Test Bank for Robbins and Cotran Pathologic Basis of Disease 9th Edition by Kumar

Similar documents
Test Bank for Robbins and Cotran Pathologic Basis of Disease 9th Edition by Kumar

Dr Rodney Itaki Lecturer Anatomical Pathology Discipline. University of Papua New Guinea School of Medicine & Health Sciences Division of Pathology

TUMOR M ARKERS MARKERS

Neoplasia literally means "new growth.

NEOPLASIA! Terminology and Classification of Neoplastic cells! Objectives: Asst. Prof. Prasit Suwannalert, Ph.D. Leading Questions

Cancer Genetics. What is Cancer? Cancer Classification. Medical Genetics. Uncontrolled growth of cells. Not all tumors are cancerous

Cancer genetics

number Done by Corrected by Doctor Maha Shomaf

NEOPLASIA! Terminology and Classification of Neoplastic cells! Asst. Prof. Prasit Suwannalert, Ph.D. Objectives:

Section D. Genes whose Mutation can lead to Initiation

Mohammed El-Khateeb. Tumor Genetics. MGL-12 May 13 th Chapter 22 slide 1 台大農藝系遺傳學

Information for You and Your Family

oncogenes-and- tumour-suppressor-genes)

3 cell types in the normal ovary

American Society of Cytopathology Core Curriculum in Molecular Biology

Renal tumors of adults

Introduction. Cancer Biology. Tumor-suppressor genes. Proto-oncogenes. DNA stability genes. Mechanisms of carcinogenesis.

Neoplasia. (4&5 of 6)

Chapter 9, Part 1: Biology of Cancer and Tumor Spread

Colorectal adenocarcinoma leading cancer in developed countries In US, annual deaths due to colorectal adenocarcinoma 57,000.

Neoplasia part I. Dr. Mohsen Dashti. Clinical Medicine & Pathology nd Lecture

SHN-1 Human Digestive Panel Test results

Lecture 8 Neoplasia II. Dr. Nabila Hamdi MD, PhD

Oncogenes and Tumor Suppressors MCB 5068 November 12, 2013 Jason Weber

3 cell types in the normal ovary

1. Basic principles 2. 6 hallmark features 3. Abnormal cell proliferation: mechanisms 4. Carcinogens: examples. Major Principles:

Multistep nature of cancer development. Cancer genes

Section D: The Molecular Biology of Cancer

ONCOLOGY. Csaba Bödör. Department of Pathology and Experimental Cancer Research november 19., ÁOK, III.

Biochemistry of Cancer and Tumor Markers

Development of Carcinoma Pathways

Karyotype analysis reveals transloction of chromosome 22 to 9 in CML chronic myelogenous leukemia has fusion protein Bcr-Abl

Mohammed El-Khateeb. Tumor Genetics. MGL-12 July 21 st 2013 台大農藝系遺傳學 Chapter 22 slide 1

NEOPLASIA. 3. Which of the following tumour is benign a. Chondrosarcoma b. Osteochondroma c. Chondroblastoma d. Ewing s tumour e.

Hereditary Non Polyposis Colorectal Cancer(HNPCC) From clinic to genetics

Sarah Burton. Lead Gynae Oncology Nurse Specialist Cancer Care Cymru

Bowel obstruction and tumors

PATHOBIOLOGY OF NEOPLASIA

SCOPE OF PRACTICE PGY-5

Neoplasia 18 lecture 6. Dr Heyam Awad MD, FRCPath

Colonic Polyp. Najmeh Aletaha. MD

Lecture 1: Carcinogenesis

Present State of Gene Diagnosis and Future Prospects

What All of Us Should Know About Cancer and Genetics

Carcinogenesis. Carcinogenesis. 1. Basic principles 2. 6 hallmark features 3. Abnormal cell proliferation: mechanisms 4. Carcinogens: examples

OVARIES. MLS Basic histological diagnosis MLS HIST 422 Semester 8- batch 7 L13 Dr: Ali Eltayb.

BIOLOGY OF CANCER. Definition: Cancer. Why is it Important to Understand the Biology of Cancer? Regulation of the Cell Cycle 2/13/2015

Joseph Misdraji, M.D. GI pathology Unit Massachusetts General Hospital

Cancer. The fundamental defect is. unregulated cell division. Properties of Cancerous Cells. Causes of Cancer. Altered growth and proliferation

1. Esophageal diverticulum located above the upper esophageal sphincter is called

Deregulation of signal transduction and cell cycle in Cancer

AllinaHealthSystems 1

Tumour Structure and Nomenclature. Paul Edwards. Department of Pathology and Cancer Research UK Cambridge Institute, University of Cambridge

CANCER. Inherited Cancer Syndromes. Affects 25% of US population. Kills 19% of US population (2nd largest killer after heart disease)

colorectal cancer Colorectal cancer hereditary sporadic Familial 1/12/2018

Oncology 101. Cancer Basics

Chapter 4 Cellular Oncogenes ~ 4.6 -

Neoplasia 2018 lecture 11. Dr H Awad FRCPath

Cancer. Questions about cancer. What is cancer? What causes unregulated cell growth? What regulates cell growth? What causes DNA damage?

Célia DeLozier-Blanchet

FINALIZED SEER SINQ S MAY 2012

For more information about how to cite these materials visit

Chapter 9. Cells Grow and Reproduce

Cancer Fundamentals. Julie Randolph-Habecker, Ph.D. Director, Experimental Histopathology Shared Resource

Cell Cycle and Cancer

What causes cancer? Physical factors (radiation, ionization) Chemical factors (carcinogens) Biological factors (virus, bacteria, parasite)

CentoCancer STRIVE FOR THE MOST COMPLETE INFORMATION

CELL BIOLOGY - CLUTCH CH CANCER.

Cancer statistics (US)

Epithelial tumors. Dr. F.F. Khuzin, PhD Dr. M.O. Mavlikeev

COLON AND RECTUM SOLID TUMOR RULES ABSTRACTORS TRAINING

Molecular Cell Biology. Prof. D. Karunagaran. Department of Biotechnology. Indian Institute of Technology Madras

Invited Re vie W. Molecular genetics of ovarian carcinomas. Histology and Histo pathology

CARCINOGENESIS THE MOLECULAR BASIS OF CANCER

Gastrointestinal pathology 2018 lecture 4. Dr Heyam Awad FRCPath

Bihong Zhao, M.D, Ph.D Department of Pathology

Molecular biology :- Cancer genetics lecture 11

Tumor Immunology. Tumor (latin) = swelling

List of Available TMAs in the PRN

Colon and Rectum: 2018 Solid Tumor Rules

Policy Specific Section: Medical Necessity and Investigational / Experimental. October 14, 1998 March 28, 2014

Ovarian cancer: 2012 Update Srini Prasad MD Univ Texas MD Anderson Cancer Center

Icd 10 ovarian stroma

Early Embryonic Development

NEOPLASIA-I CANCER. Nam Deuk Kim, Ph.D.

Lecture 2. [Pathophysiology]

Neoplasia 2018 Lecture 2. Dr Heyam Awad MD, FRCPath

Abdulrahman Alhanbali. Bahaa Najjar. Maha shomaf

Urinary Bladder: WHO Classification and AJCC Staging Update 2017

Cancer. The fundamental defect is. unregulated cell division. Properties of Cancerous Cells. Causes of Cancer. Altered growth and proliferation

Familial and Hereditary Colon Cancer

Gastrointestinal Malignancies. Dr Rodney ITAKI Pathology Division, SMHS, UPNG Anatomical Pathology Discipline

Page 1 of 8 TABLE OF CONTENTS

Introduction to Cancer Biology

A 64 y.o. man presents to the hospital with persistent cough and hemoptysis. Fernando Mut Montevideo - Uruguay

Determination Differentiation. determinated precursor specialized cell

Tumori eredofamiliari: sorveglianza di donne ad alto rischio

IS THROAT CANCER HEREDITARY

Diseases of the breast (2 of 2) Breast cancer

SUPPLEMENTARY INFORMATION

Transcription:

Link full download: http://testbankair.com/download/test-bank-for-robbins-cotran-pathologic-basis-of-disease-9th-edition-bykumar-abbas-and-aster Test Bank for Robbins and Cotran Pathologic Basis of Disease 9th Edition by Kumar Chapter 07: Neoplasia MULTIPLE CHOICE 1. Which of the following tumors occurs most often in the ovary? A. Chondroma B. Hemangioma C. Leiomyoma D. Transitional cell papilloma E. Cystadenoma ANS: E, Cystadenomas, which may contain serous fluid or mucin and are thus called serous or mucinous cystadenomas, are typically found in the ovary. These benign tumors have malignant counterparts known as cystadenocarcinomas. 2. Which one of the following carcinomas is locally invasive but rarely forms metastases in lymph nodes and distant sites? A. Basal cell carcinoma of the skin B. Squamous cell carcinoma of the skin C. Oat cell carcinoma of the lung D. Transitional cell carcinoma of the urinary bladder E. Adenocarcinoma of the stomach ANS: A, Basal cell carcinomas of the skin, the most common malignant tumor in the human body, is a locally invasive malignant tumor, which, if untreated, could ultimately kill the host. However, these tumors are usually diagnosed early and removed adequately, so that they almost never metastasize. 3. Pseudomyxoma peritonei is a complication of which tumor? A. Serous cystadenoma of the ovary B. Mucinous cystadenoma of the ovary C. Ovarian fibroma D. Myxoma of the heart E. Myxosarcoma of the lower extremity

ANS: B, Pseudomyxoma of the ovary usually results from peritoneal seeding of mucin-secreting tumors of the ovary or the gastrointestinal tract, and most often the appendix. Although the ovarian tumor is benign, the implants of the tumor cells seeding the peritoneal cavity can be difficult to eradicate. The cells continue to secrete mucin and fill the abdominal cavity, colloquially known as jelly-belly. 4. Which mechanism affecting the genes or chromosomes accounts for the activation of the c-myc protooncogene in Burkitt lymphoma cells? A. Overexpression B. Amplification C. Point mutation D. Translocation E. Inactivation of its promotor ANS: D, Translocation of the c-myc protooncogene from its normal site on chromosome 8 to chromosome 14 results in the formation of the myc oncogene and plays a major role in the pathogenesis of Burkitt lymphoma. 5. Homogeneous staining regions (HSR) of chromosome 2p, the site of the Nmyc gene, are adverse prognostic signs if found in neuroblastoma cells. HRS are evidence of gene A. deletion B. amplification C. point mutation D. translocation E. inversion ANS: B, Homogeneous staining regions and double minutes are signs of gene amplification. Amplification of the N-myc oncogene in neuroblastoma cells is a poor prognostic finding. 6. In which cell function is BRCA1, a gene mutated in women with familial breast carcinoma, involved? A. Cell adhesion B. Growth inhibition C. Signal transduction D. Cell surface channel E. Transcriptional regulation and DNA repair ANS: E, BRCA1 and BRCA2 are tumor suppressor genes whose true function has not been fully elucidated. It is thought that they participate in the transcriptional

regulation and interact with proteins that regulate double-strand DNA repair. 7. Germ line mutation of E-cadherin is found in familial cases of A. lymphoblastic lymphoma B. Ewing sarcoma C. neuroblastoma D. gastric carcinoma E. seminoma ANS: D, E-cadherin is a cell-to-cell adhesion molecule that serves to hold many epithelial cells together. This surface adhesion molecule is often lost in adenocarcinomas, accounting for the invasive growth of these neoplasms. Germ line mutation of the E-cadherin gene has been found in families with gastric carcinoma. 8. Germ line mutation of the Von Hippel Lindau (VHL) gene is associated with formation of retinal angiomas and A. glioblastoma multiforme B. oligodendroglioma C. neurinomas D. ependymomas E. cerebellar hemangioblastomas ANS: E, Von Hippel Lindau syndrome was originally described as a syndrome comprising angiomas of the retina and hemangioblastomas of the cerebellum. It is linked to the germ line mutation of the VHL tumor suppressor gene. These patients are at risk of developing renal cell carcinoma and pheochromocytomas. Mutations of the VHL gene also have been found in sporadic renal carcinomas unrelated to Von Hippel Lindau syndrome. 9. Microsatellite instability, a marker of DNA mismatch repair, is typically found in A. hereditary nonpolyposis colon cancer B. familial adenomatous polyposis coli C.T-cell lymphoma D.B-cell lymphoma E.myelogenous leukemia ANS: A, Mutations of human DNA mismatch repair genes play a pathogenetic role in the development of colonic cancers in families with hereditary nonpolyposis colon cancer (HNPCC). Due to the error in mismatch repair, the microsatellite sequences (normally fixed for life and the same in every tissue) expand. They account for the microsatellite instability, a hallmark of all conditions with defective DNA mismatch repair.

10. Which enzymes in the liver account for the activation of most procarcinogens into carcinogens? A. Cytochrome P-450-dependent mono-oxidases B. Aminotransferases C. Hydroxylases D. Glutathione dehydrogenase E. Caspases ANS: A, Most of the exogenous procarcinogens are activated into carcinogens in the liver through the action of microsomal cytochrome P-450 dependent monooxidases found in the smooth endoplasmic reticulum of hepatocytes. Susceptibility to carcinogens is in part determined by the polymorphism of genes that encode these enzymes. 11. Which is the most common radiation-induced cancer in humans? A. Thyroid cancer B. Chronic lymphocytic leukemia C. Breast cancer D. Lung cancer E. Salivary gland carcinoma ANS: B, Leukemias represent the most common radiation-induced cancer in humans, closely followed by thyroid cancer, which is the most common malignancy in young persons. 12. Helicobacter pylori infection predisposes to formation of gastric tumors, but the association between the bacterial infection and a gastric tumor is the strongest for A. adenocarcinoma of the stomach B. gastrointestinal stromal tumors C. marginal zone lymphomas D. T-cell lymphoma E. Burkitt lymphoma ANS: C, The best and strongest evidence links Helicobacter pylori infection with the onset of mucosa-associated B-cell lymphomas (MALTomas) of the stomach, which are also known as marginal zone lymphomas. It is thought that H. pylori activates T cells, which in turn promote polyclonal proliferation of B cells in the gastric mucosa. In this process, some cells obviously become malignant and give rise to T-cell independent low-grade monoclonal lymphomas. 13. Clubbing of the digits, periosteal new bone formation on the metatarsals, metacarpals, and proximal phalanges, and arthritis of adjacent joints is a paraneoplastic syndrome most often associated

with carcinoma of the A. thyroid B. larynx C. bronchi D. liver E. stomach ANS: C, Clubbing of the fingers and related bone and joint changes of the hand and fingers are signs of hypertrophic osteoarthropathy, which most often occurs in patients with bronchogenic carcinoma. The pathogenesis of these changes is not known.