Marker Identification of the Grade of Dysplasia of Intraductal Papillary
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INTRINSIC FACTORS in the ETIOLOGY of NEOPLASMS' It Is
INTRINSIC FACTORS IN THE ETIOLOGY OF NEOPLASMS' CARL V. WELLER, MS., M.D. (From the Department of Pathology, University of Michigan) It is as true as it is trite that the cause of disease is never a single factor. Two elements always enter into etiology. One of these is inherent in the germ plasm of the individual; the other brought to bear upon the organism from beyond the confines of the germinal elements from which it has devel- oped. Better than internal and external, endogenous and exogenous, or con- stitutional and environmental, to designate these two groups of factors, are the terms intrinsic and extrinsic. Practical experience directs us to seek the relative importance of intrinsic and extrinsic factors whenever the causation of disease is studied, and we find that the two ingredients may be combined in every possible proportion. At one end of the series are diseases such as deaf mutism, transmitted as a simple recessive, in which the intrinsic element almost crowds out all other considerations. In the recessively sex-linked hemophilia, again the intrinsic element is so prominent that we see at once the mendelian significance of the process, although the bleeder may not be made known until the extrinsic factor, trauma, opens his blood vessels. The asthenic, dolichomorphic bodily configuration, which marks the phthisical habitus, is a familial character and therefore intrinsic, but it conditions infection by the tubercle bacillus in such a way as to give it serious or even lethal possibilities. When we consider syphilis, we find that the Treponema is no respecter of genetic constitution, yet sex and race may modify the character of the disease. -
Structural Forms of the Human Amylase Locus and Their Relationships to Snps, Haplotypes, and Obesity
Structural Forms of the Human Amylase Locus and Their Relationships to SNPs, Haplotypes, and Obesity The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Usher, Christina Leigh. 2015. Structural Forms of the Human Amylase Locus and Their Relationships to SNPs, Haplotypes, and Obesity. Doctoral dissertation, Harvard University, Graduate School of Arts & Sciences. Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467224 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Structural forms of the human amylase locus and their relationships to SNPs, haplotypes, and obesity A dissertation presented by Christina Leigh Usher to The Division of Medical Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the subject of Genetics and Genomics Harvard University Cambridge, Massachusetts March 2015 © 2015 Christina Leigh Usher All rights reserved. Dissertation Advisor: Professor Steven McCarroll Christina Leigh Usher Structural forms of the human amylase locus and their relationships to SNPs, haplotypes, and obesity Abstract Hundreds of human genes reside in structurally complex loci that elude molecular analysis and assessment in genome-wide association studies (GWAS). One such locus contains the three different amylase genes (AMY2B, AMY2A, and AMY1) responsible for digesting starch into sugar. The copy number of AMY1 is reported to be the genome’s largest influence on obesity, yet has gone undetected in GWAS. -
Updates in Molecular Pathology of Central Nervous System Gliomas in Adults
UPDATES IN ONCOLOGY: PART 2 Updates in Molecular Pathology of Central Nervous System Gliomas in Adults MICHAEL PUNSONI, MD; JOHN E. DONAHUE, MD; HEINRICH D. ELINZANO, MD; TIMOTHY KINSELLA, MD 17 19 EN ABSTRACT Epidemiology Central nervous system (CNS) tumors are a heteroge- The incidence of CNS malignancies has been increasing. neous group of neoplasms divided into two broad cate- Most commonly, CNS tumors arise from glial cells, partic- gories, glial and non-glial. Non-glial tumors are derived ularly astrocytes and oligodendrocytes. Gliomas account from such diverse structures as the pineal gland, menin- for approximately 77% of primary malignant brain tumors ges, germ cells, and hematopoietic cells, as well as metas- (3). Most patients present between the fifth and seventh tases. Primary glial neoplasms, or those which originate decade of life. High-grade tumors are more common than from astrocytes, oligodendrocytes, or ependymal cells, low-grade and present a high risk of morbidity and mortal- include astrocytomas, oligodendrogliomas, ependymo- ity. The World Health Organization (WHO) in 2000 formu- mas, and mixed gliomas. Each entity has a unique mor- lated a classification system based on histologic findings phology and pattern of biologic behavior which portends that is used to stratify brain tumors into prognostic grades. a distinct prognosis and outcome. Individual outcomes High-grade gliomas (WHO grade III and IV) are most com- show some variability based on tumor location and age of monly seen in middle-aged to older adults, while grade II symptom onset; however, the underlying aggressiveness astrocytomas mainly affect younger adults. Management for of the tumor often dictates the time course of the disease. -
797 Circulating Tumor DNA and Circulating Tumor Cells for Cancer
Medical Policy Circulating Tumor DNA and Circulating Tumor Cells for Cancer Management (Liquid Biopsy) Table of Contents • Policy: Commercial • Coding Information • Information Pertaining to All Policies • Policy: Medicare • Description • References • Authorization Information • Policy History • Endnotes Policy Number: 797 BCBSA Reference Number: 2.04.141 Related Policies Biomarkers for the Diagnosis and Cancer Risk Assessment of Prostate Cancer, #336 Policy1 Commercial Members: Managed Care (HMO and POS), PPO, and Indemnity Plasma-based comprehensive somatic genomic profiling testing (CGP) using Guardant360® for patients with Stage IIIB/IV non-small cell lung cancer (NSCLC) is considered MEDICALLY NECESSARY when the following criteria have been met: Diagnosis: • When tissue-based CGP is infeasible (i.e., quantity not sufficient for tissue-based CGP or invasive biopsy is medically contraindicated), AND • When prior results for ALL of the following tests are not available: o EGFR single nucleotide variants (SNVs) and insertions and deletions (indels) o ALK and ROS1 rearrangements o PDL1 expression. Progression: • Patients progressing on or after chemotherapy or immunotherapy who have never been tested for EGFR SNVs and indels, and ALK and ROS1 rearrangements, and for whom tissue-based CGP is infeasible (i.e., quantity not sufficient for tissue-based CGP), OR • For patients progressing on EGFR tyrosine kinase inhibitors (TKIs). If no genetic alteration is detected by Guardant360®, or if circulating tumor DNA (ctDNA) is insufficient/not detected, tissue-based genotyping should be considered. Other plasma-based CGP tests are considered INVESTIGATIONAL. CGP and the use of circulating tumor DNA is considered INVESTIGATIONAL for all other indications. 1 The use of circulating tumor cells is considered INVESTIGATIONAL for all indications. -
Connections Between Warburg's and Szentgyorgyi's Approach About The
Research iMedPub Journals Journal of Neoplasm 2017 http://www.imedpub.com/ ISSN 2576-3903 Vol.1 No.2:8 DOI: 10.217672576-3903.100008 Connections between Warburg’s and Szentgyorgyi’s Approach about the Causes of Cancer Szigeti GP1, Szasz O2 and Hegyi G3 1Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Hungary 2Department of Biotechnics, St. Istvan University, Hungary 3Department of Complementary and Alternative Medicine, University of Pecs, Hungary Corresponding author: Gabriella Hegyi, Department of Complementary and Alternative Medicine, University of Pecs, Hungary, Tel: +36 30 922-5347; E-mail: [email protected] Rec date: November 30, 2016; Acc date: December 26, 2016; Pub date: December 30, 2016 Citation: Szigeti GP, Szasz O, Hegyi G. Connections Between Warburg’s and Szentgyorgyi’s Approach About Causes of Cancer. J Neoplasm. 2017, 1: 2. to the environmental, diet and habit origins of malignant Abstract diseases [21-23]. Most widely, cancer is believed to be an abnormal tissue Numerous theories and hypotheses are published about triggered by a gene mutation. However, the proto-oncogene the causes of cancer and its hallmarks. Two remarkable and the oncogene appear not only in cancerous cases [24], but principles were established and debated for a long time. with pregnancy [25], with embryogenesis [26,27], with the The first is the Warburg-effect, which based on healing of wounds [28] and with the synthesis of growth mitochondrial dysfunction, connected to the intensive factors [29]. Oncogenes show a great variety of anti-apoptotic metabolic activity of the malignancy. The other is the functions with the cells taking part in the wound-healing [30]. -
Differential Proteomic Analysis of the Pancreas of Diabetic Db/Db Mice Reveals the Proteins Involved in the Development of Complications of Diabetes Mellitus
Int. J. Mol. Sci. 2014, 15, 9579-9593; doi:10.3390/ijms15069579 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 www.mdpi.com/journal/ijms Article Differential Proteomic Analysis of the Pancreas of Diabetic db/db Mice Reveals the Proteins Involved in the Development of Complications of Diabetes Mellitus Victoriano Pérez-Vázquez 1,*, Juan M. Guzmán-Flores 1, Daniela Mares-Álvarez 1, Magdalena Hernández-Ortiz 2, Maciste H. Macías-Cervantes 1, Joel Ramírez-Emiliano 1 and Sergio Encarnación-Guevara 2 1 Depto. de Ciencias Médicas, División de Ciencias de la Salud, Campus León, Universidad de Guanajuato, León, Guanajuato 37320, Mexico; E-Mails: [email protected] (J.M.G.-F.); [email protected] (D.M.-A.); [email protected] (M.H.M.-C.); [email protected] (J.R.-E.) 2 Centro de Ciencias Genómicas, Universidad Nacional Autónoma de México, Cuernavaca, Morelos 62210, Mexico; E-Mails: [email protected] (M.H.-O.); [email protected] (S.E.-G.) * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +52-477-7143-812; Fax: +52-477-7167-623. Received: 4 April 2014; in revised form: 14 May 2014 / Accepted: 19 May 2014 / Published: 30 May 2014 Abstract: Type 2 diabetes mellitus is characterized by hyperglycemia and insulin-resistance. Diabetes results from pancreatic inability to secrete the insulin needed to overcome this resistance. We analyzed the protein profile from the pancreas of ten-week old diabetic db/db and wild type mice through proteomics. Pancreatic proteins were separated in two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and significant changes in db/db mice respect to wild type mice were observed in 27 proteins. -
Injury and Cancer
Case Western Reserve Law Review Volume 5 Issue 2 Article 4 1954 Injury and Cancer Lester Adelson Follow this and additional works at: https://scholarlycommons.law.case.edu/caselrev Part of the Law Commons Recommended Citation Lester Adelson, Injury and Cancer, 5 W. Rsrv. L. Rev. 150 (1954) Available at: https://scholarlycommons.law.case.edu/caselrev/vol5/iss2/4 This Article is brought to you for free and open access by the Student Journals at Case Western Reserve University School of Law Scholarly Commons. It has been accepted for inclusion in Case Western Reserve Law Review by an authorized administrator of Case Western Reserve University School of Law Scholarly Commons. [Winter Injury and Cancer by Lester Adelson, M.D. WITH LEGAL ANNOTATIONS BY OLIVER SCHROEDER, JR.* INTRODUCTION THE WORD "cancer" is one which is charged with emotion and fear, carrying with it implications of prolonged disability and slow, certain and painful death.' In considering and discussing the subject of cancer, diffi- culties frequently arise, not because not enough is known, but because so much is known that-is incorrect and untrue. A vast fund of misinformation and false information mis- leads the unwary stranger THE AUTHOR (A.B., 1935, Harvard Univer- and the uncritical observer. sity; M.D., 1939, Tufts College Medical School) is Chief Deputy Coroner and Patholo- Cancer is the second gist at the Coroner's Office, Cuyahoga County, leading cause of death, and Ohio, and Assistant Professor of Legal Medi- problems which arise in cine at the School of Medicine of Western Reserve University. connection with it are seen frequently. -
Chuanxiong Rhizoma Compound on HIF-VEGF Pathway and Cerebral Ischemia-Reperfusion Injury’S Biological Network Based on Systematic Pharmacology
ORIGINAL RESEARCH published: 25 June 2021 doi: 10.3389/fphar.2021.601846 Exploring the Regulatory Mechanism of Hedysarum Multijugum Maxim.-Chuanxiong Rhizoma Compound on HIF-VEGF Pathway and Cerebral Ischemia-Reperfusion Injury’s Biological Network Based on Systematic Pharmacology Kailin Yang 1†, Liuting Zeng 1†, Anqi Ge 2†, Yi Chen 1†, Shanshan Wang 1†, Xiaofei Zhu 1,3† and Jinwen Ge 1,4* Edited by: 1 Takashi Sato, Key Laboratory of Hunan Province for Integrated Traditional Chinese and Western Medicine on Prevention and Treatment of 2 Tokyo University of Pharmacy and Life Cardio-Cerebral Diseases, Hunan University of Chinese Medicine, Changsha, China, Galactophore Department, The First 3 Sciences, Japan Hospital of Hunan University of Chinese Medicine, Changsha, China, School of Graduate, Central South University, Changsha, China, 4Shaoyang University, Shaoyang, China Reviewed by: Hui Zhao, Capital Medical University, China Background: Clinical research found that Hedysarum Multijugum Maxim.-Chuanxiong Maria Luisa Del Moral, fi University of Jaén, Spain Rhizoma Compound (HCC) has de nite curative effect on cerebral ischemic diseases, *Correspondence: such as ischemic stroke and cerebral ischemia-reperfusion injury (CIR). However, its Jinwen Ge mechanism for treating cerebral ischemia is still not fully explained. [email protected] †These authors share first authorship Methods: The traditional Chinese medicine related database were utilized to obtain the components of HCC. The Pharmmapper were used to predict HCC’s potential targets. Specialty section: The CIR genes were obtained from Genecards and OMIM and the protein-protein This article was submitted to interaction (PPI) data of HCC’s targets and IS genes were obtained from String Ethnopharmacology, a section of the journal database. -
Hematopoietic and Lymphoid Neoplasm Coding Manual
Hematopoietic and Lymphoid Neoplasm Coding Manual Effective with Cases Diagnosed 1/1/2010 and Forward Published August 2021 Editors: Jennifer Ruhl, MSHCA, RHIT, CCS, CTR, NCI SEER Margaret (Peggy) Adamo, BS, AAS, RHIT, CTR, NCI SEER Lois Dickie, CTR, NCI SEER Serban Negoita, MD, PhD, CTR, NCI SEER Suggested citation: Ruhl J, Adamo M, Dickie L., Negoita, S. (August 2021). Hematopoietic and Lymphoid Neoplasm Coding Manual. National Cancer Institute, Bethesda, MD, 2021. Hematopoietic and Lymphoid Neoplasm Coding Manual 1 In Appreciation NCI SEER gratefully acknowledges the dedicated work of Drs, Charles Platz and Graca Dores since the inception of the Hematopoietic project. They continue to provide support. We deeply appreciate their willingness to serve as advisors for the rules within this manual. The quality of this Hematopoietic project is directly related to their commitment. NCI SEER would also like to acknowledge the following individuals who provided input on the manual and/or the database. Their contributions are greatly appreciated. • Carolyn Callaghan, CTR (SEER Seattle Registry) • Tiffany Janes, CTR (SEER Seattle Registry) We would also like to give a special thanks to the following individuals at Information Management Services, Inc. (IMS) who provide us with document support and web development. • Suzanne Adams, BS, CTR • Ginger Carter, BA • Sean Brennan, BS • Paul Stephenson, BS • Jacob Tomlinson, BS Hematopoietic and Lymphoid Neoplasm Coding Manual 2 Dedication The Hematopoietic and Lymphoid Neoplasm Coding Manual (Heme manual) and the companion Hematopoietic and Lymphoid Neoplasm Database (Heme DB) are dedicated to the hard-working cancer registrars across the world who meticulously identify, abstract, and code cancer data. -
Cancer Risk Assessment and Cancer Prevention: Promises and Challenges
CommentaryCancer Prevention Research Cancer Risk Assessment and Cancer Prevention: Promises and Challenges Brian J. Reid “Acquired genetic lability permits stepwise selection of variant cancer itself, but morphologic assessment may be limited in its sublines and underlies tumor progression” (1). ability to distinguish asymptomatic indolent conditions from Despite intense efforts to cure cancers through advances in those that will progress to advanced malignancies and death staging, surgery, chemo- and radiation therapy, treatment of (3–5, 13). Examining cancer from an evolutionary perspective most advanced, symptomatic epithelial malignancies con- can open new approaches for cancer risk assessment, diagnosis, tinues to be challenging, and age-adjusted cancer mortality therapy and prevention. The evolution of multicellular organ- in the United States has decreased by only 5%since 1950 isms has been accompanied by constraint of cellular evolution, (2). The clinical course of treated cancer patients all too often and cancer represents a breakdown of the mechanisms that culminates in relapse and death. Ironically, growing evidence suppress cellular evolution. Cairns hypothesized that the archi- also suggests that many patients with premalignancy or even tecture of proliferating epithelial tissues would suppress tumor malignancy follow benign courses and die far more often of formation by restricting and sequestering stem cells in epithe- non-cancer causes than of cancer (3–5). These paradoxical phe- lial proliferative units, for example, at the base of intestinal nomena form the dilemma of early detection-underdetection crypts (14). Opportunities for competition between variants of life-threatening early disease and overdetection of indolent that might arise would be restrained by shedding differentiated early disease. -
Role of Amylase in Ovarian Cancer Mai Mohamed University of South Florida, [email protected]
University of South Florida Scholar Commons Graduate Theses and Dissertations Graduate School July 2017 Role of Amylase in Ovarian Cancer Mai Mohamed University of South Florida, [email protected] Follow this and additional works at: http://scholarcommons.usf.edu/etd Part of the Pathology Commons Scholar Commons Citation Mohamed, Mai, "Role of Amylase in Ovarian Cancer" (2017). Graduate Theses and Dissertations. http://scholarcommons.usf.edu/etd/6907 This Dissertation is brought to you for free and open access by the Graduate School at Scholar Commons. It has been accepted for inclusion in Graduate Theses and Dissertations by an authorized administrator of Scholar Commons. For more information, please contact [email protected]. Role of Amylase in Ovarian Cancer by Mai Mohamed A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy Department of Pathology and Cell Biology Morsani College of Medicine University of South Florida Major Professor: Patricia Kruk, Ph.D. Paula C. Bickford, Ph.D. Meera Nanjundan, Ph.D. Marzenna Wiranowska, Ph.D. Lauri Wright, Ph.D. Date of Approval: June 29, 2017 Keywords: ovarian cancer, amylase, computational analyses, glycocalyx, cellular invasion Copyright © 2017, Mai Mohamed Dedication This dissertation is dedicated to my parents, Ahmed and Fatma, who have always stressed the importance of education, and, throughout my education, have been my strongest source of encouragement and support. They always believed in me and I am eternally grateful to them. I would also like to thank my brothers, Mohamed and Hussien, and my sister, Mariam. I would also like to thank my husband, Ahmed. -
A Circulating Tumor DNA
Journal of Tumor Research Editorial A Circulating Tumor DNA Loay Parrella* Laboratory of Cellular and Molecular Endocrinology, Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy EDITORIAL NOTE Fragmentation of this length can be indicative of apoptotic DNA fragmentation, suggesting that necrobiosis is also the first Circulating Tumor DNA (CTDNA) is tumor-derived fragmented technique of CTDNA unleash. The fragmentation of CFDNA is DNA within the blood that's not related to cells. CTDNA altered with in the plasma of cancer patients. The main charm of mustn't be confused with non-cellular DNA (CFDNA), a CTDNA analysis is that it's extracted in an exceedingly broader term that describes DNA that's freely current within the noninvasive manner through blood assortment. Acquisition of blood, however isn't essentially of neoplasm origin. As a result of CFDNA or CTDNA usually needs assortment of roughly 3mL CTDNA could replicate the complete neoplasm ordination, its of blood into EDTA- coated tubes. The employment of EDTA is gained traction for its potential clinical utility; “liquid biopsies” vital to cut back curdling of blood. The plasma and humor within the type of blood attracts is also taken at numerous time fractions of blood are often separated through an action step. points to observe neoplasm progression throughout the CTDNA or CFDNA are often later extracted from these treatment program. CTDNA originates directly from the Tumor fractions. Though humor tends to possess larger levels of or from Current Tumor Cells (CTCs), that describes viable, CFDNA, this can be primarily attributed to DNA from intact neoplasm cells that shed from primary tumors and enter lymphocytes.