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Utaroh Motosugi,
Hiroshi Yamaguchi,
Toru Furukawa,
Tomoaki Ichikawa,
Takashi Hatori, Izumi Fujita,
Masakazu Yamamoto,
Fuyuhiko Motoi,
Atsushi Kanno,
Tomoo Watanabe,
Naoto Koike,
Isamu Koyama,
Junya Kobayashi,
Michio Shimizu
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ABSTRACT: OBJECTIVE: The objective of this study was to describe the imaging findings for intraductal tubulopapillary neoplasms of the pancreas. METHODS: Eleven pancreatic tumors pathologically confirmed as intraductal tubulopapillary neoplasm were retrospectively collected. The dynamic contrast-enhanced computed tomography (CT), magnetic resonance (MR) imaging including MR cholangiopancreatography (MRCP), ultrasound, and endoscopic retrograde cholangiopancreatography (ERCP) results were reviewed. The 2-tone duct sign and cork-of-wine-bottle sign were reviewed as indicators of intraductal tumor growth on CT/MR and MRCP/ERCP images, respectively. RESULTS: A 2-tone duct sign was noted on the dynamic CT images (7/10, 70%) and on the MR imaging (5/8, 63%). The distal main pancreatic duct was dilated in all the patients except one, who had a branch duct lesion. A cork-of-wine-bottle sign was observed on the MRCP image (3/8, 38%) and on the ERCP image (3/6, 50%). CONCLUSIONS: Intraductal tubulopapillary neoplasms are rare tumors showing characteristic imaging findings such as the 2-tone duct sign and the cork-of-wine-bottle sign that represent their intraductal growth.
Journal of computer assisted tomography 11/2012; 36(6):710-717. · 1.38 Impact Factor
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Toru Furukawa,
Takashi Hatori, Izumi Fujita,
Masakazu Yamamoto,
Makio Kobayashi,
Nobuyuki Ohike,
Toshio Morohoshi,
Shinichi Egawa,
Michiaki Unno,
Sonshin Takao,
Masahiko Osako,
Suguru Yonezawa,
Mari Mino-Kenudson,
Gregory Y Lauwers,
Hiroshi Yamaguchi,
Shinichi Ban,
Michio Shimizu
[show abstract]
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ABSTRACT: The clinicopathological significance of four morphological types of intraductal papillary mucinous neoplasms of the pancreas (IPMNs; gastric, intestinal, pancreatobiliary and oncocytic) was assessed.
Retrospective multicentre analysis of 283 surgically resected IPMNs.
Of the 283 IPMNs, 139 were of the gastric type, 101 were intestinal, 19 were pancreatobiliary and 24 were oncocytic. These types were significantly associated with clinicopathological factors including sex (p = 0.0032), age (p = 0.00924), ectatic duct size (p = 0.0245), detection of mural nodules (p = 4.09 × 10⁻⁶), histological grade (p < 2.20 × 10⁻¹⁶), macroscopic types with differential involvement of the pancreatic duct system (p = 3.91 × 10⁻⁵), invasive phenotypes (p = 3.34 × 10⁻¹²), stage (p < 2.20 × 10⁻¹⁶) and recurrence (p = 0.00574). Kaplan-Meier analysis showed significant differences in patient survival by morphological type (p = 5.24 × 10⁻⁶). Survival rates at 5 and 10 years, respectively, were 0.937 (95% CI 0.892 to 0.984) for patients with gastric-type IPMNs; 0.886 (95% CI 0.813 to 0.965) and 0.685 (95% CI 0.553 to 0.849) for those with intestinal-type IPMNs; 0.839 (95% CI 0.684 to 1.000) and 0.734 (95% CI 0.526 to 1.000) for those with oncocytic-type IPMNs; and 0.520 (95% CI 0.298 to 0.909) and undetermined for those with pancreatobiliary-type IPMNs. Analysis by the Cox proportional hazards model comparing prognostic risks determined by stage and the morphological and macroscopic types indicated that staging was the most significant predictor of survival (p = 3.68×10⁻⁸) followed by the morphological type (p = 0.0435). Furthermore, the morphological type remained a significant predictor in a subcohort of invasive cases (p = 0.0089).
In this multicentre retrospective analysis, the morphological type of IPMN appears to be an independent predictor of patient prognosis.
Gut 12/2010; 60(4):509-16. · 10.11 Impact Factor
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ABSTRACT: The molecular pathobiology of pancreatic cystic neoplasms is poorly understood. The aim of this study was to know the involvement of epidermal growth factor receptor (EGFR) and its downstream targets in the serous cystic neoplasms and the mucinous cystic neoplasms of the pancreas. In a total of 72 pancreatic cystic neoplasms, including 39 serous cystic neoplasms and 33 mucinous cystic neoplasms, we examined the expression of native and phosphorylated EGFR, mitogen-activated protein kinase (MAPK), and AKT by immunohistochemistry and somatic mutations in EGFR, KRAS, BRAF, and PIK3CA, by direct sequencing. We also assessed the copy numbers of EGFR transcripts and the amplification of the EGFR gene in some of the samples. We found that EGFR, phosphorylated EGFR, MAPK, and phosphorylated MAPK were evidently expressed in 100, 54, 100, and 69% of the serous cystic neoplasms, and in 12%, none, 33, and 27% of the mucinous cystic neoplasms, respectively; the expression was significantly higher and more prevalent in the serous cystic neoplasms than in the mucinous cystic neoplasms. The expression of AKT and phosphorylated AKT was low in both the types of neoplasms. On average, EGFR transcripts in the serous cystic neoplasms and the mucinous cystic neoplasms increased 53.5- and 2.5-fold, respectively, as compared with that in normal tissues, with the increase in the former being significantly greater than that in the latter. Amplification of the EGFR gene was not detected in any of the examined serous cystic neoplasms. None of the tumors had mutations in any of the examined portions of the genes, except two mucinous cystic neoplasms with mutations in codon-12 of KRAS. These results indicate that EGFR and MAPK are actively involved in the pathobiology of serous cystic neoplasms and may therefore be potential diagnostic markers and therapeutic targets in patients with the above mentioned types of neoplasms.
Modern Pathology 05/2010; 23(8):1127-35. · 4.79 Impact Factor
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ABSTRACT: Total pancreatectomy (TP) is sometimes performed to treat low-grade malignant neoplasms that are spreading to the entire pancreas. However, TP impairs quality of life, due to the resulting loss of pancreatic exocrine and endocrine function, and an organ-preserving procedure should be chosen to minimize the impact of pancreatic dysfunction. Recently, we performed four duodenum-preserving TPs (DPTPs) on patients with low-grade malignant neoplasms of the entire pancreas and we introduce our operative technique and results herein.
DPTP is performed with the objective of preserving the arterial arcade of the posterior pancreas so as to maintain good blood flow in the duodenum and common bile duct. Care must also be taken to preserve the splenic artery and vein to protect the spleen. When patients are also undergoing a bile duct resection, an end-to-side choledochoduodenostomy is also performed to reconstruct the biliary tract.
Patient 1: DPTP with preservation of the spleen, conserving splenic vessels, was performed on a patient with hereditary pancreatic carcinoma with pancreatic intraepithelial neoplasia-3 (PanIN-3). Patient 2: DPTP with splenectomy was performed on a patient with multiple metastases of the entire pancreas from renal cell carcinoma. Patient 3: DPTP with preservation of the common bile duct and the spleen, conserving splenic vessels, was performed on a patient with minimally invasive carcinoma derived from intraductal papillary mucinous neoplasm (IPMN). Patient 4: DPTP with preservation of the spleen, conserving splenic vessels, was performed on a patient with minimally invasive carcinoma derived from IPMN. No deaths or morbidity occurred. All patients were placed on pancreatic enzyme replacement therapy and given a daily dose of insulin of approximately 30 U. Complete professional rehabiliation was achieved in all patients. All patients except one gained weight, and the hemoglobin A1c (HbA1c) levels have been maintained at around 7%.
DPTP is a useful organ-preserving procedure for low-grade malignant neoplasms spreading within the entire pancreas. This procedure minimizes the impact of pancreatic dysfunction and allows the patient to maintain good nutrition after surgery.
Journal of hepato-biliary-pancreatic sciences. 10/2009; 17(6):824-30.
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Hiroshi Yamaguchi,
Michio Shimizu,
Shinichi Ban,
Isamu Koyama,
Takashi Hatori, Izumi Fujita,
Masakazu Yamamoto,
Shunji Kawamura,
Makio Kobayashi,
Kazuyuki Ishida, [......],
Michiaki Unno,
Atsushi Kanno,
Kennichi Satoh,
Tooru Shimosegawa,
Hideki Orikasa,
Tomoo Watanabe,
Kazuhiko Nishimura,
Yoshiro Ebihara,
Naoto Koike,
Toru Furukawa
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ABSTRACT: We have encountered cases of unusual intraductal pancreatic neoplasms with predominant tubulopapillary growth. We collected data on 10 similar cases of "intraductal tubulopapillary neoplasms (ITPNs)" and analyzed their clinicopathologic and molecular features. Tumor specimens were obtained from 5 men and 5 women with a mean age of 58 years. ITPNs were solid and nodular tumors obstructing dilated pancreatic ducts and did not contain any visible mucin. The tumor cells formed tubulopapillae and contained little cytoplasmic mucin. The tumors exhibited uniform high-grade atypia. Necrotic foci were frequently observed, and invasion was observed in some cases. The ITPNs were immunohistochemically positive for cytokeratin 7 and/or cytokeratin 19 and negative for trypsin, MUC2, MUC5AC, and fascin. Molecular studies revealed abnormal expressions of TP53 and SMAD4 in 1 case, but aberrant expression of beta-catenin was not observed. No mutations in KRAS and BRAF were observed in the 8 cases that were examined. Eight patients are alive without recurrence, 1 patient died of liver metastases, and 1 patient is alive but had a recurrence and underwent additional pancreatectomy. The mitotic count and Ki-67 labeling index were significantly associated with invasion. All the features of ITPN were distinct from those of other known intraductal pancreatic neoplasms, including pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasm, and the intraductal variant of acinar cell carcinoma. Intraductal tubular carcinomas showed several features that were similar to those of ITPN, except for the tubulopapillary growth pattern. In conclusion, ITPNs can be considered to represent a new disease entity encompassing intraductal tubular carcinoma as a morphologic variant.
The American journal of surgical pathology 06/2009; 33(8):1164-72. · 4.06 Impact Factor
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Pancreas 04/2009; 38(2):235-7. · 2.39 Impact Factor
