosis, when not associated with a PDAC component [3,5,6]. Some studies have demonstrated that UC and UCOGC have a molecular landscape very similar to PDAC, based on alterations that affect the classic PDAC drivers, including the oncogene KRAS and the tumor suppressor genes TP53, SMAD4, and CDKN2A [5,7,8]. As such, somatic mutations are unlikely to explain the unique phenotype of UC and UCOGC.…”
Section: Introductionmentioning
confidence: 99%
“…In the interim of tions, c.35G>A and c.35G>T at codon 12 and codon 34. [3][4][5][6][7][8] KRAS Q61H and TP53 Q100X mutations are also recently discovered to be present in both components. 3 In a case series by Ruess, molecular analysis of these tumors revealed that pancreatic carcinosarcomas are of monoclonal origin.…”
Section: Discussionmentioning
confidence: 99%
“…[3][4][5][6][7][8] KRAS Q61H and TP53 Q100X mutations are also recently discovered to be present in both components. 3 In a case series by Ruess, molecular analysis of these tumors revealed that pancreatic carcinosarcomas are of monoclonal origin. KRAS mutation is a distinctive driver mutation in pancreatic ductal adenocarcinoma.…”
Section: Discussionmentioning
confidence: 99%
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“…Previous studies suggested that most pancreatic carcinosarcomas appear to be of monoclonal origin and seem to arise from a carcinoma via metaplastic transformation of a subclone of the tumor, probably by the epithelial–mesenchymal transition mechanism [ 3 , 7 ]. In one report, clonality of the two distinct tumor components was assessed by microdissection with subsequent genetic analysis for KRAS and TP53 gene mutation and showed the same genetic alterations in the carcinomatous and the sarcomatous components, strongly suggesting a common origin [ 8 ]. Another study demonstrated that an identical mutation (G to A transition) at exon 2 of the KRAS gene was detected in both the carcinomatous and sarcomatous components [ 9 ].…”
Section: Discussionmentioning
confidence: 99%