About Bile Duct Cancer Overview and Types
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Carcinoid) Tumours Gastroenteropancreatic
Downloaded from gut.bmjjournals.com on 8 September 2005 Guidelines for the management of gastroenteropancreatic neuroendocrine (including carcinoid) tumours J K Ramage, A H G Davies, J Ardill, N Bax, M Caplin, A Grossman, R Hawkins, A M McNicol, N Reed, R Sutton, R Thakker, S Aylwin, D Breen, K Britton, K Buchanan, P Corrie, A Gillams, V Lewington, D McCance, K Meeran, A Watkinson and on behalf of UKNETwork for neuroendocrine tumours Gut 2005;54;1-16 doi:10.1136/gut.2004.053314 Updated information and services can be found at: http://gut.bmjjournals.com/cgi/content/full/54/suppl_4/iv1 These include: References This article cites 201 articles, 41 of which can be accessed free at: http://gut.bmjjournals.com/cgi/content/full/54/suppl_4/iv1#BIBL Rapid responses You can respond to this article at: http://gut.bmjjournals.com/cgi/eletter-submit/54/suppl_4/iv1 Email alerting Receive free email alerts when new articles cite this article - sign up in the box at the service top right corner of the article Topic collections Articles on similar topics can be found in the following collections Stomach and duodenum (510 articles) Pancreas and biliary tract (332 articles) Guidelines (374 articles) Cancer: gastroenterological (1043 articles) Liver, including hepatitis (800 articles) Notes To order reprints of this article go to: http://www.bmjjournals.com/cgi/reprintform To subscribe to Gut go to: http://www.bmjjournals.com/subscriptions/ Downloaded from gut.bmjjournals.com on 8 September 2005 iv1 GUIDELINES Guidelines for the management of gastroenteropancreatic neuroendocrine (including carcinoid) tumours J K Ramage*, A H G Davies*, J ArdillÀ, N BaxÀ, M CaplinÀ, A GrossmanÀ, R HawkinsÀ, A M McNicolÀ, N ReedÀ, R Sutton`, R ThakkerÀ, S Aylwin`, D Breen`, K Britton`, K Buchanan`, P Corrie`, A Gillams`, V Lewington`, D McCance`, K Meeran`, A Watkinson`, on behalf of UKNETwork for neuroendocrine tumours .............................................................................................................................. -
Cholangiocarcinoma 2020: the Next Horizon in Mechanisms and Management
CONSENSUS STATEMENT Cholangiocarcinoma 2020: the next horizon in mechanisms and management Jesus M. Banales 1,2,3 ✉ , Jose J. G. Marin 2,4, Angela Lamarca 5,6, Pedro M. Rodrigues 1, Shahid A. Khan7, Lewis R. Roberts 8, Vincenzo Cardinale9, Guido Carpino 10, Jesper B. Andersen 11, Chiara Braconi 12, Diego F. Calvisi13, Maria J. Perugorria1,2, Luca Fabris 14,15, Luke Boulter 16, Rocio I. R. Macias 2,4, Eugenio Gaudio17, Domenico Alvaro18, Sergio A. Gradilone19, Mario Strazzabosco 14,15, Marco Marzioni20, Cédric Coulouarn21, Laura Fouassier 22, Chiara Raggi23, Pietro Invernizzi 24, Joachim C. Mertens25, Anja Moncsek25, Sumera Rizvi8, Julie Heimbach26, Bas Groot Koerkamp 27, Jordi Bruix2,28, Alejandro Forner 2,28, John Bridgewater 29, Juan W. Valle 5,6 and Gregory J. Gores 8 Abstract | Cholangiocarcinoma (CCA) includes a cluster of highly heterogeneous biliary malignant tumours that can arise at any point of the biliary tree. Their incidence is increasing globally, currently accounting for ~15% of all primary liver cancers and ~3% of gastrointestinal malignancies. The silent presentation of these tumours combined with their highly aggressive nature and refractoriness to chemotherapy contribute to their alarming mortality, representing ~2% of all cancer-related deaths worldwide yearly. The current diagnosis of CCA by non-invasive approaches is not accurate enough, and histological confirmation is necessary. Furthermore, the high heterogeneity of CCAs at the genomic, epigenetic and molecular levels severely compromises the efficacy of the available therapies. In the past decade, increasing efforts have been made to understand the complexity of these tumours and to develop new diagnostic tools and therapies that might help to improve patient outcomes. -
Papilla with Separate Bile and Pancreatic Duct Orifices
JOP. J Pancreas (Online) 2013 May 10; 14(3):302-303. MULTIMEDIA ARTICLE – Clinical Imaging Papilla with Separate Bile and Pancreatic Duct Orifices Surinder Singh Rana, Deepak Kumar Bhasin Department of Gastroenterology, Post Graduate Institute of Medical Education and Research (PGIMER). Chandigarh, India A 32-year-old male, a known case of alcohol related Conflict of interest The authors have no potential chronic non calcific pancreatitis, was referred to us for conflicts of interest pancreatic endotherapy for relief of intractable abdominal pain. The cross sectional imaging studies References had revealed an irregularly dilated main pancreatic duct. The examination of the major duodenal papilla 1. Silvis SE, Vennes JA, Dreyer M. Variation in the normal duodenal papilla. Gastrointest Endosc 1983; 29:132-133 [PMID; revealed the presence of two separate orifices at 6852473] endoscopic retrograde cholangiopancreatography (ERCP) (Image). The cranial orifice was located at 11- 12 clock position whereas the caudal orifice was located at 4-5 clock position. The caudal orifice was selectively cannulated and the injection of the contrast revealed presence of an irregularly dilated main pancreatic duct. The cannula and the guide wire introduced through the caudal orifice selectively entered the pancreatic duct and did not come out through the cranial orifice. During ERCP, bile could be seen coming out of the cranial orifice, confirming it to be the orifice of common bile duct. Following selective cannulation of the main pancreatic duct, a 5-Fr stent was placed into the pancreatic duct. Following this, the patient had complete pain relief and is planned for further sessions of pancreatic endotherapy along with pancreatic sphincterotomy. -
The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Inherited Polyposis Syndromes Daniel Herzig, M.D
CLINICAL PRACTICE GUIDELINES The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Inherited Polyposis Syndromes Daniel Herzig, M.D. • Karin Hardimann, M.D. • Martin Weiser, M.D. • Nancy Yu, M.D. Ian Paquette, M.D. • Daniel L. Feingold, M.D. • Scott R. Steele, M.D. Prepared by the Clinical Practice Guidelines Committee of The American Society of Colon and Rectal Surgeons he American Society of Colon and Rectal Surgeons METHODOLOGY (ASCRS) is dedicated to ensuring high-quality pa- tient care by advancing the science, prevention, and These guidelines are built on the last set of the ASCRS T Practice Parameters for the Identification and Testing of management of disorders and diseases of the colon, rectum, Patients at Risk for Dominantly Inherited Colorectal Can- and anus. The Clinical Practice Guidelines Committee is 1 composed of society members who are chosen because they cer published in 2003. An organized search of MEDLINE have demonstrated expertise in the specialty of colon and (1946 to December week 1, 2016) was performed from rectal surgery. This committee was created to lead interna- 1946 through week 4 of September 2016 (Fig. 1). Subject tional efforts in defining quality care for conditions related headings for “adenomatous polyposis coli” (4203 results) to the colon, rectum, and anus, in addition to the devel- and “intestinal polyposis” (445 results) were included, us- opment of Clinical Practice Guidelines based on the best ing focused search. The results were combined (4629 re- available evidence. These guidelines are inclusive and not sults) and limited to English language (3981 results), then prescriptive. -
Germline Fumarate Hydratase Mutations in Patients with Ovarian Mucinous Cystadenoma
European Journal of Human Genetics (2006) 14, 880–883 & 2006 Nature Publishing Group All rights reserved 1018-4813/06 $30.00 www.nature.com/ejhg SHORT REPORT Germline fumarate hydratase mutations in patients with ovarian mucinous cystadenoma Sanna K Ylisaukko-oja1, Cezary Cybulski2, Rainer Lehtonen1, Maija Kiuru1, Joanna Matyjasik2, Anna Szyman˜ska2, Jolanta Szyman˜ska-Pasternak2, Lars Dyrskjot3, Ralf Butzow4, Torben F Orntoft3, Virpi Launonen1, Jan Lubin˜ski2 and Lauri A Aaltonen*,1 1Department of Medical Genetics, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland; 2International Hereditary Cancer Center, Department of Genetics and Pathology, Pomeranian Medical University, Szczecin, Poland; 3Department of Clinical Biochemistry, Aarhus University Hospital, Skejby, Denmark; 4Pathology and Obstetrics and Gynecology, University of Helsinki, Helsinki, Finland Germline mutations in the fumarate hydratase (FH) gene were recently shown to predispose to the dominantly inherited syndrome, hereditary leiomyomatosis and renal cell cancer (HLRCC). HLRCC is characterized by benign leiomyomas of the skin and the uterus, renal cell carcinoma, and uterine leiomyosarcoma. The aim of this study was to identify new families with FH mutations, and to further examine the tumor spectrum associated with FH mutations. FH germline mutations were screened from 89 patients with RCC, skin leiomyomas or ovarian tumors. Subsequently, 13 ovarian and 48 bladder carcinomas were analyzed for somatic FH mutations. Two patients diagnosed with ovarian mucinous cystadenoma (two out of 33, 6%) were found to be FH germline mutation carriers. One of the changes was a novel mutation (Ala231Thr) and the other one (435insAAA) was previously described in FH deficiency families. These results suggest that benign ovarian tumors may be associated with HLRCC. -
HPV-Negative Penile Squamous Cell Carcinoma
Modern Pathology (2017) 30, 1013–1020 © 2017 USCAP, Inc All rights reserved 0893-3952/17 $32.00 1013 HPV-negative penile squamous cell carcinoma: disruptive mutations in the TP53 gene are common Karl Kashofer, Elke Winter, Iris Halbwedl, Andrea Thueringer, Marisa Kreiner, Stefan Sauer and Sigrid Regauer Institute of Pathology, Medical University of Graz, Graz, Austria The majority of penile squamous cell carcinomas is caused by transforming human papilloma virus (HPV) infection. The etiology of HPV-negative cancers is unclear, but TP53 mutations have been implicated. Archival tissues of 108 invasive squamous cell carcinoma from a single pathology institution in a low-incidence area were analyzed for HPV-DNA and p16ink4a overexpression and for TP53 mutations by ion torrent next-generation sequencing. Library preparation failed in 32/108 squamous cell carcinomas. Institutional review board approval was obtained. Thirty of 76 squamous cell carcinomas (43%; average 63 years) were HPV-negative with 8/33 squamous cell carcinomas being TP53 wild-type (24%; average 63 years). Twenty-five of 33 squamous cell carcinomas (76%; average 65 years) showed 32 different somatic TP53 mutations (23 missense mutations in exons 5–8, 6 nonsense, 1 frameshift and 2 splice-site mutations). Several hotspot mutations were detected multiple times (R175H, R248, R282, and R273). Eighteen of 19 squamous cell carcinomas with TP53 expression in immunohistochemistry had TP53 mutations. Fifty percent of TP53-negative squamous cell carcinomas showed mostly truncating loss-of-function TP53 mutations. Patients without mutations had longer survival (5 years: 86% vs 61%; 10 years: 60% vs 22%), but valid clinically relevant conclusions cannot be drawn due to different tumor stages and heterogeneous treatment of the cases presented in this study. -
Review of Intra-Arterial Therapies for Colorectal Cancer Liver Metastasis
cancers Review Review of Intra-Arterial Therapies for Colorectal Cancer Liver Metastasis Justin Kwan * and Uei Pua Department of Vascular and Interventional Radiology, Tan Tock Seng Hospital, Singapore 388403, Singapore; [email protected] * Correspondence: [email protected] Simple Summary: Colorectal cancer liver metastasis occurs in more than 50% of patients with colorectal cancer and is thought to be the most common cause of death from this cancer. The mainstay of treatment for inoperable liver metastasis has been combination systemic chemotherapy with or without the addition of biological targeted therapy with a goal for disease downstaging, for potential curative resection, or more frequently, for disease control. For patients with dominant liver metastatic disease or limited extrahepatic disease, liver-directed intra-arterial therapies including hepatic arterial chemotherapy infusion, chemoembolization and radioembolization are alternative treatment strategies that have shown promising results, most commonly in the salvage setting in patients with chemo-refractory disease. In recent years, their role in the first-line setting in conjunction with concurrent systemic chemotherapy has also been explored. This review aims to provide an update on the current evidence regarding liver-directed intra-arterial treatment strategies and to discuss potential trends for the future. Abstract: The liver is frequently the most common site of metastasis in patients with colorectal cancer, occurring in more than 50% of patients. While surgical resection remains the only potential Citation: Kwan, J.; Pua, U. Review of curative option, it is only eligible in 15–20% of patients at presentation. In the past two decades, Intra-Arterial Therapies for Colorectal major advances in modern chemotherapy and personalized biological agents have improved overall Cancer Liver Metastasis. -
Fact Sheet - Symptoms of Pancreatic Cancer
Fact Sheet - Symptoms of Pancreatic Cancer Diagnosis Pancreatic cancer is often difficult to diagnose, because the pancreas lies deep in the abdomen, behind the stomach, so tumors are not felt during a physical exam. Pancreatic cancer is often called the “silent” cancer because the tumor can grow for many years before it causes pressure, pain, or other signs of illness. When symptoms do appear, they can vary depending on the size of the tumor and where it is located on the pancreas. For these reasons, the symptoms of pancreatic cancer are seldom recognized until the cancer has progressed to an advanced stage and often spread to other areas of the body. General Symptoms Pain The first symptom of pancreatic cancer is often pain, because the tumors invade nerve clusters. Pain can be felt in the stomach area and/or in the back. The pain is generally worse after eating and when lying down, and is sometimes relieved by bending forward. Pain is more common in cancers of the body and tail of the pancreas. The abdomen may also be generally tender or painful if the liver, pancreas or gall bladder are inflamed or enlarged. It is important to keep in mind that there are many other causes of abdominal and back pain! Jaundice More than half of pancreatic cancer sufferers have jaundice, a yellowing of the skin and whites of the eyes. Jaundice is caused by a build-up bilirubin, a substance which is made in the liver and a component of bile. Bilirubin contains a lot of yellow pigment, and gives bile it’s color. -
Common Bile Duct Exploration
Education Common Bile Duct Exploration What is a common bile duct exploration? The common bile duct is a tube that connects the liver, gallbladder, and pancreas to the small intestine. It helps deliver fluids for digestion. A common bile duct exploration is a procedure used to see if a stone is blocking the flow of bile from your liver and gallbladder to your intestine. When is it used? When a stone gets stuck in the common bile duct it may cause bile to back up into the liver. This causes jaundice. Jaundice is a condition in which the skin and the whites of the eyes become yellowish. If the stone is not removed, the common bile duct may become infected and need emergency surgery. It can also cause pancreatitis, a reaction in the pancreas that can be life threatening. Common bile duct exploration is often done during surgery to remove the gallbladder. An alternative procedure is an endoscopic retrograde cholangiopancreatography (ERCP). When an ERCP is done, a tube is inserted through your mouth and stomach into the small intestine. The tube can be used to put contrast dye into the duct to look for stones with x-rays. If there are stones, a small opening is made in the common duct to allow the stone or stones to pass into the intestine. You should ask your health care provider about these choices. How do I prepare for a common bile duct exploration? Plan for your care and recovery after the operation. Allow for time to rest and try to find people to help you with your day-to- day duties. -
Pancreatic Cancer and Liver Cancer Are the Deadliest Cancers; and Still No Effective Chemotherapy
International Journal of ISSN 2692-5877 Clinical Studies & Medical Case Reports DOI: 10.46998/IJCMCR.2021.10.000240 Perspective Pancreatic Cancer and Liver Cancer Are the Deadliest Cancers; and Still No Effective Chemotherapy. Why? Leslie C Costello* and Renty B Franklin Department of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry and the University of Maryland Greenebaum Comprehensive Cancer Center, USA *Corresponding author: Adel Ekladious, Department of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry; and the University of Maryland Greenebaum Comprehensive Cancer Center, Baltimore, Md. 21201, USA. Email: [email protected]. Received: May 28, 2021 Published: June 14, 2021 Abstract In 2020, there were about 60,400 cases and 48,200 due to pancreatic cancer; an estimated death rate of 80%. For liver cancer the values are 42,800 new cases and 30,000 deaths; an estimated death rate of 72%. The 5-year survival rate is 9% for pancreatic cancer and 18% for liver cancer. During the recent period of 30 years, there has been no decrease in the incidence of pancreatic cancer deaths or liver deaths; and instead, there has been an increase death. The reason is the continued absence of an efficacious systemic chemotherapy. That is due to the failure of the identification of the important factors that are implicated in the develop- ment and progression of those cancers. However, information does exist, which is likely to represent a viable and compelling concept of the manifestation of both cancers; and will provide the basis for a potential effective chemotherapy. The status of zinc is the likely important factor that manifests the development and progression pancreatic and liver cancers and clioquinol zinc ionophore is the treatment. -
Mtorc1 and FGFR1 Signaling in Fibrolamellar Hepatocellular
Modern Pathology (2015) 28, 103–110 & 2015 USCAP, Inc. All rights reserved 0893-3952/15 $32.00 103 mTORC1 and FGFR1 signaling in fibrolamellar hepatocellular carcinoma Kimberly J Riehle1,2,3,4, Matthew M Yeh1,2, Jeannette J Yu1,4, Heidi L Kenerson3, William P Harris1,5, James O Park1,3 and Raymond S Yeung1,2,3 1The Northwest Liver Research Program, University of Washington, Seattle, WA, USA; 2Department of Pathology, University of Washington, Seattle, WA, USA; 3Department of Surgery, University of Washington, Seattle, WA, USA; 4Seattle Children’s Hospital, Seattle, WA, USA and 5Department of Medicine, University of Washington, Seattle, WA, USA Fibrolamellar hepatocellular carcinoma, or fibrolamellar carcinoma, is a rare form of primary liver cancer that afflicts healthy young men and women without underlying liver disease. There are currently no effective treatments for fibrolamellar carcinoma other than resection or transplantation. In this study, we sought evidence of mechanistic target of rapamycin complex 1 (mTORC1) activation in fibrolamellar carcinoma, based on anecdotal reports of tumor response to rapamycin analogs. Using a tissue microarray of 89 primary liver tumors, including a subset of 10 fibrolamellar carcinomas, we assessed the expression of phosphorylated S6 ribosomal protein (P-S6), a downstream target of mTORC1, along with fibroblast growth factor receptor 1 (FGFR1). These results were extended and confirmed using an additional 13 fibrolamellar carcinomas, whose medical records were reviewed. In contrast to weak staining in normal livers, all fibrolamellar carcinomas on the tissue microarray showed strong immunostaining for FGFR1 and P-S6, whereas only 13% of non-fibrolamellar hepatocellular carcinomas had concurrent activation of FGFR1 and mTORC1 signaling (Po0.05). -
Primary Hepatic Carcinoid Tumor with Poor Outcome Om Parkash Aga Khan University, [email protected]
eCommons@AKU Section of Gastroenterology Department of Medicine March 2016 Primary Hepatic Carcinoid Tumor with Poor Outcome Om Parkash Aga Khan University, [email protected] Adil Ayub Buria Naeem Sehrish Najam Zubair Ahmed Aga Khan University See next page for additional authors Follow this and additional works at: https://ecommons.aku.edu/ pakistan_fhs_mc_med_gastroenterol Part of the Gastroenterology Commons Recommended Citation Parkash, O., Ayub, A., Naeem, B., Najam, S., Ahmed, Z., Jafri, W., Hamid, S. (2016). Primary Hepatic Carcinoid Tumor with Poor Outcome. Journal of the College of Physicians and Surgeons Pakistan, 26(3), 227-229. Available at: https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterol/220 Authors Om Parkash, Adil Ayub, Buria Naeem, Sehrish Najam, Zubair Ahmed, Wasim Jafri, and Saeed Hamid This report is available at eCommons@AKU: https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterol/220 CASE REPORT Primary Hepatic Carcinoid Tumor with Poor Outcome Om Parkash1, Adil Ayub2, Buria Naeem2, Sehrish Najam2, Zubair Ahmed, Wasim Jafri1 and Saeed Hamid1 ABSTRACT Primary Hepatic Carcinoid Tumor (PHCT) represents an extremely rare clinical entity with only a few cases reported to date. These tumors are rarely associated with metastasis and surgical resection is usually curative. Herein, we report two cases of PHCT associated with poor outcomes due to late diagnosis. Both cases presented late with non-specific symptoms. One patient presented after a 2-week history of symptoms and the second case had a longstanding two years symptomatic interval during which he remained undiagnosed and not properly worked up. Both these cases were diagnosed with hepatic carcinoid tumor, which originates from neuroendocrine cells. Case 1 opted for palliative care and expired in one month’s time.