Distinction of Invasive Carcinoma Derived from Intraductal Papillary Mucinous Neoplasms from Concomitant Ductal Adenocarcinoma of the Pancreas Using Molecular Biomarkers

Koji Tamura, Takao Ohtsuka, Kenjiro Date, Takaaki Fujimoto, Taketo Matsunaga, Hideyo Kimura, Yusuke Watanabe, Tetsuyuki Miyazaki, Kenoki Ohuchida, Shunichi Takahata, Kousei Ishigami, Yoshinao Oda, Kazuhiro Mizumoto, Masafumi Nakamura, Masao Tanaka

Research output: Contribution to journalArticle

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Abstract

Objectives To clarify the usefulness of molecular biomarkers for distinguishing invasive carcinoma derived from intraductal papillary mucinous neoplasms (IPMNs [Inv-IPMN]) from concomitant pancreatic ductal adenocarcinoma (PDAC). Methods Data from 19 patients with resected concomitant PDAC were retrospectively reviewed. KRAS/GNAS mutations and immunohistochemical (IHC) expression of p53 and p16/CDKN2A were assessed in both IPMN and distinct PDAC. As controls, KRAS/GNAS mutations and IHC labeling were assessed between invasive and noninvasive components in 1 lesion of 22 independent patients. Results KRAS/GNAS mutation status of invasive and noninvasive components in Inv-IPMN was consistent in 18 (86%) of 21 patients. Conversely, mutational patterns in IPMN and distinct PDAC in the same pancreas differed from each other in 17 (89%) of 19. There were 10 (53%) and 8 (42%) of 19 patients who showed the same p53 and p16/CDKN2A staining between concomitant PDAC and distinct IPMN. In the Inv-IPMN cohort, 19 (86%) of 22 patients showed the same IHC expression pattern between the noninvasive and invasive components. Conclusions It may be possible to distinguish Inv-IPMN from concomitant PDAC by assessing these molecular biomarkers. More precise distinction of Inv-IPMN and concomitant PDAC will lead to adequate recognition of the natural history of IPMNs and hence optimal management.

Original languageEnglish
Pages (from-to)826-835
Number of pages10
JournalPancreas
Volume45
Issue number6
DOIs
Publication statusPublished - Jul 1 2016

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Carcinoma, Intraductal, Noninfiltrating
Pancreas
Adenocarcinoma
Biomarkers
Neoplasms
Mutation
Natural History
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Hepatology
  • Endocrinology

Cite this

Distinction of Invasive Carcinoma Derived from Intraductal Papillary Mucinous Neoplasms from Concomitant Ductal Adenocarcinoma of the Pancreas Using Molecular Biomarkers. / Tamura, Koji; Ohtsuka, Takao; Date, Kenjiro; Fujimoto, Takaaki; Matsunaga, Taketo; Kimura, Hideyo; Watanabe, Yusuke; Miyazaki, Tetsuyuki; Ohuchida, Kenoki; Takahata, Shunichi; Ishigami, Kousei; Oda, Yoshinao; Mizumoto, Kazuhiro; Nakamura, Masafumi; Tanaka, Masao.

In: Pancreas, Vol. 45, No. 6, 01.07.2016, p. 826-835.

Research output: Contribution to journalArticle

Tamura, Koji ; Ohtsuka, Takao ; Date, Kenjiro ; Fujimoto, Takaaki ; Matsunaga, Taketo ; Kimura, Hideyo ; Watanabe, Yusuke ; Miyazaki, Tetsuyuki ; Ohuchida, Kenoki ; Takahata, Shunichi ; Ishigami, Kousei ; Oda, Yoshinao ; Mizumoto, Kazuhiro ; Nakamura, Masafumi ; Tanaka, Masao. / Distinction of Invasive Carcinoma Derived from Intraductal Papillary Mucinous Neoplasms from Concomitant Ductal Adenocarcinoma of the Pancreas Using Molecular Biomarkers. In: Pancreas. 2016 ; Vol. 45, No. 6. pp. 826-835.
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abstract = "Objectives To clarify the usefulness of molecular biomarkers for distinguishing invasive carcinoma derived from intraductal papillary mucinous neoplasms (IPMNs [Inv-IPMN]) from concomitant pancreatic ductal adenocarcinoma (PDAC). Methods Data from 19 patients with resected concomitant PDAC were retrospectively reviewed. KRAS/GNAS mutations and immunohistochemical (IHC) expression of p53 and p16/CDKN2A were assessed in both IPMN and distinct PDAC. As controls, KRAS/GNAS mutations and IHC labeling were assessed between invasive and noninvasive components in 1 lesion of 22 independent patients. Results KRAS/GNAS mutation status of invasive and noninvasive components in Inv-IPMN was consistent in 18 (86{\%}) of 21 patients. Conversely, mutational patterns in IPMN and distinct PDAC in the same pancreas differed from each other in 17 (89{\%}) of 19. There were 10 (53{\%}) and 8 (42{\%}) of 19 patients who showed the same p53 and p16/CDKN2A staining between concomitant PDAC and distinct IPMN. In the Inv-IPMN cohort, 19 (86{\%}) of 22 patients showed the same IHC expression pattern between the noninvasive and invasive components. Conclusions It may be possible to distinguish Inv-IPMN from concomitant PDAC by assessing these molecular biomarkers. More precise distinction of Inv-IPMN and concomitant PDAC will lead to adequate recognition of the natural history of IPMNs and hence optimal management.",
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AU - Tamura, Koji

AU - Ohtsuka, Takao

AU - Date, Kenjiro

AU - Fujimoto, Takaaki

AU - Matsunaga, Taketo

AU - Kimura, Hideyo

AU - Watanabe, Yusuke

AU - Miyazaki, Tetsuyuki

AU - Ohuchida, Kenoki

AU - Takahata, Shunichi

AU - Ishigami, Kousei

AU - Oda, Yoshinao

AU - Mizumoto, Kazuhiro

AU - Nakamura, Masafumi

AU - Tanaka, Masao

PY - 2016/7/1

Y1 - 2016/7/1

N2 - Objectives To clarify the usefulness of molecular biomarkers for distinguishing invasive carcinoma derived from intraductal papillary mucinous neoplasms (IPMNs [Inv-IPMN]) from concomitant pancreatic ductal adenocarcinoma (PDAC). Methods Data from 19 patients with resected concomitant PDAC were retrospectively reviewed. KRAS/GNAS mutations and immunohistochemical (IHC) expression of p53 and p16/CDKN2A were assessed in both IPMN and distinct PDAC. As controls, KRAS/GNAS mutations and IHC labeling were assessed between invasive and noninvasive components in 1 lesion of 22 independent patients. Results KRAS/GNAS mutation status of invasive and noninvasive components in Inv-IPMN was consistent in 18 (86%) of 21 patients. Conversely, mutational patterns in IPMN and distinct PDAC in the same pancreas differed from each other in 17 (89%) of 19. There were 10 (53%) and 8 (42%) of 19 patients who showed the same p53 and p16/CDKN2A staining between concomitant PDAC and distinct IPMN. In the Inv-IPMN cohort, 19 (86%) of 22 patients showed the same IHC expression pattern between the noninvasive and invasive components. Conclusions It may be possible to distinguish Inv-IPMN from concomitant PDAC by assessing these molecular biomarkers. More precise distinction of Inv-IPMN and concomitant PDAC will lead to adequate recognition of the natural history of IPMNs and hence optimal management.

AB - Objectives To clarify the usefulness of molecular biomarkers for distinguishing invasive carcinoma derived from intraductal papillary mucinous neoplasms (IPMNs [Inv-IPMN]) from concomitant pancreatic ductal adenocarcinoma (PDAC). Methods Data from 19 patients with resected concomitant PDAC were retrospectively reviewed. KRAS/GNAS mutations and immunohistochemical (IHC) expression of p53 and p16/CDKN2A were assessed in both IPMN and distinct PDAC. As controls, KRAS/GNAS mutations and IHC labeling were assessed between invasive and noninvasive components in 1 lesion of 22 independent patients. Results KRAS/GNAS mutation status of invasive and noninvasive components in Inv-IPMN was consistent in 18 (86%) of 21 patients. Conversely, mutational patterns in IPMN and distinct PDAC in the same pancreas differed from each other in 17 (89%) of 19. There were 10 (53%) and 8 (42%) of 19 patients who showed the same p53 and p16/CDKN2A staining between concomitant PDAC and distinct IPMN. In the Inv-IPMN cohort, 19 (86%) of 22 patients showed the same IHC expression pattern between the noninvasive and invasive components. Conclusions It may be possible to distinguish Inv-IPMN from concomitant PDAC by assessing these molecular biomarkers. More precise distinction of Inv-IPMN and concomitant PDAC will lead to adequate recognition of the natural history of IPMNs and hence optimal management.

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