DOCSLIB.ORG

Pancreatic Adenocarcinoma, Multiple Insular-Ductualr Alterations and Malignant Ppoma in a Patient Treated with Glp-1 Analogs

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pancreatic Adenocarcinoma, Multiple Insular-Ductualr Alterations and Malignant Ppoma in a Patient Treated with Glp-1 Analogs JOP. J Pancreas (Online) 2017 Sep 29; 18(5):399-408. ORIGINAL ARTICLE Pancreatic Adenocarcinoma, Multiple Insular-Ductualr Alterations and Malignant PPoma in a Patient Treated With Glp-1 Analogs Parviz M Pour1,2, Geoffrey Talmon2 1UNMC Eppley Cancer Center and 2Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE ABSTRACT Background According to numerous studies in the hamster pancreatic cancer model, islet cells are the most vulnerable to a carcinogen’s insult and the induction of islet cell proliferation enhances the neoplastic process, however, the prevention of islet cell neogenesis inhibits it. In humans, however, discrepancies exist on the nature of the cancer progenitor cells. The recent discovery of islet cell expansion by GLP-1 analogs in type 2 diabetics offered a unique opportunity for comparative studies. Materials and Methods The pancreatic tissue of a type 2 diabetic who was treated with Victoza and Byetta for 25 months and died about a year later from pancreatic cancer, was evaluated histologically and by immunohistochemistry. Results Differences were found relative to the patterns of the distribution of islets in the tissue derived from the ventral and dorsal anlage of the pancreas. In the glucagon-rich and PP-poor dorsal pancreas, most islets were well circumscribed and atrophic but many contained intrainsular ductules that were malignant in one case. In the PP-rich, glucagon- presented malignant growth. In the PP cell dominated area, islet cell transformation to normal, atypical and malignant ductular structures inpoor various ventral stages pancreas, of differentiation the islets were were ill-defined, found, and varied remarkably in size inand multiple shape, weresites. Conclusionmuch larger than in the control tissue, and in one area 1) as in the hamster pancreatic cancer model, human islets also appear to present a source of pancreatic ductal neoplasms; and 2) the alterations seem to be related to the effects of GLP-1 analogs. This is the first report demonstrating that: INTRODUCTION cancer formation [1]. In humans, however, such a possibility was doubted, as comparable studies in humans No clues have emerged on the histogenesis of pancreatic cancer in humans. Induction of acinar cell lesions by pancreatic islet cells in diabetic patients treated with the chemical carcinogens in rodents led to the assumption GLP-1were absent. analog Recent[3] provide findings an opportunityof a massive for proliferation comparative of that acinar cells are the primary targets of the carcinogens. Moreover, the partial ductal cell appearance of some able to obtain the pancreas of a patient who was treated of these tumors was considered evidence that ductal withstudies. Victoza With thisand inByetta mind, for we 25 identified months a andcase died and werefrom adenocarcinomas are the result of acinar cell to ductal cell complications of pancreatic cancer a year later. transdifferentiation. This hypothesis contrasted with the virus- and carcinogen-induced primary adenocarcinoma MATERIALS AND METHODS in the Guinea fowl and Syrian Golden hamsters, The 66-year-old, type 2 insulin-dependent diabetic respectively [1, 2]. In fact, in the hamster model, the initial man, was treated with Victoza on September 20, 2009. For step in neoplasia begins within the islets [1]. Numerous an unknown reason, the treatment was changed to Byetta studies concerned with the role of islet cells in pancreatic on October 20, 2010 and continued until December 2011. islet cell proliferation and regeneration enhances, whereas was switched back to insulin. No serious diseases of the thecarcinogenesis prevention verifiedof islet cellthat neogenesis any condition inhibits that pancreaticstimulates patientDue to werethe patient's known untilfinancial March limitations, 6, 2013, whenthe treatment invasive pancreatic adenocarcinoma was diagnosed and removed Received July 19th, 2017 - Accepted September 20th, 2017 by Whipple operation two weeks later. After recovery from Keywords Carcinoma in Situ; Cell Transdifferentiation; Glucagon-Like the surgery, the patient received adjuvant Gemcitabine for Peptide 1; Islets of Langerhans; Pancreatic Neoplasms Abbreviation CGA chomogranin A; GLP-1 Glucagon-like peptide-1; PP pancreatic polypeptide in September 2013 with liver metastases and was treated Correspondence Parviz M Pour withfive cycles palliative and FOLFRINOXinsulin. He was until re-admitted he expired to in the September hospital 9727 Spring Street 2014. An autopsy limited to the abdomen revealed Omaha, NE, 68124, USA Tel +4023978724 “extensive carcinomatosis with a gelatinous reddish tan Fax +402 5176384 E-mail [email protected] mass, necrosis and fibrosis throughout the abdomen with JOP. Journal of the Pancreas - http://pancreas.imedpub.com/ - Vol. 18 No. 5 –Sep 2017.extreme [ISSN difficulty 1590-8577] locating the remnant of the pancreas.”399 JOP. J Pancreas (Online) 2017 Sep 29; 18(5):399-408. The pre-operative comprehensive metabolic panel the lesions that occur during pancreatic carcinogenesis in showed hyper glucosemia, increased Anion Gap, hamsters [1] (Figure 1f). decreased albumin and increased alanine and aspartamine The tissue from the uncinate process (ventral pancreas) transferase, alkaline phosphatase and total bilirubin. No to be well preserved; however, in sections immunostained metabolic panel showed almost the same abnormalities. withwas free CGA of andcancer pancreatic and in the polypeptide H&E stained (PP) slides antibodies, appeared Otherhormonal values, profiles including were the estimatedmeasured. GFR, The were post-Whipple within the a massive expansion of islet cells was noticed, forming normal range. ovoid, trabecular, branched, linear or an irregular mass The pancreaticogastroduodenectomy specimen was a with indistinct outlines, consistent with the reported 4.8×4.2×3 cm mass that extended into the peri-pancreatic PPoma cases [4, 5, 6] (Figure 1e). Remarkably, the islet fat, within 0.4 cm of the distal pancreatic neck margin, and cells stained with the anti-PP antibody appeared extremely abutted the SMV/SMA vascular groove margins. Metastases dark and the concentration of the antibody had to be (stage PT3,PN1). The pancreatic parenchyma in the region a concentration of 40 ml was required to visualize the ofwere the identifieduncinate process within wasone grossly peri-pancreatic unremarkable. lymph node PPreduced cells into theavoid normal unspecific control immunoreactivity. tissue, a solution Althoughof 10 ml still strongly stained the PP cells in this case but not in the Tissue Processing control tissue. Many islet cells of generally large and poor delineation formalin and processed for histology by conventional were intermingled with ductular structures of different methods.Pancreatic Serial tissue sections was fixedfrom inthe 10% tissues phosphate that appeared buffered epithelial size and large hypo-chromatic nuclei (Figures 1f, 2a). These insular-ductular complexes could be best immunohistochemistry by Avidin-Biotin method using to be intact were stained for H&E or processed for differentiated and visualized with the dual staining with anti-PP and anti-CA19-9 antibodies (Figure 2a). incubation),the following anti-glucagon antibodies: (Cellanti-insulin Signaling (Cell Technology, Signaling The proportion of the insular and ductular elements Technology, Danvers, MA; 1:100 dilution,45 minute varied in different islets. In general, the more ductular chromogranin A (Ventana Medical Systems, Tucson, AZ, cells, the less islet cells (Figures 2b-2d). In some areas, pre-dilutedDanvers, MA; by 1:100 manufacturer, dilution,30 36-minute minute incubation), anti- almost the entire islet was replaced by ductular elements. Indisputable evidence for the development of ductular incubation), and the pre-diluted anti-CA 19-9 antibody elements from islet cells was the presence of intermediary [PA0424]PP (Abcam, from Cambridge, Leica Biosystems,MA; 1:1,200 dilution,Buffalo Grove,45-minute IL. cells, the ductular cells that contained traces of endocrine Multiplex dual chromagen staining (insulin+glucagon, granules (Figures 2d-2f, 3a). With a decreasing number PP plus insulin, PP plus CA19-9) was performed using of islet cells, the ductular cells showed increasing the Novocasra mouse monoclonal antibody (product hypertrophy, atypia and patterns consistent with in situ carcinoma (Figures 3a-3d). In such lesions, only a few PA0620(R-T-u), was used. Normal pancreatic tissue or no islet cells were detectable (Figures 4a, 4b). The fromcode: aNCL-L-Insulin), non-diabetic case and wasclone used 2D11-HS, as a control the same for allas multiplicity of the lesion at different stages of islet cell antibodies. transdifferentiation was extraordinary. In one area of Histopathological Finding aboutIn a6 sectionmm in diameter,taken from five the such peri-pancreatic lesions were tissueidentified. near The invasive tumors presented a wide variation in the pancreas head, colonies of PP cells (Figure 4d) were histological make-ups from well-differentiated areas detected within the connective tissue, presenting features to poorly differentiated and anaplastic patterns. The consistent with malignant PPoma. The original site of the remaining pancreatic tissue of the dorsal pancreas was malignant tumor could not be visualized. Some differentiated areas of the adenocarcinoma The islets were generally atrophic with most containing a reducedatrophic numberand showed of insulin-positive chronic pancreatitis cells, a relative and
Load more

Recommended publications
  • Tumour-Agnostic Therapy for Pancreatic Cancer and Biliary Tract Cancer
    diagnostics Review Tumour-Agnostic Therapy for Pancreatic Cancer and Biliary Tract Cancer Shunsuke Kato Department of Clinical Oncology, Juntendo University Graduate School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo 113-8421, Japan; [email protected]; Tel.: +81-3-5802-1543 Abstract: The prognosis of patients with solid tumours has remarkably improved with the develop- ment of molecular-targeted drugs and immune checkpoint inhibitors. However, the improvements in the prognosis of pancreatic cancer and biliary tract cancer is delayed compared to other carcinomas, and the 5-year survival rates of distal-stage disease are approximately 10 and 20%, respectively. How- ever, a comprehensive analysis of tumour cells using The Cancer Genome Atlas (TCGA) project has led to the identification of various driver mutations. Evidently, few mutations exist across organs, and basket trials targeting driver mutations regardless of the primary organ are being actively conducted. Such basket trials not only focus on the gate keeper-type oncogene mutations, such as HER2 and BRAF, but also focus on the caretaker-type tumour suppressor genes, such as BRCA1/2, mismatch repair-related genes, which cause hereditary cancer syndrome. As oncogene panel testing is a vital approach in routine practice, clinicians should devise a strategy for improved understanding of the cancer genome. Here, the gene mutation profiles of pancreatic cancer and biliary tract cancer have been outlined and the current status of tumour-agnostic therapy in these cancers has been reported. Keywords: pancreatic cancer; biliary tract cancer; targeted therapy; solid tumours; driver mutations; agonist therapy Citation: Kato, S. Tumour-Agnostic Therapy for Pancreatic Cancer and 1.
    [Show full text]
  • Case Report Metastasis of Pancreatic Cancer Within Primary Colon Cancer by Overtaking the Stromal Microenvironment
    Int J Clin Exp Pathol 2018;11(6):3141-3146 www.ijcep.com /ISSN:1936-2625/IJCEP0075771 Case Report Metastasis of pancreatic cancer within primary colon cancer by overtaking the stromal microenvironment Takeo Nakaya1, Hisashi Oshiro1, Takumi Saito2, Yasunaru Sakuma2, Hisanaga Horie2, Naohiro Sata2, Akira Tanaka1 Departments of 1Pathology, 2Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan Received March 10, 2018; Accepted April 15, 2018; Epub June 1, 2018; Published June 15, 2018 Abstract: We report a unique case of a 74-old man, who presented with double cancers, showing metastasis of pancreatic cancer to colon cancer. Histopathological examination after surgery revealed that the patient had as- cending colon cancer, which metastasized to the liver (pT4N0M1), as well as pancreatic cancer (pT2N1M1) that metastasized to the most invasive portion of the colon cancer, namely the serosal to subserosal layers. Although the mechanisms for this scenario have yet to be elucidated, we speculate that the metastatic pancreatic carcinoma overtook the stromal microenvironment of the colon cancer. Namely, the cancer microenvironment enriched by can- cer-associated fibroblasts, which supported the colon cancer, might be suitable for the invasion and engraftment by pancreatic carcinoma. The similarity of histological appearance might make it difficult to distinguish metastatic pancreatic carcinoma within colon cancer. Furthermore, the metastasis of pancreatic carcinoma in colon carcinoma might be more common, despite it not having been previously reported. Keywords: Cancer metastasis, metastatic pancreatic cancer, colon cancer, double cancer, tumor microenviron- ment Introduction Case report Prevention and control of cancer metastasis is Clinical history one of the most important problems in cancer care [1-4].
    [Show full text]
  • Pancreatic Cancer
    A Patient’s Guide to Pancreatic Cancer COMPREHENSIVE CANCER CENTER Staff of the Comprehensive Cancer Center’s Multidisciplinary Pancreatic Cancer Program provided information for this handbook GI Oncology Program, Patient Education Program, Gastrointestinal Surgery Department, Medical Oncology, Radiation Oncology and Surgical Oncology Digestive System Anatomy Esophagus Liver Stomach Gallbladder Duodenum Colon Pancreas (behind the stomach) Anatomy of the Pancreas Celiac Plexus Pancreatic Duct Common Bile Duct Sphincter of Oddi Head Body Tail Pancreas ii A Patient’s Guide to Pancreatic Cancer ©2012 University of Michigan Comprehensive Cancer Center Table of Contents I. Overview of pancreatic cancer A. Where is the pancreas located?. 1 B. What does the pancreas do? . 2 C. What is cancer and how does it affect the pancreas? .....................2 D. How common is pancreatic cancer and who is at risk?. .3 E. Is pancreatic cancer hereditary? .....................................3 F. What are the symptoms of pancreatic cancer? ..........................4 G. How is pancreatic cancer diagnosed?. 7 H. What are the types of cancer found in the pancreas? .....................9 II. Treatment A. Treatment of Pancreatic Cancer. 11 1. What are the treatment options?. 11 2. How does a patient decide on treatment? ..........................12 3. What factors affect prognosis and recovery?. .12 D. Surgery. 13 1. When is surgery a treatment?. 13 2. What other procedures are done?. .16 E. Radiation therapy . 19 1. What is radiation therapy? ......................................19 2. When is radiation therapy given?. 19 3. What happens at my first appointment? . 20 F. Chemotherapy ..................................................21 1. What is chemotherapy? ........................................21 2. How does chemotherapy work? ..................................21 3. When is chemotherapy given? ...................................21 G.
    [Show full text]
  • FDG PET/CT in Pancreatic and Hepatobiliary Carcinomas Value to Patient Management and Patient Outcomes
    FDG PET/CT in Pancreatic and Hepatobiliary Carcinomas Value to Patient Management and Patient Outcomes Ujas Parikh, MAa, Charles Marcus, MDa, Rutuparna Sarangi, MAa, Mehdi Taghipour, MDa, Rathan M. Subramaniam, MD, PhD, MPHa,b,c,* KEYWORDS 18F-FDG PET/CT Pancreatic cancer Hepatocellular carcinoma KEY POINTS Fludeoxyglucose F 18 (18F-FDG) PET/CT has not been shown to offer additional benefit in the initial diagnosis of pancreatic cancer, but studies show benefit of 18F-FDG PET/CT in staging, particularly in the detection of distant metastasis, and in patient prognosis. There is good evidence for 18F-FDG PET and 18F-FDG PET/CT in the staging and prognosis of both cholangiocarcinoma and gallbladder cancer. 18F-FDG PET/CT has shown promise in the staging of liver malignancies by detecting extrahepatic metastasis. There is good evidence supporting the ability of PET/CT in predicting prognosis in patients with hepatocellular carcinoma (HCC). Evidence is evolving for the role of 18F-FDG PET/CT in predicting prognosis and survival in patients with colorectal liver metastasis (CRLM). INTRODUCTION the time of diagnosis, only 20% of tumors are curative with resection.2 Invasive ductal adenocar- Pancreatic cancer is the tenth most common cinoma is the most common pancreatic malig- malignancy and fourth most common cause of nancy, accounting for more than 80% of cancer deaths in the United States, with a lifetime 1 pancreatic cancers. Other less common malig- risk of 1.5%. It was estimated that 46,420 people nancies include neuroendocrine tumors and were expected to be diagnosed with pancreatic exocrine acinar cell neoplasms.3,4 Although smok- cancer in the United States in 2014.
    [Show full text]
  • APC Haploinsufficiency Coupled with P53 Loss Sufficiently Induces
    Oncogene (2016) 35, 2223–2234 © 2016 Macmillan Publishers Limited All rights reserved 0950-9232/16 www.nature.com/onc ORIGINAL ARTICLE APC haploinsufficiency coupled with p53 loss sufficiently induces mucinous cystic neoplasms and invasive pancreatic carcinoma in mice T-L Kuo1, C-C Weng1, K-K Kuo2,3, C-Y Chen3,4, D-C Wu3,5,6, W-C Hung7 and K-H Cheng1,3,8 Adenomatous polyposis coli (APC), a tumor-suppressor gene critically involved in familial adenomatous polyposis, is integral in Wnt/β-catenin signaling and is implicated in the development of sporadic tumors of the distal gastrointestinal tract including pancreatic cancer (PC). Here we report for the first time that functional APC is required for the growth and maintenance of pancreatic islets and maturation. Subsequently, a non-Kras mutation-induced premalignancy mouse model was developed; in this model, APC haploinsufficiency coupled with p53 deletion resulted in the development of a distinct type of pancreatic premalignant precursors, mucinous cystic neoplasms (MCNs), exhibiting pathomechanisms identical to those observed in human MCNs, including accumulation of cystic fluid secreted by neoplastic and ovarian-like stromal cells, with 100% penetrance and the presence of hepatic and gastric metastases in 430% of the mice. The major clinical implications of this study suggest targeting the Wnt signaling pathway as a novel strategy for managing MCN. Oncogene (2016) 35, 2223–2234; doi:10.1038/onc.2015.284; published online 28 September 2015 INTRODUCTION polyposis who presented concurrent solid pseudopapillary tumor, Pancreatic cancer (PC) is the fourth most common cause of adult a large encapsulated pancreatic mass with cystic and solid 12 cancer mortality and among the most lethal human cancers.
    [Show full text]
  • 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.
    [Show full text]
  • What Is a Gastrointestinal Carcinoid Tumor?
    cancer.org | 1.800.227.2345 About Gastrointestinal Carcinoid Tumors Overview and Types If you have been diagnosed with a gastrointestinal carcinoid tumor or are worried about it, you likely have a lot of questions. Learning some basics is a good place to start. ● What Is a Gastrointestinal Carcinoid Tumor? Research and Statistics See the latest estimates for new cases of gastrointestinal carcinoid tumor in the US and what research is currently being done. ● Key Statistics About Gastrointestinal Carcinoid Tumors ● What’s New in Gastrointestinal Carcinoid Tumor Research? What Is a Gastrointestinal Carcinoid Tumor? Gastrointestinal carcinoid tumors are a type of cancer that forms in the lining of the gastrointestinal (GI) tract. Cancer starts when cells begin to grow out of control. To learn more about what cancer is and how it can grow and spread, see What Is Cancer?1 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 To understand gastrointestinal carcinoid tumors, it helps to know about the gastrointestinal system, as well as the neuroendocrine system. The gastrointestinal system The gastrointestinal (GI) system, also known as the digestive system, processes food for energy and rids the body of solid waste. After food is chewed and swallowed, it enters the esophagus. This tube carries food through the neck and chest to the stomach. The esophagus joins the stomachjust beneath the diaphragm (the breathing muscle under the lungs). The stomach is a sac that holds food and begins the digestive process by secreting gastric juice. The food and gastric juices are mixed into a thick fluid, which then empties into the small intestine.
    [Show full text]
  • Synchronous Pancreatic Ductal Adenocarcinoma and Hepatocellular Carcinoma: Report of a Case and Review of the Literature JENNY Z
    ANTICANCER RESEARCH 38 : 3009-3012 (2018) doi:10.21873/anticanres.12554 Synchronous Pancreatic Ductal Adenocarcinoma and Hepatocellular Carcinoma: Report of a Case and Review of the Literature JENNY Z. LAI 1,2 , YIHUA ZHOU 3 and DENGFENG CAO 2 1University College, Washington University in St. Louis, St. Louis, MO, U.S.A.; 2Department of Pathology and Immunology, Washington University in Saint Louis School of Medicine, St. Louis, MO, U.S.A.; 3Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, U.S.A. Abstract. Two or more histologically distinct malignancies adenocarcinoma (PDAC) is one of the fatal cancers with diagnosed during the same hospital admission are short-term survival rates. The case fatality rate for the uncommon, but they do exist. Cases with synchronous disease is approximately 97% and has declined slightly (from primary pancreatic ductal adenocarcinoma and 99% to 97%) in the last 12 years (3). To date, the causes of hepatocellular carcinoma are rarely seen. This is a case pancreatic cancer are not thoroughly understood, though report of a 56 years old Caucasian female with the chief certain risk factors such as smoking, obesity, lifestyle, complaint of jaundice over a duration of 10 days. CT diabetes mellitus, alcohol, dietary factors and chronic imaging findings revealed a 3.5 cm ill-defined pancreatic pancreatitis have been proposed. Hepatocellular carcinoma head mass and a 1.5 cm liver mass in the segment 5. EUS- (HCC) is the second leading cause and the fastest rising FNA cytology showed pancreatic head ductal cause of cancer-related death worldwide (4). One of the most adenocarcinoma (PDAC).
    [Show full text]
  • Nomina Histologica Veterinaria, First Edition
    NOMINA HISTOLOGICA VETERINARIA Submitted by the International Committee on Veterinary Histological Nomenclature (ICVHN) to the World Association of Veterinary Anatomists Published on the website of the World Association of Veterinary Anatomists www.wava-amav.org 2017 CONTENTS Introduction i Principles of term construction in N.H.V. iii Cytologia – Cytology 1 Textus epithelialis – Epithelial tissue 10 Textus connectivus – Connective tissue 13 Sanguis et Lympha – Blood and Lymph 17 Textus muscularis – Muscle tissue 19 Textus nervosus – Nerve tissue 20 Splanchnologia – Viscera 23 Systema digestorium – Digestive system 24 Systema respiratorium – Respiratory system 32 Systema urinarium – Urinary system 35 Organa genitalia masculina – Male genital system 38 Organa genitalia feminina – Female genital system 42 Systema endocrinum – Endocrine system 45 Systema cardiovasculare et lymphaticum [Angiologia] – Cardiovascular and lymphatic system 47 Systema nervosum – Nervous system 52 Receptores sensorii et Organa sensuum – Sensory receptors and Sense organs 58 Integumentum – Integument 64 INTRODUCTION The preparations leading to the publication of the present first edition of the Nomina Histologica Veterinaria has a long history spanning more than 50 years. Under the auspices of the World Association of Veterinary Anatomists (W.A.V.A.), the International Committee on Veterinary Anatomical Nomenclature (I.C.V.A.N.) appointed in Giessen, 1965, a Subcommittee on Histology and Embryology which started a working relation with the Subcommittee on Histology of the former International Anatomical Nomenclature Committee. In Mexico City, 1971, this Subcommittee presented a document entitled Nomina Histologica Veterinaria: A Working Draft as a basis for the continued work of the newly-appointed Subcommittee on Histological Nomenclature. This resulted in the editing of the Nomina Histologica Veterinaria: A Working Draft II (Toulouse, 1974), followed by preparations for publication of a Nomina Histologica Veterinaria.
    [Show full text]
  • What Is the Origin of Pancreatic Adenocarcinoma?
    University of Nebraska Medical Center DigitalCommons@UNMC Journal Articles: Biochemistry & Molecular Biology Biochemistry & Molecular Biology Winter 1-22-2013 What is the origin of pancreatic adenocarcinoma? Parviz M. Pour University of Nebraska Medical Center, [email protected] K. K. Panday University of Nebraska Medical Center Surinder K. Batra University of Nebraska Medical Center, [email protected] Follow this and additional works at: https://digitalcommons.unmc.edu/com_bio_articles Part of the Medical Biochemistry Commons, and the Medical Molecular Biology Commons Recommended Citation Pour, Parviz M.; Panday, K. K.; and Batra, Surinder K., "What is the origin of pancreatic adenocarcinoma?" (2013). Journal Articles: Biochemistry & Molecular Biology. 99. https://digitalcommons.unmc.edu/com_bio_articles/99 This Article is brought to you for free and open access by the Biochemistry & Molecular Biology at DigitalCommons@UNMC. It has been accepted for inclusion in Journal Articles: Biochemistry & Molecular Biology by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. Molecular Cancer Bio Med Central Review Open Access What is the origin of pancreatic adenocarcinoma? Parviz M Pour* 1,2, Krishan K Pandey 3 and Surinder K Batra 3 Address: 1The Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 986805 Nebraska Medical Center, Omaha, NE 68198 USA, 2Department of Pathology and Microbiology University of Nebraska Medical Center, 986805 Nebraska
    [Show full text]
  • What Is Pancreatic Cancer?
    cancer.org | 1.800.227.2345 About Pancreatic Cancer Overview and Types If you have been diagnosed with pancreatic cancer or worried about it, you likely have a lot of questions. Learning some basics is a good place to start. ● What Is Pancreatic Cancer? Research and Statistics See the latest estimates for new cases of pancreatic cancer and deaths in the US and what research is currently being done. ● Key Statistics for Pancreatic Cancer ● What’s New in Pancreatic Cancer Research? What Is Pancreatic Cancer? Pancreatic cancer is a type of cancer that starts in the pancreas. (Cancer starts when cells in the body begin to grow out of control. To learn more about how cancers start and spread, see What Is Cancer?1) Pancreatic adenocarcinoma is the most common type of pancreatic cancer. Pancreatic neuroendocrine tumors (NETs) are a less common type and are discussed in Pancreatic Neuroendocrine Tumors2. 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 Where pancreatic cancer starts The pancreas The pancreas is an organ that sits behind the stomach. It's shaped a bit like a fish with a wide head, a tapering body, and a narrow, pointed tail. In adults it's about 6 inches (15 centimeters) long but less than 2 inches (5 centimeters) wide. ● The head of the pancreas is on the right side of the abdomen (belly), behind where the stomach meets the duodenum (the first part of the small intestine). ● The body of the pancreas is behind the stomach. ● The tail of the pancreas is on the left side of the abdomen next to the spleen.
    [Show full text]
  • What Is Pancreatic Polypeptide and What Does It Do?
    What is Pancreatic Polypeptide and what does it do? This document aims to evaluate current understanding of pancreatic polypeptide (PP), a gut hormone with several functions contributing towards the maintenance of energy balance. Successful regulation of energy homeostasis requires sophisticated bidirectional communication between the gastrointestinal tract and central nervous system (CNS; Williams et al. 2000). The coordinated release of numerous gastrointestinal hormones promotes optimal digestion and nutrient absorption (Chaudhri et al., 2008) whilst modulating appetite, meal termination, energy expenditure and metabolism (Suzuki, Jayasena & Bloom, 2011). The Discovery of a Peptide Kimmel et al. (1968) discovered PP whilst purifying insulin from chicken pancreas (Adrian et al., 1976). Subsequent to extraction of avian pancreatic polypeptide (aPP), mammalian homologues bovine (bPP), porcine (pPP), ovine (oPP) and human (hPP), were isolated by Lin and Chance (Kimmel, Hayden & Pollock, 1975). Following extensive observation, various features of this novel peptide witnessed its eventual classification as a hormone (Schwartz, 1983). Molecular Structure PP is a member of the NPY family including neuropeptide Y (NPY) and peptide YY (PYY; Holzer, Reichmann & Farzi, 2012). These biologically active peptides are characterized by a single chain of 36-amino acids and exhibit the same ‘PP-fold’ structure; a hair-pin U-shaped molecule (Suzuki et al., 2011). PP has a molecular weight of 4,240 Da and an isoelectric point between pH6 and 7 (Kimmel et al., 1975), thus carries no electrical charge at neutral pH. Synthesis Like many peptide hormones, PP is derived from a larger precursor of 10,432 Da (Leiter, Keutmann & Goodman, 1984). Isolation of a cDNA construct, synthesized from hPP mRNA, proposed that this precursor, pre-propancreatic polypeptide, comprised 95 residues (Boel et al., 1984) and is processed to produce three products (Leiter et al., 1985); PP, an icosapeptide containing 20-amino acids and a signal peptide (Boel et al., 1984).
    [Show full text]