Cancer Cause: Biological, Chemical and Physical Carcinogens
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Meat, Fish and Dairy Products and the Risk of Cancer: a Summary Matrix 7 2
Meat, fish and dairy products and the risk of cancer 2018 Contents World Cancer Research Fund Network 3 Executive summary 5 1. Meat, fish and dairy products and the risk of cancer: a summary matrix 7 2. Summary of Panel judgements 9 3. Definitions and patterns 11 3.1 Red meat 11 3.2 Processed meat 12 3.3 Foods containing haem iron 13 3.4 Fish 13 3.5 Cantonese-style salted fish 13 3.6 Grilled (broiled) or barbecued (charbroiled) meat and fish 14 3.7 Dairy products 14 3.8 Diets high in calcium 15 4. Interpretation of the evidence 16 4.1 General 16 4.2 Specific 16 5. Evidence and judgements 27 5.1 Red meat 27 5.2 Processed meat 31 5.3 Foods containing haem iron 35 5.4 Fish 36 5.5 Cantonese-style salted fish 37 5.6 Grilled (broiled) or barbecued (charbroiled) meat and fish 40 5.7 Dairy products 41 5.8 Diets high in calcium 51 5.9 Other 52 6. Comparison with the 2007 Second Expert Report 52 Acknowledgements 53 Abbreviations 57 Glossary 58 References 65 Appendix 1: Criteria for grading evidence for cancer prevention 71 Appendix 2: Mechanisms 74 Our Cancer Prevention Recommendations 79 2 Meat, fish and dairy products and the risk of cancer 2018 WORLD CANCER RESEARCH FUND NETWORK Our Vision We want to live in a world where no one develops a preventable cancer. Our Mission We champion the latest and most authoritative scientific research from around the world on cancer prevention and survival through diet, weight and physical activity, so that we can help people make informed choices to reduce their cancer risk. -
Evaluation of the Frequency of Patients with Cancer Presenting to an Emergency Department
ORIGINAL ARTICLE Evaluation of the frequency of patients with cancer presenting to an emergency department Cem Isikber1 Muge Gulen1 Salim Satar2 Akkan Avci1 Selen Acehan1 Gulistan Gul Isikber3 Onder Yesiloglu1 1. Adana City Training and Research Hospital, Department of Emergency Medicine, Adana, Turkey. 2. Associate Professor, Adana City Training and Research Hospital, Department of Emergency Medicine, Adana, Turkey. 3. Adana City Training and Research Hospital, Department of Infectious Diseases and Microbiology, Adana, Turkey. http://dx.doi.org/10.1590/1806-9282.66.10.1402 SUMMARY OBJECTIVE: This study aims to determine the demographic characteristics of cancer patients admitted to an emergency department and determine the relationship between the frequency of admission to the emergency department and oncological emergencies and their effect on mortality. METHODS: This observational, prospective, diagnostic accuracy study was performed in the ED of a tertiary care hospital. Patients over the age of 18 who were previously diagnosed with cancer and admitted to the emergency service for medical reasons were included in the study. We recorded baseline characteristics including age, gender, complaints, oncological diagnosis, metastasis status, cancer treatments received, the number of ED admissions, structural and metabolic oncological emergency diagnoses in the ED, discharge status, length of hospital stay, and mortality status. RESULTS: In our study, 1205 applications related to the oncological diagnosis of 261 patients were examined. 55.6% of the patients were male, and 44.4% were female. The most common metabolic oncological emergency was anemia (19.5%), and the most common structural oncological emergency was bone metastasis-fracture (4.6%.) The mean score of admission of patients to the emergency department was four times (min: 1 max: 29) during the study period. -
Exposure to Carcinogens and Work-Related Cancer: a Review of Assessment Methods
European Agency for Safety and Health at Work ISSN: 1831-9343 Exposure to carcinogens and work-related cancer: A review of assessment methods European Risk Observatory Report Exposure to carcinogens and work-related cancer: A review of assessment measures Authors: Dr Lothar Lißner, Kooperationsstelle Hamburg IFE GmbH Mr Klaus Kuhl (task leader), Kooperationsstelle Hamburg IFE GmbH Dr Timo Kauppinen, Finnish Institute of Occupational Health Ms Sanni Uuksulainen, Finnish Institute of Occupational Health Cross-checker: Professor Ulla B. Vogel from the National Working Environment Research Centre in Denmark Project management: Dr Elke Schneider - European Agency for Safety and Health at Work (EU-OSHA) Europe Direct is a service to help you find answers to your questions about the European Union Freephone number (*): 00 800 6 7 8 9 10 11 (*) Certain mobile telephone operators do not allow access to 00 800 numbers, or these calls may be billed. More information on the European Union is available on the Internet ( 48TU http://europa.euU48T). Cataloguing data can be found on the cover of this publication. Luxembourg: Publications Office of the European Union, 2014 ISBN: 978-92-9240-500-7 doi: 10.2802/33336 Cover pictures: (clockwise): Anthony Jay Villalon (Fotolia); ©Roman Milert (Fotolia); ©Simona Palijanskaite; ©Kari Rissa © European Agency for Safety and Health at Work, 2014 Reproduction is authorised provided the source is acknowledged. European Agency for Safety and Health at Work – EU-OSHA 1 Exposure to carcinogens and work-related cancer: -
Carcinogens Are Mutagens
-Proc. Nat. Acad. Sci. USA Vol. 70, No. 8, pp. 2281-2285, August 1973 Carcinogens are Mutagens: A Simple Test System Combining Liver Homogenates for Activation and Bacteria for Detection (frameshift mutagens/aflatoxin/benzo(a)pyrene/acetylaminofluorene) BRUCE N. AMES, WILLIAM E. DURSTON, EDITH YAMASAKI, AND FRANK D. LEE Biochemistry Department, University of California, Berkeley, Calif. 94720 Contributed by Bruce N. Ames, May 14, 1973 ABSTRACT 18 Carcinogens, including aflatoxin Bi, methylsulfoxide (Me2SO), spectrophotometric grade, was ob- benzo(a)pyrene, acetylaminofluorene, benzidine, and di- tained from Schwarz/Mann, sodium phenobarbital from methylamino-trans-stilbene, are shown to be activated by liver homogenates to form potent frameshift mutagens. Mallinckrodt, aflatoxin B1 from Calbiochem, and 3-methyl- We believe that these carcinogens have in common a ring cholanthrene from Eastman; 7,12-dimethylbenz(a)anthracene system sufficiently planar for a stacking interaction with was a gift of P. L. Grover. Schuchardt (Munich) was the DNA base pairs and a part of the molecule capable of being source for the other carcinogens. metabolized to a reactive group: these structural features are discussed in terms of the theory of frameshift muta- Bacterial Strains used are mutants of S. typhimurium LT-2 genesis. We propose that these carcinogens, and many have been discussed in detail others that are mutagens, cause cancer by somatic muta- and (2). tion. A simple, inexpensive, and extremely sensitive test for Source Liver. Male rats (Sprague-Dawley/Bio-1 strain, detection of carcinogens as mutagens is described. It con- of sists of the use of a rat or human liver homogenate for Horton Animal Laboratories) were maintained on Purina carcinogen activation (thus supplying mammalian metab- laboratory chow. -
A Study on Tumor Suppressor Genes Mutations Associated with Different Pppathologicalpathological Cccolorectalcolorectal Lllesions.Lesions
A Study on Tumor Suppressor Genes Mutations Associated with Different PPPathologicalPathological CCColorectalColorectal LLLesions.Lesions. Thesis Submitted for partial fulfillment of the requirements for the Ph.D. degree of Science in Biochemistry By Salwa Naeim Abd ElEl----KaderKader Mater M.Sc. in Biochemistry, 2002 Biological Applications Department Nuclear Research Center Atomic Energy Authority Under the supervision of Prof. Dr. Amani F.H Nour El ---Deen Prof. Dr. Abdel Hady Ali Abdel Wahab Professor of Biochemistry Professor of Biochemistry Biochemistry Department and Molecular Biology Faculty of Science Cancer Biology Department Ain Shams University National Cancer Institute Cairo University Prof. DrDr.MohsenMohsen Ismail Mohamed Dr. Azza Salah Helmy Professor of Clinical Pathology Biological Assistant Professor of Biochemistry Applications Department Biochemistry Department Nuclear Research Center Faculty of Science Atomic Energy Authority Ain Shams University 2012011111 ﺑﺴﻢ ﺍﷲ ﺍﻟﺮﺣﻤﻦ ﺍﻟﺮﺣﻴﻢ ﺇِﻧﻤﺎ ﺃﹶﻣﺮﻩ ﺇِﺫﹶﺍ ﺃﹶﺭﺍﺩ ﺷﻴﺌﹰﺎ ﺃﹶﹾﻥ ﻳﹸﻘﻮﻝﹶ ﻟﹶﻪ ﻛﹸـﻦ ﻓﹶﻴﻜﹸـﻮ ﻥ ﹸ ””” ٨٢٨٨٢٢٨٢““““ﻓﹶﺴﺒﺤﺎﻥﹶ ﺍﱠﻟﺬِﻱ ﺑِﻴﺪِﻩِ ﻣﻠﹶﻜﹸﻮﺕ ﻛﹸـﻞﱢ ﺷـﻲﺀٍ ﻭﺇِﻟﹶﻴـﻪِ ﺗﺮﺟﻌﻮﻥﹶ ””” ٨٣٨٨٣٣٨٣““““ ﺻﺪﻕ ﺍﷲ ﺍﻟﻌﻈﻴﻢ رة (٨٢-٨٣) I declare that this thesis has been composed by myself and the work there in has not been submitted for a degree at this or any other university. Salwa Naeim Abd El-Kader Matter To my dear husband and family Their love, encouragement and help made my studies possible and to them I owe everything. Thank you Salwa Naeim Abd El-Kader Matter Acknowledgement First of all, thanks to Allah the most merciful for guiding me and giving me the strength to complete this work. It is pleasure to express my deepest thanks and profound respect to Prof. -
Environmental Causes of Cancer
British Toxicology Society http://www.thebts.org/ Environmental Causes of Cancer What is cancer? Cancer is the uncontrolled replication of cells. Such cells have different characteristics from regular cells, enabling them to escape the normal mechanisms controlling cell division and fate. Cancer develops when cells progressively acquire several of these characteristics. Cancer is a major cause of morbidity and mortality throughout the world. During their lifetime, approximately 50% of the population will develop cancer and, globally, almost 17% will die of cancer. Cancer is spoken of as if it were a single disease, but it is a multiplicity of diseases, each with its own aetiology, risk factors and population trends. Nevertheless, amongst adverse health effects, it is amongst those diseases treated with most dread, not surprisingly given that some forms of cancer are untreatable and have a very high mortality rate. Cancer is a progressive and persistent disease and it typically takes approx. 25% of a lifespan to develop cancer in a solid tissue, such as the liver or lung. A corollary of this is that most cancers are diseases of older age, and almost 50% of cancer deaths are in the over 70s. Hence, as the population ages, the proportion dying of cancer increases. This, in part, reflects the effectiveness of improving population longevity. Given the above, there has been intense focus over the last 50 years in trying to identify the causes of cancer, in that prevention would be the most effective public health strategy. Early studies concluded that the majority of cancer was environmental in origin and some inferred that this was because of the presence of chemicals in the environment, whereas in fact it meant that most cancers were not obviously inherited, i.e. -
Inflammation and Cancer: a Comparative View
Review J Vet Intern Med 2012;26:18–31 Inflammation and Cancer: A Comparative View Wallace B. Morrison Rudolph Virchow first speculated on a relationship between inflammation and cancer more than 150 years ago. Subse- quently, chronic inflammation and associated reactive free radical overload and some types of bacterial, viral, and parasite infections that cause inflammation were recognized as important risk factors for cancer development and account for one in four of all human cancers worldwide. Even viruses that do not directly cause inflammation can cause cancer when they act in conjunction with proinflammatory cofactors or when they initiate or promote cancer via the same signaling path- ways utilized in inflammation. Whatever its origin, inflammation in the tumor microenvironment has many cancer-promot- ing effects and aids in the proliferation and survival of malignant cells and promotes angiogenesis and metastasis. Mediators of inflammation such as cytokines, free radicals, prostaglandins, and growth factors can induce DNA damage in tumor suppressor genes and post-translational modifications of proteins involved in essential cellular processes including apoptosis, DNA repair, and cell cycle checkpoints that can lead to initiation and progression of cancer. Key words: Cancer; Comparative; Infection; Inflammation; Tumor. pidemiologic evidence suggests that approximately that has documented similar or identical genetic E25% of all human cancer worldwide is associated expression, inflammatory cell infiltrates, cytokine and with chronic inflammation, chronic infection, or both chemokine expression, and other biomarkers in (Tables 1 and 2).1–5 Local inflammation as an anteced- humans and many domestic mammals with morpho- ent event to cancer development has long been recog- logically equivalent cancers.65–78 The author is una- nized in cancer patients. -
Toxicological Profile for Radon
RADON 205 10. GLOSSARY Some terms in this glossary are generic and may not be used in this profile. Absorbed Dose, Chemical—The amount of a substance that is either absorbed into the body or placed in contact with the skin. For oral or inhalation routes, this is normally the product of the intake quantity and the uptake fraction divided by the body weight and, if appropriate, the time, expressed as mg/kg for a single intake or mg/kg/day for multiple intakes. For dermal exposure, this is the amount of material applied to the skin, and is normally divided by the body mass and expressed as mg/kg. Absorbed Dose, Radiation—The mean energy imparted to the irradiated medium, per unit mass, by ionizing radiation. Units: rad (rad), gray (Gy). Absorbed Fraction—A term used in internal dosimetry. It is that fraction of the photon energy (emitted within a specified volume of material) which is absorbed by the volume. The absorbed fraction depends on the source distribution, the photon energy, and the size, shape and composition of the volume. Absorption—The process by which a chemical penetrates the exchange boundaries of an organism after contact, or the process by which radiation imparts some or all of its energy to any material through which it passes. Self-Absorption—Absorption of radiation (emitted by radioactive atoms) by the material in which the atoms are located; in particular, the absorption of radiation within a sample being assayed. Absorption Coefficient—Fractional absorption of the energy of an unscattered beam of x- or gamma- radiation per unit thickness (linear absorption coefficient), per unit mass (mass absorption coefficient), or per atom (atomic absorption coefficient) of absorber, due to transfer of energy to the absorber. -
Risk Factors and Causes of Cancers in Adolescents
cancer.org | 1.800.227.2345 Risk Factors and Causes of Cancers in Adolescents A risk factor is anything that increases a person's chances of getting a disease such as cancer. Different cancers have different risk factors. In older adults, many cancers are linked to lifestyle-related risk factors such as smoking, being overweight, eating an unhealthy diet, not getting enough exercise, and drinking too much alcohol. Exposures to things in the environment, such as radon, air pollution, asbestos, or radiation during medical tests or procedures, also play a role in some adult cancers. These types of risk factors usually take many years to influence cancer risk, so they are not thought to play much of a role in cancers in children or teens. Cancer occurs as a result of changes (mutations) in the genes1 inside our cells. Genes, which are made of DNA, control nearly everything our cells do. Some genes affect when our cells grow, divide into new cells, and die. Changes in these genes can cause cells to grow out of control, which can sometimes lead to cancer. Some people inherit gene mutations from a parent that increase their risk of certain cancers. In people who inherit such a mutation, this can sometimes lead to cancer earlier in life than would normally be expected. But most cancers are not caused by inherited gene changes. We know some of the causes of gene changes that can lead to adult cancers (such as the lifestyle-related and environmental risk factors mentioned above), but the reasons for gene changes that cause most cancers in teens are not known. -
Radiation and Your Patient: a Guide for Medical Practitioners
RADIATION AND YOUR PATIENT: A GUIDE FOR MEDICAL PRACTITIONERS A web module produced by Committee 3 of the International Commission on Radiological Protection (ICRP) What is the purpose of this document ? In the past 100 years, diagnostic radiology, nuclear medicine and radiation therapy have evolved from the original crude practices to advanced techniques that form an essential tool for all branches and specialties of medicine. The inherent properties of ionising radiation provide many benefits but also may cause potential harm. In the practice of medicine, there must be a judgement made concerning the benefit/risk ratio. This requires not only knowledge of medicine but also of the radiation risks. This document is designed to provide basic information on radiation mechanisms, the dose from various medical radiation sources, the magnitude and type of risk, as well as answers to commonly asked questions (e.g radiation and pregnancy). As a matter of ease in reading, the text is in a question and answer format. Interventional cardiologists, radiologists, orthopaedic and vascular surgeons and others, who actually operate medical x-ray equipment or use radiation sources, should possess more information on proper technique and dose management than is contained here. However, this text may provide a useful starting point. The most common ionising radiations used in medicine are X, gamma, beta rays and electrons. Ionising radiation is only one part of the electromagnetic spectrum. There are numerous other radiations (e.g. visible light, infrared waves, high frequency and radiofrequency electromagnetic waves) that do not posses the ability to ionize atoms of the absorbing matter. -
Molecular Mechanisms of the Preventable Causes of Cancer in the United States
Downloaded from genesdev.cshlp.org on October 2, 2021 - Published by Cold Spring Harbor Laboratory Press REVIEW Molecular mechanisms of the preventable causes of cancer in the United States Erica A. Golemis,1 Paul Scheet,2 Tim N. Beck,1,3 Ed Scolnick,4 David J. Hunter,5 Ernest Hawk,6 and Nancy Hopkins7 1Program in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA; 2Department of Epidemiology, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; 3Molecular and Cell Biology and Genetics Program, Drexel University College of Medicine, Philadelphia, Pennsylvania 19129, USA; 4Eli and Edythe L. Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02142, USA; 5Nuffield Department of Population Health, University of Oxford, Medical Sciences Division, Oxford OX3 7LF, United Kingdom; 6Division of Cancer Prevention and Population Sciences, University of Texas M.D. Anderson Cancer Center, Houston Texas 77030, USA; 7Koch Institute for Integrative Cancer Research, Biology Department, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA Annually, there are 1.6 million new cases of cancer and cause skin cancer, only a small fraction of the public is nearly 600,000 cancer deaths in the United States alone. aware that smoking increases the incidence of cancer in The public health burden associated with these numbers more than a dozen sites or that viruses cause essentially has motivated enormous research efforts into understand- all cervical cancers, all head and neck cancers (HNCs) ing the root causes of cancer. These efforts have led to the not caused by smoking, and most liver cancers not caused recognition that between 40% and 45% of cancers are as- by obesity or hepatotoxins (such as chronic alcohol use). -
New Discoveries in Radiation Science
cancers Editorial New Discoveries in Radiation Science Géza Sáfrány 1,*, Katalin Lumniczky 1 and Lorenzo Manti 2 1 Department Radiobiology and Radiohygiene, National Public Health Center, 1221 Budapest, Hungary; [email protected] 2 Department of Physics, University of Naples Federico II, 80126 Naples, Italy; [email protected] * Correspondence: [email protected]; Tel.: +36-309199218 This series of 16 articles (8 original articles and 8 reviews) was written by internation- ally recognized scientists attending the 44th Congress of the European Radiation Research Society (Pécs, Hungary). Ionizing radiation is an interesting agent because it is used to cure cancers and can also induce cancer. The effects of ionizing radiation at the organism level depend on the response of the cells. When radiation hits a cell, it might damage any cellular organelles and macromolecules. Unrepairable damage leads to cell death, while misrepaired alterations leave mutations in surviving cells. If the repair is errorless, normal cells will survive. However, in a small percentage of the seemingly healthy cells the number of spontaneous mutations will increase, which is a sign of radiation-induced genomic instability. Radiation-induced cell death is behind the development of acute radiation syndromes and the killing of tumorous and normal cells during radiation therapy. Radiation-induced mutations in surviving cells might lead to the induction of tumors. According to the central paradigm of radiation biology, the genetic material, that is the DNA, is the main cellular target of ionizing radiation. Many different types of damage are induced by radiation in the DNA, but the most deleterious effects arise from double strand breaks (DSBs).