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http://en.wikipedia.org/wiki/Carcinogenic
Carcinogen
From Wikipedia, the free encyclopedia
(Redirected from Carcinogenic) A carcinogen is any substance, radionuclide, or radiation that is an agent directly involved in causing cancer. This may be due to the ability to damage the genome or to the disruption of cellular metabolic processes. Several radioactive substances are considered carcinogens, but their carcinogenic activity is attributed to the radiation, for example gamma rays and alpha particles, which they emit. Common examples of non-radioactive carcinogens are inhaled asbestos, certain dioxins, and tobacco smoke. Although the public generally associates carcinogenicity with synthetic chemicals, it is equally likely to arise in both natural and synthetic substances.[1] Carcinogens are not necessarily immediately toxic, thus their effect can be insidious. Cancer is any disease in which normal cells are damaged and do not undergo programmed cell death as fast as they divide via mitosis. Carcinogens may increase the risk of cancer by altering cellular metabolism or damaging DNA directly in cells, which interferes with biological processes, and induces the uncontrolled, malignant division, ultimately leading to the formation of tumors. Usually, severe DNA damage leads to apoptosis, but if the programmed cell death pathway is damaged, then the cell cannot prevent itself from becoming a cancer cell. There are many natural carcinogens. Aflatoxin B1, which is produced by the fungus Aspergillus flavus growing on stored grains, nuts and peanut butter, is an example of a potent, naturally occurring microbial carcinogen. Certain viruses such as Hepatitis B and human papilloma virus have been found to cause cancer in humans. The first one shown to cause cancer in animals is Rous sarcoma virus, discovered in 1910 by Peyton Rous. Dioxins and dioxin-like compounds, benzene, kepone, EDB, and asbestos have all been classified as carcinogenic. [2] As far back as the 1930s, industrial smoke and tobacco smoke were identified as sources of dozens of carcinogens, including benzo[a]pyrene, tobaccospecific nitrosamines such as nitrosonornicotine, and reactive aldehydes such as formaldehydewhich is also a hazard in embalming and making plastics. Vinyl chloride, from which PVC is manufactured, is a carcinogen and thus a hazard in PVC production. Co-carcinogens are chemicals that do not necessarily cause cancer on their own, but promote the activity of other carcinogens in causing cancer. After the carcinogen enters the body, the body makes an attempt to eliminate it through a process called biotransformation. The purpose of these reactions is to make the carcinogen more water-soluble so that it can be removed from the body. But these reactions can also convert a less toxic carcinogen into a more toxic carcinogen. DNA is nucleophilic, therefore soluble carbon electrophiles are carcinogenic, because DNA attacks them. For example, some alkenes are toxicated by human enzymes to produce an electrophilic epoxide. DNA attacks the epoxide, and is bound permanently to it. This is the mechanism behind the carcinogenicity of benzo[a]pyrene in tobacco smoke, other aromatics, aflatoxin and mustard gas.
The hazard symbol for carcinogenic chemicals in the Globally Harmonized System.
Contents
IUPAC definition
Carcinogenicity: Ability or tendency to produce cancer.
1 Radiation Note: In general, polymers are not known as carcinogens or mutagens, 2 Carcinogens in prepared food however, residual monomers or additives can cause genetic mutations.[3] 3 Carcinogens in cigarettes 4 Mechanisms of carcinogenicity 5 Classification of carcinogens 5.1 International Agency for Research on Cancer 5.2 Globally Harmonized System 5.3 U.S. National Toxicology Program 5.4 American Conference of Governmental Industrial Hygienists 5.5 European Union 5.6 Safe Work Australia 6 Procarcinogen 7 Common carcinogens 7.1 Occupational carcinogens 7.2 Others
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8 Major carcinogens implicated in the four most common cancers worldwide 8.1 Lung cancer 8.2 Breast cancer 8.3 Colon cancer 8.4 Stomach cancer 9 See also 10 References 11 External links
Radiation
Main article: radiation-induced cancer CERCLA identifies all radionuclides as carcinogens, although the nature of the emitted radiation (alpha, beta, gamma, or neutron and the radioactive strength), its consequent capacity to cause ionization in tissues, and the magnitude of radiation exposure, determine the potential hazard. Carcinogenicity of radiation depends of the type of radiation, type of exposure, and penetration. For example, alpha radiation has low penetration and is not a hazard outside the body, but emitters are carcinogenic when inhaled or ingested. For example, Thorotrast, a (incidentally radioactive) suspension previously used as a contrast medium in x-ray diagnostics, is a potent human carcinogen known because of its retention within various organs and persistent emission of alpha particles. Not all types of electromagnetic radiation are in fact carcinogenic. Low-energy waves on the electromagnetic spectrum are thought not to be including radio waves, microwave radiation, infrared radiation and visible light. There are many many documented cases of radar technicians experiencing prolonged exposure and a higher incidence of cancer. http://www.ncbi.nlm.nih.gov/pubmed/10926722 Higherenergy radiation, including ultraviolet radiation (present in sunlight), x-rays, and gamma radiation, generally is carcinogenic, if received in sufficient doses. Low level ionizing radiation may induce irreparable DNA damage (leading to replicational and transcriptional errors needed for neoplasia or may trigger viral interactions) leading to pre-mature aging and cancer.[4][5][6] Substances or foods irradiated with electrons or electromagnetic radiation (such as microwave, X-ray or gamma) are not carcinogenic. [citation needed] In contrast, non-electromagnetic neutron radiation produced inside nuclear reactors can produce secondary radiation through nuclear transmutation.
Carcinogens in cigarettes
Main article: Tobacco and health
Mechanisms of carcinogenicity
Carcinogens can be classified as genotoxic or nongenotoxic. Genotoxins cause irreversible genetic damage or mutations by binding to DNA. Genotoxins include chemical agents like N-nitroso-N-methylurea (NMU) or non-chemical agents such as ultraviolet light and
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ionizing radiation. Certain viruses can also act as carcinogens by interacting with DNA. Nongenotoxins do not directly affect DNA but act in other ways to promote growth. These include hormones and some organic compounds.[10]
Classification of carcinogens
International Agency for Research on Cancer
The International Agency for Research on Cancer (IARC) is an intergovernmental agency established in 1965, which forms part of the World Health Organization of the United Nations. It is based in Lyon, France. Since 1971 it has published a series of Monographs on the Evaluation of Carcinogenic Risks to Humans [11] that have been highly influential in the classification of possible carcinogens. Approximate equivalences between classification schemes IARC Group 1 Group 2A Group 2B GHS Cat. 1A Cat. 1B NTP Known Reasonably suspected ACGIH EU A1 A2 Cat. 1 Cat. 2
Cat. 2 A3 Cat. 3 Group 1: the agent (mixture) is definitely carcinogenic to humans. The exposure Group 3 circumstance entails exposures that are carcinogenic to humans. A4 Group 2A: the agent (mixture) is probably carcinogenic to humans. The Group 4 A5 exposure circumstance entails exposures that are probably carcinogenic to humans. Group 2B: the agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. Group 3: the agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. Group 4: the agent (mixture) is probably not carcinogenic to humans.
European Union
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The European Union classification of carcinogens is contained in the Dangerous Substances Directive and the Dangerous Preparations Directive. It consists of three categories: Category 1: Substances known to be carcinogenic to humans. Category 2: Substances which should be regarded as if they are carcinogenic to humans. Category 3: Substances which cause concern for humans, owing to possible carcinogenic effects but in respect of which the available information is not adequate for making a satisfactory assessment. This assessment scheme is being phased out in favor of the GHS scheme (see above), to which it is very close in category definitions.
Procarcinogen
A procarcinogen is a precursor to a carcinogen. One example is nitrites when taken in by the diet. They are not carcinogenic themselves, but turn into nitrosamines in the body, which are carcinogenic.[14]
Common carcinogens
Occupational carcinogens
Occupational carcinogens are agents that pose a risk of cancer in several specific work-locations: Carcinogen Associated cancer sites or types Occupational uses or sources Smelting byproduct Component of: Alloys Electrical and semiconductor devices Medications (e.g. melarsoprol) Herbicides Fungicides Animal dips Drinking water from contaminated aquifers.
Not in widespread use, but found in: Lungs Asbestosis Gastrointestinal tract Pleural Mesothelioma Peritoneal Mesothelioma Constructions Roofing papers Floor tiles Fire-resistant textiles Friction linings (only outside Europe) Replacement friction linings for automobiles still may contain asbestos
Asbestos
Benzene
Leukemia
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Hodgkin lymphoma
Former use as solvent and fumigant Printing Lithography Paint Rubber Dry cleaning Adhesives Coatings Detergents
Lung
Prostate
Lung
Lung[16] Bladder[16]
Ethylene oxide
Leukemia
Ripening agent for fruits and nuts Rocket propellant Fumigant for foodstuffs and textiles Sterilant for hospital equipment
Nickel
Nose Lung
Lung
Uranium decay Quarries and mines Cellars and poorly ventilated places
Vinyl chloride
Hemangiosarcoma Liver
Refrigerant Production of polyvinyl chloride Adhesive for plastics Former use in pressurized containers
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circadian disruption[17] Involuntary smoking (Passive smoking)[18] Radium-226, Radium-224, Plutonium-238, Plutonium-239[19] and other alpha particle emitters with high atomic weight
Unless else specified in boxes, then ref is:[20]
Lung
Others
Gasoline (contains aromatics) Lead and its compounds Alkylating antineoplastic agents (e.g. mechlorethamine) Other alkylating agents (e.g. dimethyl sulfate) Ultraviolet radiation from the sun and UV lamps Alcohol (causing head and neck cancers) Other ionizing radiation (X-rays, gamma rays, etc.)
Lung cancer
Lung cancer is the most common cancer in the world, both in terms of cases (1.6 million cases; 12.7% of total cancer cases) and deaths (1.4 million deaths; 18.2% of total cancer deaths).[23] Lung cancer is largely caused by tobacco smoke. Risk estimates for lung cancer in the United States indicate that tobacco smoke is responsible for 90% of lung cancers. Other factors are implicated in lung cancer, and these factors can interact synergistically with smoking, so that total attributable risk adds up to more than 100%. These factors include occupational exposure to carcinogens (about 9-15%), radon (10%) and outdoor air pollution (1-2%).[24] Tobacco smoke is a complex mixture of more than 5,300 identified chemicals. The most important carcinogens in tobacco smoke have been determined by a Margin of Exposure approach.[25] Using this approach, the most important tumorigenic compounds in tobacco smoke were, in order of importance, acrolein, formaldehyde, acrylonitrile, 1,3-butadiene, cadmium, acetaldehyde, ethylene oxide and isoprene. Most of these compounds cause DNA damage by forming DNA adducts or by inducing other alterations in DNA.[22] DNA damages are subject to error-prone DNA repair or can cause replication errors. Such errors in repair or replication can result in mutations in tumor suppressor genes or oncogenes leading to cancer.
Breast cancer
Breast cancer is the second most common cancer [(1.4 million cases, 10.9%), but ranks 5th as cause of death (458,000, 6.1%)].[23] Increased risk of breast cancer is associated with persistently elevated blood levels of estrogen.[26] Estrogen appears to contribute to breast carcinogenesis by three processes; (1) the metabolism of estrogen to genotoxic, mutagenic carcinogens, (2) the stimulation of tissue growth, and (3) the repression of phase II detoxification enzymes that metabolize ROS leading to increased oxidative DNA damage.[27][28][29] The major estrogen in humans, estradiol, can be metabolized to quinone derivatives that form adducts with DNA.[30] These derivatives can cause dupurination, the removal of bases from the phosphodiester backbone of DNA, followed by inaccurate repair or replication of the apurinic site leading to mutation and eventually cancer. This genotoxic mechanism may interact in synergy with estrogen receptor-mediated, persistent cell proliferation to ultimately cause breast cancer.[30] Genetic background, dietary practices and environmental factors also likely contribute to the incidence of DNA damage and breast cancer risk.
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Colon cancer
Colorectal cancer is the third most common cancer [1.2 million cases (9.4%), 608,000 deaths (8.0%)].[23] Tobacco smoke may be responsible for up to 20% of colorectal cancers in the United States. [31] In addition, substantial evidence implicates bile acids as an important factor in colon cancer. Twelve studies (summarized in Bernstein et al. [32]) indicate that the bile acids deoxycholic acid (DCA) and/or lithocholic acid (LCA) induce production of DNA damaging reactive oxygen species and/or reactive nitrogen species in human or animal colon cells. Furthermore 14 studies showed that DCA and LCA induce DNA damage in colon cells. Also 27 studies reported that bile acids cause programmed cell death (apoptosis). Increased apoptosis can result in selective survival of cells that are resistant to induction of apoptosis.[32] Colon cells with reduced ability to undergo apoptosis in response to DNA damage would tend to accumulate mutations, and such cells may give rise to colon cancer.[32] Epidemiologic studies have found that fecal bile acid concentrations are increased in populations with a high incidence of colon cancer. Dietary increases in total fat or saturated fat result in elevated DCA and LCA in feces and elevated exposure of the colon epithelium to these bile acids. When the bile acid DCA was added to the standard diet of wild-type mice invasive colon cancer was induced in 56% of the mice after 8 to 10 months.[33] Overall, the available evidence indicates that DCA and LCA are centrally important DNA-damaging carcinogens in colon cancer.
Stomach cancer
Stomach cancer is the fourth most common cancer [990,000 cases (7.8%), 738,000 deaths (9.7%)].[23] Helicobacter pylori infection is the main causative factor in stomach cancer. Chronic gastritis (inflammation) caused by H. pylori is often long-standing if not treated. Infection of gastric epithelial cells with H. pylori results in increased production of reactive oxygen species (ROS). [34][35] ROS cause oxidative DNA damage including the major base alteration 8-hydroxydeoxyguanosine (8-OHdG). 8-OHdG resulting from ROS is increased in chronic gastritis. The altered DNA base can cause errors during DNA replication that have mutagenic and carcinogenic potential. Thus H. pylori-induced ROS appear to be the major carcinogens in stomach cancer because they cause oxidative DNA damage leading to carcinogenic mutations.
See also
Acrylamide Asian Dust Carcinogenesis History of cancer Industrial Union Department v. American Petroleum Institute International Agency for Research on Cancer Mutagen Possible carcinogen Safe handling of carcinogens Teratogen Warburg hypothesis
References
1. ^ Ames, Bruce N; Gold, Lois Swirsky (2000). "Paracelsus to parascience: The environmental cancer distraction". Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 447: 3. doi:10.1016/S0027-5107(99)00194-3 (http://dx.doi.org /10.1016%2FS0027-5107%2899%2900194-3). 2. ^ a b Report on Carcinogens, Eleventh Edition (http://ntp.niehs.nih.gov/index.cfm?objectid=32BA9724F1F6-975E-7FCE50709CB4C932); U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program (2011). 3. ^ "Terminology for biorelated polymers and applications (IUPAC Recommendations 2012)" (http://pac.iupac.org/publications/pac/pdf /2012/pdf/8402x0377.pdf). Pure and Applied Chemistry 84 (2): 377410. 2012. doi:10.1351/PAC-REC-10-12-04 (http://dx.doi.org /10.1351%2FPAC-REC-10-12-04). 4. ^ Acharya, PVN; The Effect of Ionizing Radiation on the Formation of Age-Correlated Oligo Deoxyribo Nucleo Phospheryl Peptides in Mammalian Cells; 10th International Congress of Gerontology, Jerusalem. Abstract No. 1; January 1975. Work done while employed by Dept. of Pathology, University of Wisconsin, Madison. 5. ^ Acharya, PVN; Implicatons of The Action of Low Level Ionizing Radiation on the Inducement of Irreparable DNA Damage Leading to Mammalian Aging and Chemical Carcinogenesis.; 10th International Congress of Biochemistry, Hamburg, Germany. Abstract No. 01-1-079; July 1976. Work done while employed by Dept. of Pathology, University of Wisconsin, Madison. ^ Acharya, PV Narasimh; Irreparable DNA-Damage by Industrial Pollutants in Pre-mature Aging, Chemical Carcinogenesis and Cardiac Hypertrophy: Experiments and Theory; 1st International Meeting of Heads of Clinical Biochemistry Laboratories, Jerusalem, Israel. April 1977. Work conducted at Industrial Safety Institute and Behavioral Cybernetics Laboratory, University of Wisconsin, Madison. ^ Wei Zheng, Deborah R Gustafson, Rashmi Sinha, James R Cerhan, et al. "Well-done meat intake and the risk of breast cancer." Journal of the National Cancer Institute. Oxford: Nov 18, 1998.Vol. 90, Iss. 22; pg. 1724, 6 pgs. ^ "National Cancer Institute, 2004 analysis and recommendations" (http://www.cancer.gov/cancertopics/factsheet/Risk/heterocyclicamines). Cancer.gov. 2004-09-15. Retrieved 2010-09-22. ^ "Acrylamide" (http://www.food.gov.uk/safereating/chemsafe /acrylamide_branch/). ^ "The Gale Encyclopedia of Cancer: A guide to Cancer and its Treatments, Second Edition. Page no. 137". ^ "IARC Monographs" (http://monographs.iarc.fr/). Monographs.iarc.fr. Retrieved 2010-09-22. ^ Section 301(b)(4) of the Public Health Service Act, as amended
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by Section 262, Pub. L. 95622. 13. ^ Safe Work Australia (http://www.safeworkaustralia.gov.au /AboutSafeWorkAustralia/WhatWeDo/Publications/Documents /504/Approved_Criteria_classifying_Hazardous_Substances_NOHS C1008_1999_2nd_Edition.pdf), NOHSC. (1999). Approved criteria for classifying hazardous substances [NOHSC:1008(1999)] 4.76. Accessed 21/05/2011 14. ^ "Web definitions for Procarcinogen" (http://www.lactospore.com /glossary.htm). Lactospore.com. Retrieved 2010-09-22. 15. ^ Hartwig, Andrea (2013). "Chapter 15. Cadmium and cancer". In Astrid Sigel, Helmut Sigel and Roland K. O. Sigel. Cadmium: From Toxicology to Essentiality. Metal Ions in Life Sciences 11. Springer. pp. 491507. doi:10.1007/978-94-007-5179-8_15 (http://dx.doi.org /10.1007%2F978-94-007-5179-8_15). 16. ^ a b "IARC: DIESEL ENGINE EXHAUST CARCINOGENIC" (http://press.iarc.fr/pr213_E.pdf) (Press release). International Agency for Research on Cancer (IARC). Retrieved June 12, 2012. "June 12, 2012 -- After a week-long meeting of international experts, the International Agency for Research on Cancer (IARC), which is part of the World Health Organization (WHO), today classified diesel engine exhaust as carcinogenic to humans (Group 1), based on sufficient evidence that exposure is associated with an increased risk for lung cancer" 17. ^ "IARC Monographs Programme finds cancer hazards associated with shiftwork, painting and firefighting, International Agency for Research on Cancer" (http://www.iarc.fr/en/media-centre/pr/2007 /pr180.html). Retrieved 2011-07-01 18. ^ Tobacco Smoke and Involuntary Smoking (http://monographs.iarc.fr/ENG/Monographs/vol83/), IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 83 (2004). 19. ^ Survival, causes of death, and estimated tissue doses in a group of human beings injected with plutonium (http://www.osti.gov /energycitations/purl.cover.jsp?purl=/4136654-rOiaqY /Survival,causesofdeath,andestimatedtissuedosesinagroupofhumanb eingsinjectedwithplutonium.pdf), 751053 (http://www.osti.gov /energycitations/servlets/purl/4136654-rOiaqY/4136654.pdf), R. E. Rowland and Patricia W. Durbin, 1975. 20. ^ Table 6-2 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7. 8th edition. 21. ^ Bernstein H, Payne CM, Bernstein C, Garewal H, Dvorak K (2008). Cancer and aging as consequences of un-repaired DNA damage. In: New Research on DNA Damages (Editors: Honoka Kimura and Aoi Suzuki) Nova Science Publishers, Inc., New York, Chapter 1, pp. 1-47. open access, but read only https://www.novapublishers.com/catalog /product_info.php?products_id=43247 ISBN 978-1604565812 22. ^ a b Bernstein C, Prasad AR, Nfonsam V, Bernstein H. (2013). DNA Damage, DNA Repair and Cancer, New Research Directions in DNA Repair, Prof. Clark Chen (Ed.), ISBN 978-953-51-1114-6, InTech, http://www.intechopen.com/books/new-research-directionsin-dna-repair/dna-damage-dna-repair-and-cancer
23. ^ a b c d Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. (2010). Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer 127(12):2893-917. doi: 10.1002/ijc.25516. PMID 21351269 24. ^ Alberg AJ, Ford JG, Samet JM (2007). Epidemiology of lung cancer: ACCP evidence-based clinical practice guidelines (2nd edition). American College of Chest Physicians. Chest 132(3 Suppl):29S-55S. Review. PMID 17873159 25. ^ Cunningham FH, Fiebelkorn S, Johnson M, Meredith C. (2011). A novel application of the Margin of Exposure approach: segregation of tobacco smoke toxicants. Food Chem Toxicol. 49(11):2921-33. doi: 10.1016/j.fct.2011.07.019. Review. PMID 21802474 26. ^ Yager JD, Davidson NE. (2006). Estrogen carcinogenesis in breast cancer. N Engl J Med 354(3):270-82. Review. PMID 16421368 27. ^ Ansell PJ, Espinosa-Nicholas C, Curran EM, Judy BM, Philips BJ, Hannink M, Lubahn DB. (2004). In vitro and in vivo regulation of antioxidant response element-dependent gene expression by estrogens. Endocrinology 145(1):311-317. PMID 14551226 28. ^ Belous AR, Hachey DL, Dawling S, Roodi N, Parl FF. (2007). Cytochrome P450 1B1-mediated estrogen metabolism results in estrogen-deoxyribonucleoside adduct formation. Cancer Res 67(2):812-817. PMID 17234793 29. ^ Bolton JL, Thatcher GR. (2008). Potential mechanisms of estrogen quinone carcinogenesis. Chem Res Toxicol 21(1):93-101. Review. PMID 18052105 30. ^ a b Yue W, Santen RJ, Wang JP, Li Y, Verderame MF, Bocchinfuso WP, Korach KS, Devanesan P, Todorovic R, Rogan EG, Cavalieri EL. (2003). Genotoxic metabolites of estradiol in breast: potential mechanism of estradiol induced carcinogenesis. J Steroid Biochem Mol Biol 86(3-5):477-486. Review. PMID 14623547 31. ^ Giovannucci E, Martnez ME. (1996). Tobacco, colorectal cancer, and adenomas: a review of the evidence. J Natl Cancer Inst 88(23):1717-1730. Review. PMID 8944002 32. ^ a b c Bernstein H, Bernstein C, Payne CM, Dvorak K. (2009). Bile acids as endogenous etiologic agents in gastrointestinal cancer. World J Gastroenterol 15(27):3329-3340. PMID 19610133 33. ^ Bernstein C, Holubec H, Bhattacharyya AK, Nguyen H, Payne CM, Zaitlin B, Bernstein H. (2011). Carcinogenicity of deoxycholate, a secondary bile acid. Arch Toxicol 85(8):863-71. doi: 10.1007/s00204-011-0648-7. PMID 21267546 http://www.ncbi.nlm.nih.gov/pubmed /?term=Bernstein+C%2C+Holubec+H%2C+Bhattacharyya+AK%2C+Nguyen+ 34. ^ Ding SZ, Minohara Y, Fan XJ, Wang J, Reyes VE, Patel J, Dirden-Kramer B, Boldogh I, Ernst PB, Crowe SE. (2007). Helicobacter pylori infection induces oxidative stress and programmed cell death in human gastric epithelial cells. Infect Immun 75(8):4030-4039. PMID 17562777 35. ^ Handa O, Naito Y, Yoshikawa T. (2011). Redox biology and gastric carcinogenesis: the role of Helicobacter pylori. Redox Rep 16(1):1-7. doi:10.1179/174329211X12968219310756. Review. PMID 21605492
External links
U.S. National Toxicology Programs Report on Carcinogens (http://ntp.niehs.nih.gov/index.cfm?objectid=03C9B512-ACF8-C1F3ADBA53CAE848F635) CDC Occupational Cancer Carcinogen List NIOSH Safety and Health Topic (http://www.cdc.gov/niosh/topics/cancer /npotocca.html) Recognized Carcinogens (http://www.scorecard.org/health-effects/chemicals.tcl?short_hazard_name=cancer&all_p=t) American Cancer Society (http://www.cancer.org/docroot/PED/content /PED_1_3x_Known_and_Probable_Carcinogens.asp?sitearea=PED) Database of Rodent Carcinogens (http://potency.berkeley.edu/)
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Comparing Possible Cancer Hazards from Human Exposures to Rodent Carcinogens (http://potency.berkeley.edu/MOE.html) Retrieved from "http://en.wikipedia.org/w/index.php?title=Carcinogen&oldid=580194627" Categories: Carcinogens Carcinogenesis Radiation health effects This page was last modified on 4 November 2013 at 19:03. Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization.
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