A Circulating Tumor DNA

Total Page：16

File Type：pdf, Size：1020Kb

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. High levels of contaminating CFDNA is sub- the blood or vascular system. The precise mechanism of optimal as a result of this may decrease the sensitivity of CTDNA unleash is unclear. The biological processes postulated CTDNA detection. Therefore, the bulk of studies use plasma for to be concerned in CTDNA unleash embody necrobiosis and CTDNA isolation. Plasma is then processed once more by action sphacelus from dying cells, or active unleash from viable to get rid of residual intact blood cells. The supernatant is neoplasm cells. Studies in each human (healthy and cancer employed for DNA extraction, which may be performed patients) and xeno grafted mice show that the scale of exploitation commercially obtainable kits. fragmented CFDNA is preponderantly 166bp long, that corresponds to the length of DNA wrapped around a nucleosome and a linker. *Correspondence to: Loay Parrella, Laboratory of Cellular and Molecular Endocrinology, Humanitas Clinical and Research Center - IRCCS, Rozzano, Italy, E-mail: [email protected] Received: May 05, 2021; Accepted: May 20, 2021; Published: May 27, 2021 Citation: Parrella L (2021) A Circulating Tumor DNA. J Tumor Res. 7:3. Copyright: © 2021 Parrella L. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. J Tumor Res, Vol.7 Iss.3 No: 1.

Copy Link

Recommended publications

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.
[Show full text]
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.
[Show full text]
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.
[Show full text]
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].
[Show full text]
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.
[Show full text]
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.
[Show full text]
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.
[Show full text]
Neoplasm, Lesion Or Infection
National Imaging Associates, Inc. Clinical Guideline Original Date: July 2015 SPINE SURGERY OTHER: NEOPLASM, Page 1 of 3 LESION OR INFECTION (ALL REGIONS) CPT Codes: 63265, 63266, 63267, 63268, 63270, Last Review Date: 63271, 63272, 63273, 63275, 63276, 63277, 63278, 63280, 63281, 63282, 63283, 63285, 63286, 63287, 63290, 63295. 63290, 63295, 22590, 22595, 22600, 22610, 22612, 22614.22630, 22632, 22633, 22634, 22554, 22556, 22558, 22585, 22532, 22533, 22534 Guideline Number: NIA_CG_309 Last Revised Date: Responsible Department: Implementation Date: September 2015 Clinical Operations OVERVIEW: Significant spinal cord or nerve root compression due to tumor, lesion or infection may require surgical intervention. All operative interventions must be based on a positive correlation with clinical findings, the natural history of the disease, the clinical course, and diagnostic tests or imaging results. INDICATIONS: A. FUSION SURGERY (ANY REGION) FOR THE TREATMENT OF SPINAL NEOPLASM, LESION OR INFECTION. Significant spinal cord or nerve root compression due to tumor or infection may require decompression of the cord / roots and fusion of the involved levels. Fusion is reserved for cases wherein the structural integrity of the spine has been compromised by the disease process or the surgical intervention needed to address the disease process. The following criteria must be met for urgent intervention: Positive Clinical Findings of Myelopathy with evidence of progressive neurologic deficits consistent with worsening spinal cord compression due to tumor or infection— immediate surgical evaluation is indicated. Symptoms may include any of the following: . upper extremity weakness . unsteady gait related to myelopathy/balance or generalized lower extremity weakness . disturbance with coordination . hyperreflexia . Hoffmann sign .
[Show full text]
Comprehensive Cervical Cancer Prevention and Control: a Healthier Future for Girls and Women
WHO GUIDANCE NOTE Comprehensive cervical cancer prevention and control: a healthier future for girls and women March 2013 edition Comprehensive cervical cancer prevention and control.indd 1 27/02/2013 20:39 WHO Library Cataloguing-in-Publication Data WHO guidance note: comprehensive cervical cancer prevention and control: a healthier future for girls and women. 1.Uterine cervical neoplasms – prevention and control. 2.Uterine cervical neoplasm – diagnosis. 3.Uterine cervical neoplasm – therapy. 4.Papillomavirus infections. 5.Papillomavirus vaccines. I.World Health Organization. ISBN 978 92 4 150514 7 (NLM classification: WP 480) © World Health Organization 2013 All rights reserved. Publications of the World Health Organization are available on the WHO web site (www.who.int) or can be purchased from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 3264; fax: +41 22 791 4857; e-mail: [email protected]). Requests for permission to reproduce or translate WHO publications –whether for sale or for non-commercial distribution– should be addressed to WHO Press through the WHO web site (www.who.int/about/licensing/ copyright_form/en/index.html). The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned.
[Show full text]
Circulating Tumor DNA Testing Opens New Perspectives in Melanoma Management
cancers Review Circulating Tumor DNA Testing Opens New Perspectives in Melanoma Management 1, 1, 1 1 Alessandra Sacco y , Laura Forgione y, Marianeve Carotenuto , Antonella De Luca , Paolo A. Ascierto 2 , Gerardo Botti 3 and Nicola Normanno 1,* 1 Cell Biology and Biotherapy Unit, Istituto Nazionale Tumori-IRCCS-Fondazione G. Pascale, 80131 Naples, Italy; [email protected] (A.S.); [email protected] (L.F.); [email protected] (M.C.); [email protected] (A.D.L.) 2 Department of Melanoma, Cancer Immunotherapy and Development Therapeutics, Istituto Nazionale Tumori IRCCS Fondazione Pascale, 80131 Napoli, Italy; [email protected] 3 Scientiﬁc Direction, Istituto Nazionale Tumori IRCCS Fondazione Pascale, 80131 Napoli, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-081-5903-826 These authors contributed equally to this work. y Received: 15 September 2020; Accepted: 8 October 2020; Published: 10 October 2020 Simple Summary: Melanoma, like other solid tumors, releases DNA molecules that are referred to as circulating tumor DNA (ctDNA), into the blood and other biological ﬂuids. ctDNA analysis performed with molecular biology techniques can provide important information on the aggressiveness of the disease and its genetic characteristics. This review aims to highlight all the possible clinical applications of ctDNA analysis that can contribute to an improvement in the diagnosis and therapy of melanoma. Abstract: Malignant melanoma accounts for about 1% of all skin cancers, but it causes most of the skin cancer-related deaths. Circulating tumor DNA (ctDNA) testing is emerging as a relevant tool for the diagnosis and monitoring of cancer.
[Show full text]
Chapter 4. Cancer Prevention
Part F. Chapter 4. Cancer Prevention PART F. CHAPTER 4. CANCER PREVENTION Table of Contents Introduction ............................................................................................................................................. F4-2 Review of the Science .............................................................................................................................. F4-3 Overview of Questions Addressed ....................................................................................................... F4-3 Data Sources and Process Used to Answer Questions ........................................................................ F4-4 Question 1. What is the relationship between physical activity and specific cancer incidence? ....... F4-5 Bladder Cancer ..................................................................................................................................... F4-5 Breast Cancer ....................................................................................................................................... F4-7 Colon Cancer ...................................................................................................................................... F4-15 Endometrial Cancer ........................................................................................................................... F4-18 Esophageal Cancer ............................................................................................................................. F4-22 Gastric Cancer ...................................................................................................................................
[Show full text]
Benign Brain Tumors
Table 31.1 Benign Brain Tumors A Comparison of Benign/Borderline and Malignant Brain Tumors Counts, Percents and Age-Adjusted Incidence Ratesa by WHO Histology Grouping, 2008-2012 Benign/Borderline Malignant WHO Histology Grouping Count Percent Rate Count Percent Rate Brain Diffuse astrocytoma (protoplasma, fibrillary) - - - 411 1.3% 0.1 Anaplastic astrocytoma - - - 1,734 5.6% 0.4 Glioblastoma - - - 14,140 46.1% 3.2 Pilocytic astrocytoma - - - 1,235 4.0% 0.3 Unique astrocytoma variants 371 0.6% 0.1 153 0.5% 0.0 Oligodendroglioma - - - 1,072 3.5% 0.2 Anaplastic oligodendroglioma - - - 480 1.6% 0.1 Ependymoma/anaplastic ependymoma - - - 597 1.9% 0.1 Ependymoma variants - - - - - - Mixed glioma - - - 839 2.7% 0.2 Astrocytoma, NOS - - - 1,540 5.0% 0.4 Glioma, NOS 66 0.1% 0.0 1,631 5.3% 0.4 Choroid plexus 195 0.3% 0.0 37 0.1% 0.0 Neuroepithelial - - - 76 0.2% 0.0 Neuronal/glial, neuronal and mixed 909 1.4% 0.2 69 0.2% 0.0 Embryonal/primitive/medulloblastoma - - - 937 3.1% 0.2 Nerve sheath 283 0.4% 0.1 - - - Meningioma 247 0.4% 0.1 - - - Other mesenchymal 144 0.2% 0.0 62 0.2% 0.0 Hemangioma and hemangioblastoma 1,966 2.9% 0.4 - - - Germ cell tumors, cysts, and heterotopias 81 0.1% 0.0 110 0.4% 0.0 Chordoma/chondrosarcoma - - - 27 0.1% 0.0 Craniopharyngioma 100 0.1% 0.0 - - - Neoplasm, unspecified 1,335 2.0% 0.3 1,297 4.2% 0.3 Other histologiesb 19 0.0% 0.0 40 0.1% 0.0 Intracranial Meninges Neuroepithelial - - - - - - Nerve sheath - - - - - - Meningioma 33,764 50.2% 7.7 356 1.2% 0.1 Other mesenchymal 53 0.1% 0.0 30 0.1% 0.0 Hemangioma and hemangioblastoma
[Show full text]