Sheep in wolf's clothing: squamoid cysts of the pancreatic ducts

2021 ◽  
Author(s):  
Juanita Noeline Chui ◽  
Krishna Kotecha ◽  
Grace Deng ◽  
Christopher Seng Hong Lim ◽  
Angela Chou ◽  
...  
Keyword(s):  
Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 945
Author(s):  
Ryota Sagami ◽  
Kentaro Yamao ◽  
Jun Nakahodo ◽  
Ryuki Minami ◽  
Masakatsu Tsurusaki ◽  
...  

Pancreatic ductal adenocarcinoma (PDAC) arises from precursor lesions, such as pancreatic intra-epithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasm (IPMN). The prognosis of high-grade precancerous lesions, including high-grade PanIN and high-grade IPMN, without invasive carcinoma is good, despite the overall poor prognosis of PDAC. High-grade PanIN, as a lesion preceding invasive PDAC, is therefore a primary target for intervention. However, detection of localized high-grade PanIN is difficult when using standard radiological approaches. Therefore, most studies of high-grade PanIN have been conducted using specimens that harbor invasive PDAC. Recently, imaging characteristics of high-grade PanIN have been revealed. Obstruction of the pancreatic duct due to high-grade PanIN may induce a loss of acinar cells replaced by fibrosis and lobular parenchymal atrophy. These changes and additional inflammation around the branch pancreatic ducts (BPDs) result in main pancreatic duct (MPD) stenosis, dilation, retention cysts (BPD dilation), focal pancreatic parenchymal atrophy, and/or hypoechoic changes around the MPD. These indirect imaging findings have become important clues for localized, high-grade PanIN detection. To obtain pre-operative histopathological confirmation of suspected cases, serial pancreatic-juice aspiration cytologic examination is effective. In this review, we outline current knowledge on imaging characteristics of high-grade PanIN.


1939 ◽  
Vol 128 (2) ◽  
pp. 387-398
Author(s):  
M.L. Montgomery ◽  
C. Entenman ◽  
I.L. Chaikoff

2021 ◽  
pp. 1-9
Author(s):  
Tobias J. Weismüller

<b><i>Background:</i></b> Patients with irresectable perihilar cholangiocarcinoma (PHC) have a limited prognosis with median survival times still less than 1 year. In addition to the current standard first-line systemic chemotherapy (gemcitabine and a platinum derivate), endoscopic treatment aims to ensure adequate drainage of the biliary system by placing biliary plastic or metal stents. Local ablative procedures like intraluminal biliary brachytherapy (ILBT) or photodynamic therapy (PDT) are used to improve local tumor control and to optimize the stent patency. <b><i>Summary:</i></b> Intraductal radiofrequency ablation (RFA) is another promising tool in the therapeutic armamentarium for the endoscopic management and tumor ablation of extrahepatic cholangiocarcinoma (eCCA). By applying thermal energy to the tissue through high-frequency alternating current, RFA induces coagulative necrosis and causes local destruction of the tumor. It is established as a first line percutaneous treatment of solid liver tumors, and since 2011 an endoscopic catheter is available that allows intraductal RFA in the biliary or pancreatic ducts. While the first pilot studies primarily evaluated this new method in patients with distal eCCA, there is now evidence accumulating also for PHC. Two retrospective and two prospective studies demonstrated a significantly improved overall survival and a longer stent patency with intraductal RFA, which overall had a favorable safety profile and was not associated with a significant increase in adverse events. However, prospective studies comparing the efficacy and safety of intraductal RFA, PDT, and/or ILBT are lacking. <b><i>Key Messages:</i></b> Recent studies suggest that intraductal RFA is an effective and well-tolerated additional treatment option with regard to stent patency but also overall survival. Since RFA has fewer systemic side effects and requires less logistical effort when compared to ILBT and PDT, intraductal RFA should be considered as another safe and feasible adjuvant method for the palliative care of patients with advanced PHC. Since comparative studies are lacking, the choice of the local ablative method remains in each case an individual decision.


Digestion ◽  
2015 ◽  
Vol 91 (2) ◽  
pp. 174-179 ◽  
Author(s):  
Rong Li ◽  
Lan Yu ◽  
Xiaoxi Zhang ◽  
Xia Zhou ◽  
Min Wang ◽  
...  

2003 ◽  
Vol 199 (4) ◽  
pp. 453-461 ◽  
Author(s):  
Davide Soldini ◽  
Matthias Gugger ◽  
Elisabeth Burckhardt ◽  
Andreas Kappeler ◽  
Jean A Laissue ◽  
...  

2009 ◽  
Vol 133 (3) ◽  
pp. 423-438 ◽  
Author(s):  
Olca Basturk ◽  
Ipek Coban ◽  
N. Volkan Adsay

Abstract Context.—Cystic lesions of the pancreas are being recognized with increasing frequency and have become a more common finding in clinical practice because of the widespread use of advanced imaging modalities and the sharp drop in the mortality rate of pancreatic surgery. Consequently, in the past 2 decades, the nature of many cystic tumors in this organ has been better characterized, and significant developments have taken place in the classification and in our understanding of pancreatic cystic lesions. Objective.—To provide an overview of the current concepts in classification, differential diagnosis, and clinical/biologic behavior of pancreatic cystic tumors. Data Sources.—The authors' personal experience, based on institutional and consultation materials, combined with an analysis of the literature. Conclusions.—In contrast to solid tumors, most of which are invasive ductal adenocarcinomas with dismal prognosis, cystic lesions of the pancreas are often either benign or low-grade indolent neoplasia. However, those that are mucinous, namely, intraductal papillary mucinous neoplasms and mucinous cystic neoplasms, constitute an important category because they have well-established malignant potential, representing an adenoma-carcinoma sequence. Those that are nonmucinous such as serous tumors, congenital cysts, lymphoepithelial cysts, and squamoid cyst of pancreatic ducts have no malignant potential. Only rare nonmucinous cystic tumors that occur as a result of degenerative/necrotic changes in otherwise solid neoplasia, such as cystic ductal adenocarcinomas, cystic pancreatic endocrine neoplasia, and solid-pseudopapillary neoplasm, are also malignant and have variable degrees of aggressiveness.


Development ◽  
2000 ◽  
Vol 127 (12) ◽  
pp. 2617-2627 ◽  
Author(s):  
P.J. Miettinen ◽  
M. Huotari ◽  
T. Koivisto ◽  
J. Ustinov ◽  
J. Palgi ◽  
...  

Pancreatic acini and islets are believed to differentiate from common ductal precursors through a process requiring various growth factors. Epidermal growth factor receptor (EGF-R) is expressed throughout the developing pancreas. We have analyzed here the pancreatic phenotype of EGF-R deficient (−/−) mice, which generally die from epithelial immaturity within the first postnatal week. The pancreata appeared macroscopically normal. The most striking feature of the EGF-R (−/−) islets was that instead of forming circular clusters, the islet cells were mainly located in streak-like structures directly associated with pancreatic ducts. Based on BrdU-labelling, proliferation of the neonatal EGF-R (−/−) beta-cells was significantly reduced (2.6+/−0.4 versus 5.8+/−0.9%, P&lt;0.01) and the difference persisted even at 7–11 days of age. Analysis of embryonic pancreata revealed impaired branching morphogenesis and delayed islet cell differentiation in the EGF-R (−/−) mice. Islet development was analyzed further in organ cultures of E12.5 pancreata. The proportion of insulin-positive cells was significantly lower in the EGF-R (−/−) explants (27+/−6 versus 48+/−8%, P&lt;0.01), indicating delayed differentiation of the beta cells. Branching of the epithelium into ducts was also impaired. Matrix metalloproteinase (MMP-2 and MMP-9) activity was reduced 20% in EGF-R (−/−) late-gestation pancreata, as measured by gelatinase assays. Furthermore, the levels of secreted plasminogen activator inhibitor-1 (PAI-1) were markedly higher, while no apparent differences were seen in the levels of active uPA and tPa between EGF-R (−/−) and wild-type pancreata. Our findings suggest that the perturbation of EGF-R-mediated signalling can lead to a generalized proliferation defect of the pancreatic epithelia associated with a delay in beta cell development and disturbed migration of the developing islet cells as they differentiate from their precursors. Upregulated PAI-1 production and decreased gelatinolytic activity correlated to this migration defect. An intact EGF-R pathway appears to be a prerequisite for normal pancreatic development.


Sign in / Sign up

Export Citation Format

Share Document