Pathology and Genetics of Tumours of the Digestive System
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The Homeobox Intestinal Differentiation Factor CDX2 Is Selectively Expressed in Gastrointestinal Adenocarcinomas
Modern Pathology (2004) 17, 1392–1399 & 2004 USCAP, Inc All rights reserved 0893-3952/04 $30.00 www.modernpathology.org The homeobox intestinal differentiation factor CDX2 is selectively expressed in gastrointestinal adenocarcinomas Vassil Kaimaktchiev1, Luigi Terracciano2, Luigi Tornillo2, Hanspeter Spichtin3, Dimitra Stoios2, Marcel Bundi2, Veselina Korcheva1, Martina Mirlacher2, Massimo Loda4, Guido Sauter2 and Christopher L Corless1 1OHSU Cancer Institute and Department of Pathology, Oregon Health & Science University, Portland, OR, USA; 2Institute of Pathology, University Hospital Basel, Basel, Switzerland; 3Institute of Clinical Pathology, Basel, Switzerland and 4Department of Pathology, Brigham & Women’s Hospital, Boston, MA, USA CDX2 is a homeobox domain-containing transcription factor that is important in the development and differentiation of the intestines. Based on recent studies, CDX2 expression is immunohistochemically detectable in normal colonic enterocytes and is retained in most, but not all, colorectal adenocarcinomas. CDX2 expression has also been documented in a subset of adenocarcinomas arising in the stomach, esophagus and ovary. In this study, we examined CDX2 expression in a series of large tissue microarrays representing 4652 samples of normal and neoplastic tissues. Strong nuclear staining for CDX2 was observed in 97.9% of 140 colonic adenomas, 85.7% of 1109 colonic adenocarcinomas overall and 81.8% of 55 mucinous variants. There was no significant difference in the staining of well-differentiated (96%) and moderately differentiated tumors (90.8%, P ¼ 0.18), but poorly differentiated tumors showed reduced overall expression (56.0%, Po0.000001). Correspondingly, there was an inverse correlation between CDX2 expression and tumor stage, with a significant decrease in staining between pT2 and pT3 tumors (95.8 vs 89.0%, Po0.012), and between pT3 and pT4 tumors (89.0 vs 79.8%, Po0.016). -
The Anatomy of the Rectum and Anal Canal
BASIC SCIENCE identify the rectosigmoid junction with confidence at operation. The anatomy of the rectum The rectosigmoid junction usually lies approximately 6 cm below the level of the sacral promontory. Approached from the distal and anal canal end, however, as when performing a rigid or flexible sigmoid- oscopy, the rectosigmoid junction is seen to be 14e18 cm from Vishy Mahadevan the anal verge, and 18 cm is usually taken as the measurement for audit purposes. The rectum in the adult measures 10e14 cm in length. Abstract Diseases of the rectum and anal canal, both benign and malignant, Relationship of the peritoneum to the rectum account for a very large part of colorectal surgical practice in the UK. Unlike the transverse colon and sigmoid colon, the rectum lacks This article emphasizes the surgically-relevant aspects of the anatomy a mesentery (Figure 1). The posterior aspect of the rectum is thus of the rectum and anal canal. entirely free of a peritoneal covering. In this respect the rectum resembles the ascending and descending segments of the colon, Keywords Anal cushions; inferior hypogastric plexus; internal and and all of these segments may be therefore be spoken of as external anal sphincters; lymphatic drainage of rectum and anal canal; retroperitoneal. The precise relationship of the peritoneum to the mesorectum; perineum; rectal blood supply rectum is as follows: the upper third of the rectum is covered by peritoneum on its anterior and lateral surfaces; the middle third of the rectum is covered by peritoneum only on its anterior 1 The rectum is the direct continuation of the sigmoid colon and surface while the lower third of the rectum is below the level of commences in front of the body of the third sacral vertebra. -
What You Should Know About Familial Adenomatous Polyposis (FAP)
What you should know about Familial Adenomatous Polyposis (FAP) FAP is a very rare condition that accounts for about 1% of new cases of colorectal cancer. People with FAP typically develop hundreds to thousands of polyps (adenomas) in their colon and rectum by age 30-40. Polyps may also develop in the stomach and small intestine. Individuals with FAP can develop non-cancerous cysts on the skin (epidermoid cysts), especially on the scalp. Besides having an increased risk for colon polyps and cysts, individuals with FAP are also more likely to develop sebaceous cysts, osetomas (benign bone tumors) of the jaw, impacted teeth, extra teeth, CHRPE (multiple areas of pigmentation in the retina in the eye) and desmoid disease. Some individuals have milder form of FAP, called attenuated FAP (AFAP), and develop an average of 20 polyps at a later age. The risk for cancer associated with FAP If left untreated, the polyps in the colon and rectum will develop in to cancer, usually before age 50. Individuals with FAP also have an increased risk for stomach cancer, papillary thyroid cancer, periampullary carcinoma, hepatoblastoma (in childhood), and brain tumors. The risks to family members FAP is caused by mutations in the Adenomatous Polyposis Coli (APC) gene. Approximately 1/3 of people with FAP do not have family history of the disease, and thus have a new mutation. FAP is inherited in a dominant fashion. Children of a person with an APC mutation have a 50% risk to inherit the mutation. Brothers, sisters, and parents of individuals with FAP should also be checked to see if they have an APC mutation. -
Rectum & Anal Canal
Rectum & Anal canal Dr Brijendra Singh Prof & Head Anatomy AIIMS Rishikesh 27/04/2019 EMBRYOLOGICAL basis – Nerve Supply of GUT •Origin: Foregut (endoderm) •Nerve supply: (Autonomic): Sympathetic Greater Splanchnic T5-T9 + Vagus – Coeliac trunk T12 •Origin: Midgut (endoderm) •Nerve supply: (Autonomic): Sympathetic Lesser Splanchnic T10 T11 + Vagus – Sup Mesenteric artery L1 •Origin: Hindgut (endoderm) •Nerve supply: (Autonomic): Sympathetic Least Splanchnic T12 L1 + Hypogastric S2S3S4 – Inferior Mesenteric Artery L3 •Origin :lower 1/3 of anal canal – ectoderm •Nerve Supply: Somatic (inferior rectal Nerves) Rectum •Straight – quadrupeds •Curved anteriorly – puborectalis levator ani •Part of large intestine – continuation of sigmoid colon , but lacks Mesentery , taeniae coli , sacculations & haustrations & appendices epiploicae. •Starts – S3 anorectal junction – ant to tip of coccyx – apex of prostate •12 cms – 5 inches - transverse slit •Ampulla – lower part Development •Mucosa above Houstons 3rd valve endoderm pre allantoic part of hind gut. •Mucosa below Houstons 3rd valve upto anal valves – endoderm from dorsal part of endodermal cloaca. •Musculature of rectum is derived from splanchnic mesoderm surrounding cloaca. •Proctodeum the surface ectoderm – muco- cutaneous junction. •Anal membrane disappears – and rectum communicates outside through anal canal. Location & peritoneal relations of Rectum S3 1 inch infront of coccyx Rectum • Beginning: continuation of sigmoid colon at S3. • Termination: continues as anal canal, • one inch below -
Juvenile Polyposis Syndrome Might Be
Gao et al. BMC Gastroenterology (2020) 20:167 https://doi.org/10.1186/s12876-020-01238-7 CASE REPORT Open Access Juvenile polyposis syndrome might be misdiagnosed as familial adenomatous polyposis: a case report and literature review Xian Hua Gao1,2†, Juan Li3†, Zi Ye Zhao1,2†, Xiao Dong Xu1,2,YiQiDu2,4, Hong Li Yan2,5, Lian Jie Liu1*, Chen Guang Bai2,6* and Wei Zhang1,2* Abstract Background: Juvenile polyposis syndrome (JPS) is a rare disorder characterized by the presence of multiple juvenile polyps in the gastrointestinal tract, and germline mutations in SMAD4 or BMPR1A. Due to its rarity and complex clinical manifestation, misdiagnosis often occurs in clinical practice. Case presentation: A 42-year-old man with multiple pedunculated colorectal polyps and concomitant rectal adenocarcinoma was admitted to our hospital. His mother had died of colon cancer. He was diagnosed with familial adenomatous polyposis (FAP) and underwent total proctocolectomy and ileal pouch anal anastomosis. Two polyps were selected for pathological examination. One polyp had cystically dilated glands with slight dysplasia. The other polyp displayed severe dysplasia and was diagnosed as adenoma. Three years later, his 21-year-old son underwent a colonoscopy that revealed more than 50 pedunculated colorectal juvenile polyps. Both patients harbored a germline pathogenic mutation in BMPR1A. Endoscopic resection of all polyps was attempted but failed. Finally, the son received endoscopic resection of polyps in the rectum and sigmoid colon, and laparoscopic subtotal colectomy. Ten polyps were selected for pathological examination. All were revealed to be typical juvenile polyps, with cystically dilated glands filled with mucus. -
Guidelines for the Management of Hereditary Colorectal Cancer
Guidelines Guidelines for the management of hereditary Gut: first published as 10.1136/gutjnl-2019-319915 on 28 November 2019. Downloaded from colorectal cancer from the British Society of Gastroenterology (BSG)/Association of Coloproctology of Great Britain and Ireland (ACPGBI)/ United Kingdom Cancer Genetics Group (UKCGG) Kevin J Monahan ,1,2 Nicola Bradshaw,3 Sunil Dolwani,4 Bianca Desouza,5 Malcolm G Dunlop,6 James E East,7,8 Mohammad Ilyas,9 Asha Kaur,10 Fiona Lalloo,11 Andrew Latchford,12 Matthew D Rutter ,13,14 Ian Tomlinson ,15,16 Huw J W Thomas,1,2 James Hill,11 Hereditary CRC guidelines eDelphi consensus group ► Additional material is ABSTRact having a family history of a first-degree relative published online only. To view Heritable factors account for approximately 35% of (FDR) or second degree relative (SDR) with CRC.2 please visit the journal online (http:// dx. doi. org/ 10. 1136/ colorectal cancer (CRC) risk, and almost 30% of the While highly penetrant syndromes such as Lynch gutjnl- 2019- 319915). population in the UK have a family history of CRC. syndrome (LS), familial adenomatous polyposis (FAP) The quantification of an individual’s lifetime risk of and other polyposis syndromes account for account For numbered affiliations see end of article. gastrointestinal cancer may incorporate clinical and for only 5–10% of all CRC diagnoses, advances molecular data, and depends on accurate phenotypic in genetic diagnosis, improvements in endoscopic Correspondence to assessment and genetic diagnosis. In turn this may surgical control, and medical and lifestyle interven- Dr Kevin J Monahan, Family facilitate targeted risk-reducing interventions, including tions provide opportunities for CRC prevention and Cancer Clinic, St Mark’s endoscopic surveillance, preventative surgery and effective treatment in susceptible individuals. -
Endocrine Tumors of the Pancreas
Friday, November 4, 2005 8:30 - 10:30 a. m. Pancreatic Tumors, Session 2 Chairman: R. Jensen, Bethesda, MD, USA 9:00 - 9:30 a. m. Working Group Session Pathology and Genetics Group leaders: J.–Y. Scoazec, Lyon, France Questions to be answered: 12 Medicine and Clinical Pathology Group leader: K. Öberg, Uppsala, Sweden Questions to be answered: 17 Surgery Group leader: B. Niederle, Vienna, Austria Questions to be answered: 11 Imaging Group leaders: S. Pauwels, Brussels, Belgium; D.J. Kwekkeboom, Rotterdam, The Netherlands Questions to be answered: 4 Color Codes Pathology and Genetics Medicine and Clinical Pathology Surgery Imaging ENETS Guidelines Neuroendocrinology 2004;80:394–424 Endocrine Tumors of the Pancreas - gastrinoma Epidemiology The incidence of clinically detected tumours has been reported to be 4-12 per million inhabitants, which is much lower than what is reported from autopsy series (about 1%) (5,13). Clinicopathological staging (12, 14, 15) Well-differentiated tumours are the large majority of which the two largest fractions are insulinomas (about 40% of cases) and non-functioning tumours (30-35%). When confined to the pancreas, non-angioinvasive, <2 cm in size, with <2 mitoses per 10 high power field (HPF) and <2% Ki-67 proliferation index are classified as of benign behaviour (WHO group 1) and, with the notable exception of insulinomas, are non-functioning. Tumours confined to the pancreas but > 2 cm in size, with angioinvasion and /or perineural space invasion, or >2mitoses >2cm in size, >2 mitoses per 20 HPF or >2% Ki-67 proliferation index, either non-functioning or functioning (gastrinoma, insulinoma, glucagonoma, somastatinoma or with ectopic syndromes, such as Cushing’s syndrome (ectopic ACTH syndrome), hypercaliemia (PTHrpoma) or acromegaly (GHRHoma)) still belong to the (WHO group 1) but are classified as tumours with uncertain behaviour. -
Name: David Daniella Christabel Matric Number: 18/MHS03/002 Department: Anatomy College: Medicine and Health Sciences Course Code: Ana 212
Name: David Daniella Christabel Matric Number: 18/MHS03/002 Department: Anatomy College: Medicine And Health Sciences Course Code: Ana 212 Question: Discuss the anal canal. The anal canal is the terminal segment of the large intestine between the rectum and the anus. The anal canal is located within the anal triangle of the perineum between the right and left ischioanal fosse. It is the final segment of the gastrointestinal tract, around 4cm in length. The canal begins as a continuation of the rectum and passes inferoposteriorly to terminate at the anus. Anal canal is traditionally divided into two segments, upper and lower, separated by the pectinate line also known as the dentate line. Except during defecation, the anal canal is collapsed by the internal and external sphincters to prevent the passage of faecal material. The anal canal is surrounded by internal and external anal sphincters, which play a crucial role in the maintenance of the faecal continence. • Internal Anal Sphincters: surrounds the upper 2/3 of the anal canal. It is formed from a thickening of the involuntary circular smooth muscle in the bowel wall. • External Anal Sphincter: voluntary muscle that surrounds the lower 2/3 of the anal canal (and so overlaps with the internal sphincter). It blends superiorly with the puborecrtalis muscle of the pelvic floor. At the junction of the rectum and the anal canal, there is a muscular ring known as the anorectal ring. It is formed by the fusion of the internal anal sphincter, external anal sphincter and puborectalis muscle, and is palpable on digital rectal examination. -
Comparing Right Colon Adenoma and Hyperplastic Polyp
Title: Comparing right colon adenoma and hyperplastic polyp miss rate in colonoscopy using water exchange and carbon dioxide insufflation: A prospective multicenter randomized controlled trial NCT Number: 03845933 Unique Protocol ID: EGH-2019 Date: Feb 16, 2019 頁 1 / 10 INTRODUCTION Colonoscopy is currently regarded as the gold standard to detect and prevent colorectal cancer (CRC) [1]. It estimated to prevent about 76%-90% of CRC [2], but post-colonoscopy CRCs (PCCRCs) still occur. Recent case-control studies consistently demonstrated that protection by colonoscopy against right-sided colon cancer, ranging from 40% to 60%, was lower than the 80% protection attained in the left colon [3-5]. Of all PCCRCs, 58% were attributed to lesions missed during examination [6]. In a systematic review of tandem colonoscopy studies, a 22% pooled miss-rate for all polyps was reported [7]. Colonoscopy maneuvers helping to reduce miss-rate for all polyps, particularly in the right colon, have the potential to decrease the incidence of PCCRCs. Water exchange (WE) colonoscopy is characterized by the gasless insertion to the cecum in clear water and maximizing cleanliness during insertion. WE colonoscopy has been shown to improve the overall adenoma detection rate (ADR), compared to air insufflation colonoscopy, in many prospective randomized controlled trials (RCTs) [8-13]. WE colonoscopy also has been shown to improve right colon ADR in RCTs [10-12] and meta-analyses [14,15]. In a pooled data from two multisite RCTs, WE also significantly increases right colon combined advanced and sessile serrated ADR as compared to air insufflation colonoscopy [16]. Decreased multitasking-related distraction from cleaning maneuvers has been the most recently identified explanation for the increase in ADR by WE [17]. -
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. -
Abdominal and Pelvic Imaging Findings Associated with Sex Hormone Abnormalities
UCSF UC San Francisco Previously Published Works Title Abdominal and pelvic imaging findings associated with sex hormone abnormalities. Permalink https://escholarship.org/uc/item/7cq623wg Journal Abdominal radiology (New York), 44(3) ISSN 2366-004X Authors Kurzbard-Roach, Nicole Jha, Priyanka Poder, Liina et al. Publication Date 2019-03-01 DOI 10.1007/s00261-018-1844-1 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Abdominal Radiology https://doi.org/10.1007/s00261-018-1844-1 (0123456789().,-volV)(0123456789().,-volV) REVIEW Abdominal and pelvic imaging findings associated with sex hormone abnormalities 1 1 1 2 Nicole Kurzbard-Roach • Priyanka Jha • Liina Poder • Christine Menias Ó Springer Science+Business Media, LLC, part of Springer Nature 2018 Abstract Hormones are substances that serve as chemical communication between cells. They are unique biological molecules that affect multiple organ systems and play a key role in maintaining homoeostasis. In this role, they are usually produced from a single organ and have defined target organs. However, hormones can affect non-target organs as well. As such, biochemical and hormonal abnormalities can be associated with anatomic changes in multiple target as well as non-target organs. Hormone-related changes may take the form of an organ parenchymal abnormality, benign neoplasm, or even malignancy. Given the multifocal action of hormones, the observed imaging findings may be remote from the site of production, and may actually be multi-organ in nature. Anatomic findings related to hormone level abnormalities and/or laboratory biomarker changes may be identified with imaging. The purpose of this image-rich review is to sensitize radiologists to imaging findings in the abdomen and pelvis that may occur in the context of hormone abnormalities, focusing primarily on sex hormones and their influence on these organs. -
Zollinger-Ellison Syndrome. Case Report
https://doi.org/10.15446/cr.v5n1.71686 ZOLLINGER-ELLISON SYNDROME. CASE REPORT Keywords: Gastrinoma; Zollinger-Ellison Sydrome; Multiple Endocrine Neoplasia Type 1. Palabras clave: Gastrinoma; Síndrome de Zollinger-Ellison; Neoplasia endocrina múltiple tipo 1. Juan Felipe Rivillas-Reyes Juan Leonel Castro-Avendaño Universidad Nacional de Colombia - Sede Bogotá - Facultad de Medicina - Programa de Medicina - Bogotá D.C. - Colombia. Héctor Fabián Martínez-Muñoz Universidad Nacional de Colombia - Sede Bogotá - Facultad de Medicina - Departamento de Cirugía - Bogotá D.C. - Colombia. Corresponding author Juan Felipe Rivillas-Reyes. Facultad de Medicina, Universidad Nacional de Colombia. Bogotá D.C. Colombia. Email: [email protected]. Received: 13/04/2018 Accepted: 20/11/2018 zollinger-ellison syndrome ABSTRACT RESUMEN 29 Introduction: The Zollinger-Ellison syndrome Introducción. El síndrome de Zollinger-Elli- (ZES) is a pathology caused by a neuroendo- son (SZE) es una patología producida por un crine tumor, usually located in the pancreas tumor neuroendocrino habitualmente localiza- or the duodenum, which is characterized by do a nivel duodenal o pancreático, el cual pro- elevated levels of gastrin, resulting in an ex- duce niveles elevados de gastrina, derivando cessive production of gastric acid. en hipersecreción de ácido gástrico. Case presentation: A 42-year-old female Presentación del caso. Paciente femenino patient with a history of longstanding peptic de 42 años con antecedente de enfermedad ulcer disease, who consulted due to persistent ulceropéptica de larga data, quién consulta por epigastric pain, melena and signs of peritoneal epigastralgia persistente y deposiciones meléni- irritation. Perforated peptic ulcer was suspect- cas y presenta signos de irritación peritoneal. Se ed, requiring emergency surgical intervention.