ライフサイエンスコーパス: carcinogen

1 Ionising radiation is a potent human carcinogen.

2 as a long-term biomarker of exposure to this carcinogen.

3 lamide (AA) is a known lethal neurotoxin and carcinogen.

4 s is placed on detection of benzene, a known carcinogen.

5 rtalization by nickel, a human non-genotoxic carcinogen.

6 tolochia herbs and a potent human urothelial carcinogen.

7 tion (UVR), the most prevalent environmental carcinogen.

8 olet (UV) radiation, the most important skin carcinogen.

9 sed sucrose to be scrutinized as a potential carcinogen.

10 hus, BPA may act as a complete mammary gland carcinogen.

11 spontaneous cancers not driven by a specific carcinogen.

12 Rice contains arsenic, a known skin carcinogen.

13 s an environmental and occupational chemical carcinogen.

14 n normal epithelial cells exposed to a major carcinogen.

15 Arsenic is a well-documented human carcinogen.

16 c aromatic amine (HCA) and important dietary carcinogen.

17 ic arsenic (Asi) is a chronic, non-threshold carcinogen.

18 Ionizing radiation is a well known human carcinogen.

19 nated solvent classified as a probable human carcinogen.

20 liver damage caused by alcohol, viruses, or carcinogens.

21 are commonly exhibited by established human carcinogens.

22 (TCR)-Vgamma5 chains protect from cutaneous carcinogens.

23 dentification and hazard evaluation of human carcinogens.

24 f the formation of tumors induced by tobacco carcinogens.

25 ) before treatment with low doses of tobacco carcinogens.

26 a variety of tumorigenic effects induced by carcinogens.

27 mples and liver samples exposed to genotoxic carcinogens.

28 clude natural products, hormones, drugs, and carcinogens.

29 early three-quarters of these rodent mammary carcinogens.

30 to be specifically up-regulated by genotoxic carcinogens.

31 ormation on organic solvents as human breast carcinogens.

32 reased tumor number and size when exposed to carcinogens.

33 (ITCs) that stimulate detoxification of food carcinogens.

34 es bulky DNA lesions induced by mutagens and carcinogens.

35 n the uptake and metabolism of tobacco smoke carcinogens.

36 rom both regenerative stresses and genotoxic carcinogens.

37 propagated for 20 generations or exposed to carcinogens.

38 e as biomarkers of these tobacco and dietary carcinogens.

39 e, and other PAHs are transplacental ovarian carcinogens.

40 a Th1/Th2 inflammatory response to chemical carcinogens.

41 ve stress from cigarette smoking and related carcinogens.

42 ure to a wide range of chemical and physical carcinogens.

43 acids, which rapidly convert to DNA-damaging carcinogens.

44 posed to ionizing radiation or environmental carcinogens.

45 e exposed to a complex mix of pollutants and carcinogens.

46 to give rise to tumors when challenged with carcinogens.

47 uch as benzo[a]pyrene in tobacco smoke, into carcinogens.

48 refore control the rate of detoxification of carcinogens.

49 the circadian influence on the metabolism of carcinogens.

50 clearance of the lung airway epithelium from carcinogens.

51 ions and were not exposed to liver toxins or carcinogens.

52 r fluke species are recognised as biological carcinogens.

53 wn about its role in metabolism of drugs and carcinogens.

54 ty assays is the prediction of non-genotoxic carcinogens.

55 compounds (NOC), which are possible bladder carcinogens.

56 nt in >96% of hepatocytes before exposure to carcinogens.

57 enitor cells simultaneously with exposure to carcinogens.

58 ions regarding human hazard from exposure to carcinogens.

59 ning of fuel for heating or cooking releases carcinogens.

60 t contributions to protection from cutaneous carcinogens.

61 ation in the joint effects of common dietary carcinogens.

62 elial cells (HBEC) with low doses of tobacco carcinogens.

63 sing health risks accompanied by exposure to carcinogens.

64 sreplication of DNA damage caused by tobacco carcinogens.

65 Effects of the environmental toxin and carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, di

66 ol (NNAL), a metabolite of the powerful lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanon

67 des (total NNAL), a biomarker of the tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanon

68 ors (nAChRs) binding to the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanon

69 ention of oral carcinogenesis induced by the carcinogen 4-nitroquinoline 1-oxide (4-NQO) in a mouse m

70 inar cells upon implantation of the chemical carcinogen 7,12-dimethylbenz(a)anthracene (DMBA) or tran

71 ic BrafV600E and a single application of the carcinogen 7,12-dimethylbenz(a)anthracene.

72 for reducing the formation of the suspected carcinogen acrylamide in cooked foods often rely on a re

73 nternal dose of nicotine and tobacco-derived carcinogens among ethnic/racial groups have been observe

74 induced by the concomitant application of a carcinogen and a tumor promoter (7,12-dimethylbenz[a]ant

75 Formaldehyde, a known human carcinogen and mucous membrane irritant, is emitted from

76 ss concentrations of 0.4-0.6%, is a possible carcinogen and respiratory irritant.

77 These findings confirm silica as a human carcinogen and suggest that current exposure limits in m

78 cular emphasis is placed on benzene, a known carcinogen and the most challenging BTEX analyte with re

79 fluid intake may reduce contact time between carcinogens and bladder epithelium and consequently redu

80 DMEs, is involved in the metabolism of many carcinogens and drugs and is down-regulated in HCC.

81 chronic inflammation in response to chemical carcinogens and environmental stresses, including ultrav

82 esponse also occurs with UV-mimetic chemical carcinogens and in a manner that is independent of DNA r

83 ompounds, of which 13 are known or suspected carcinogens and more than 20 are known environmental tox

84 ultural barriers, and disparate exposures to carcinogens and pathogens.

85 detoxifying antioxidant genes that detoxify carcinogens and protect against oxidative stress.

86 yclic aromatic hydrocarbons (PAHs) are known carcinogens and suspected endocrine disruptors.

87 ith substantially reduced levels of measured carcinogens and toxins relative to smoking only combusti

88 1,4-Dioxane is a likely human carcinogen, and an excess 10(-6) cancer risk is associat

89 Arsenic is a Group I human carcinogen, and chronic arsenic exposure through drinkin

90 of significant concern as Cr(VI) is a known carcinogen, and is mobile in the subsurface.

91 Inorganic arsenic is a carcinogen, and its ingestion through foods such as rice

92 chemopreventive agents, chemical toxins and carcinogens, and >80% of therapeutic drugs.

93 r formation after administration of chemical carcinogens, and in Apc(min/+) mice.

94 d environmental pollutants, known human lung carcinogens, and potent mammary carcinogens in laborator

95 combustion carbon capture systems are potent carcinogens, and their emission could pose a serious thr

96 idated to measure tobacco-related alkaloids, carcinogens, and their metabolites in raw wastewater, in

97 ompare exposure to nicotine, tobacco-related carcinogens, and toxins among smokers of combustible cig

98 In a mouse model of carcinogen (AOM)-induced colon cancer, tamoxifen-inducib

99 vidence that certain susceptibility loci and carcinogens are associated with characteristic mutations

100 I) genotoxicity when standard ATM-activating carcinogens are used as references.

101 systems to identify cancer-promoting agents (carcinogens) are established, models to identify compoun

102 N-Nitrosamines, probable human carcinogens, are a group of disinfection byproducts unde

103 Exposure to herbal remedies containing the carcinogen aristolochic acid (AA) has been widespread in

104 Key characteristics of carcinogens as a basis for organizing data on mechanisms

105 ed CYP1A2, which metabolizes tobacco-derived carcinogen, as a causative candidate gene.

106 Arsenic is a known carcinogen associated with skin, lung, bladder, kidney,

107 of exposure to tobacco-related toxicants and carcinogens at the population level is thus an essential

108 for future studies aimed at identifying the carcinogens at work.

109 eanwhile, given the mutagenic nature of most carcinogens, attention has gravitated to developing a ge

110 tion, WT mice treated with injections of the carcinogen azoxymethane (AOM) showed increased numbers o

111 ic mucosal tissue from mice treated with the carcinogen azoxymethane after 24 weeks.

112 esis of FVB/N mice treated with the chemical carcinogen azoxymethane and subsequently exposed to colo

113 ice immediately following treatment with the carcinogen azoxymethane.

114 AR (Uro-AR(-/y)) to develop BCa by using the carcinogen BBN [N-butyl-N-(4-hydroxybutyl)-nitrosamine]

115 (NNK) and N-nitrosonicotine (NNN) are potent carcinogens believed to contribute to the development of

116 lized by the powerful polycyclic hydrocarbon carcinogen benzo(a)pyrene display transversion point mut

117 us DNA lesion, formed not only by xenobiotic carcinogens but also by the endogenous methylating agent

118 Acrylamide is a neurotoxin and potential carcinogen, but is found in various thermally processed

119 Indoor tanning is a known carcinogen, but the scope of exposure to this hazard is

120 le prediction of genotoxic and non-genotoxic carcinogens, but also had the power to discriminate betw

121 acetylates arylamine and hydrazine drugs and carcinogens, but predicted acetylator NAT2 phenotypes we

122 alline silica has been classified as a human carcinogen by the International Agency for Research on C

123 and tissues from a variety of toxicants and carcinogens by increasing the expression of a number of

124 Also, skin carcinogen challenge by 7,12-dimethylbenz[a]anthracene/1

125 Acrylamide is a well-known potentially carcinogen compound formed during thermal processing as

126 Many carcinogens damage both DNA and protein constituents of

127 atobium are classified as Group 1 biological carcinogens: definitive causes of cancer.

128 atobium are classified as group 1 biological carcinogens: definitive causes of cancer.

129 ice, HCC can be initiated by exposure to the carcinogen DEN, which has been shown to rely upon activa

130 us physiochemical markers of DNA damage from carcinogens derived from cooked meats, such as DNA adduc

131 lizing enzymes UGT1A10 and CYP1A1, enhancing carcinogen detoxification.

132 erein, female mice were exposed to the liver carcinogen diethylnitrosamine (DEN) and fed diets with w

133 duced in mice treated with the known hepatic carcinogen diethylnitrosamine (DEN).

134 s and treat the mice with the hepatocellular carcinogen diethylnitrosamine (DEN).

135 distinct A-to-T signature of the initiating carcinogen dimethylbenzanthracene, but non-shared mutati

136 ow that nickel, a nonmutagenic environmental carcinogen, disrupted H3K9me2 domains, resulting in the

137 g FFPE tissues can serve as biospecimens for carcinogen DNA adduct biomarker research.

138 a more valid and precise measure of in vivo carcinogen dose than by using self-reported smoking hist

139 The employed strategy is based on carcinogen-driven immortalization of primary mouse embry

140 ears deep molecular similarities to multiple carcinogen-driven SCCs from diverse sites, suggesting th

141 esponses between non-genotoxic and genotoxic carcinogens during the initial stages of the regeneratio

142 tive interventions range from avoiding known carcinogens (e.g., tobacco or asbestos) to intervening w

143 tive interventions range from avoiding known carcinogens (e.g., tobacco or asbestos) to intervening w

144 roles in the metabolism of steroids, drugs, carcinogens, eicosanoids, and numerous other chemicals.

145 n lymphoma (NHL) pathogenesis by influencing carcinogen exposure or through immune modulation.We aime

146 offer key insights into the contribution of carcinogen exposure to enhanced cancer susceptibility.

147 ras(ex3op) allele had fewer tumors following carcinogen exposure, and this allele was mutated less of

148 Despite maintained carcinogen exposure, tumors from smokers showed a relati

149 e, many BCs still arise through occupational carcinogen exposure.

150 ny sporadic cancers is directly initiated by carcinogen exposure.

151 ovel epigenetic signatures for non-genotoxic carcinogen exposure.

152 valuating human health risks associated with carcinogen exposure.

153 iology of many cancers, assess the impact of carcinogen exposures on cancer risk, and evaluate the po

154 the environmental and occupational chemical carcinogen FA.

155 g chromatin against damage by the endogenous carcinogen FA.

156 Seventy-five of the rodent mammary carcinogens fall into 17 groups, based on exposure poten

157 of exposure to inorganic arsenic, a class I carcinogen for humans.

158 esponses to the endogenous and environmental carcinogen formaldehyde (FA) that binds to cytosolic and

159 Acrylamide (AA) is a probable human carcinogen found in carbohydrate-rich foods that have be

160 ut it can form N-nitrosopiperazine (MNPZ), a carcinogen, from nitrogen oxides (NO(x)) in flue gas fro

161 Vinyl chloride (VC) is a carcinogen generated in groundwater by reductive dechlor

162 lved circadian disruption to be a "probable" carcinogen (group 2A), noting that human evidence was li

163 revention of tumors induced by environmental carcinogens has not been achieved.

164 k factor for keratinocyte cancers, but other carcinogens have also been implicated, including tobacco

165 As non-genotoxic and genotoxic carcinogens have different cancer risks, the objective o

166 nd neck that arise from habitual exposure to carcinogens have lower cure rates than those that arise

167 he Hazard Identification Approach for Breast Carcinogens (HIA-BC), a method for detecting chemicals t

168 ric guanine adducts.Benzo[a]pyrene (BP) is a carcinogen in cigarette smoke that upon metabolic activa

169 Benzo[a]pyrene (BP) is a carcinogen in cigarette smoke which, after metabolic act

170 ll-known hepatotoxicant and could be a liver carcinogen in humans.

171 Formaldehyde (HCHO) is the most important carcinogen in outdoor air among the 187 hazardous air po

172 nd suggest that AA may be an important ccRCC carcinogen in Romania, a finding with major public healt

173 y ultraviolet (UV) radiation, the ubiquitous carcinogen in sunlight that causes skin cancer.

174 f biomarkers of exposure to potential breast carcinogens in breast cancer studies and biomonitoring.

175 n human lung carcinogens, and potent mammary carcinogens in laboratory animals.

176 develop lung carcinomas induced by chemical carcinogens in Mmp1a(-/-) mice.

177 Studies on the Joint Effects of Occupational Carcinogens in the Development of Lung Cancer).

178 des, improved awareness of the prevalence of carcinogens in the environment, along with a growing app

179 measurement of tobacco-related toxicants and carcinogens in wastewater are not available.

180 biomarkers of fumonisin B1 (FB1), a class 2B carcinogen, in blood and urine samples collected from an

181 ng enzyme that metabolizes electrophiles and carcinogens including 4-hydroxy-2-nonenal (4-HNE), an en

182 etazoan eukaryotes, unlike the other group 1 carcinogens including human papilloma virus, hepatitis C

183 etazoan eukaryotes, unlike the other Group 1 carcinogens including human papilloma virus, hepatitis C

184 able cancer hallmarks and characteristics of carcinogens; incorporate epigenetic biomarkers, in silic

185 Carcinogens induce malignancies by creating DNA lesions

186 be involved with augmenting certain types of carcinogen induced cancer.

187 Gucy2c(-/-), mice resulted in a reduction in carcinogen-induced aberrant crypt foci formation.

188 carcinogen-induced tumours, suggesting that carcinogen-induced and genetically engineered models lea

189 itumor effect to prevent clinically relevant carcinogen-induced autochthonous HCC in mice.

190 e CD8 T cells to prevent clinically relevant carcinogen-induced autochthonous HCC in mice.

191 tumor challenge and reduced the incidence of carcinogen-induced autochthonous HCC.

192 s, further enhancing the tumor prevention of carcinogen-induced autochthonous HCC.

193 Administered hCG reduces risk of carcinogen-induced breast cancer in animal models, and h

194 ty may have a significant clinical impact on carcinogen-induced cancers.

195 uppresses hepatocarcinogenesis by inhibiting carcinogen-induced compensatory hepatocyte proliferation

196 f sunlight in melanoma skin cancers, tobacco carcinogen-induced DNA damage in lung cancers and aristo

197 Deregulated cell survival under carcinogen-induced genotoxic stress is vital for cancer

198 However, the role of autophagy following carcinogen-induced genotoxic stress remains unclear.

199 up-regulated in a time-dependent manner in a carcinogen-induced HCC mouse model, and STO-609 treatmen

200 increases rates of both spontaneous and DEN carcinogen-induced HCC.

201 L6 promoter SNP affects basal expression and carcinogen-induced IL-6 secretion.

202 SPARC reduced carcinogen-induced inflammation and accumulation of reac

203 helial cells and sensitizes mice to chemical carcinogen-induced intestinal and skin tumorigenesis.

204 s of mutant and WT Ras alleles in vivo using carcinogen-induced lung and skin carcinogenesis in mice

205 gene complex (NKC) in immunosurveillance for carcinogen-induced lung cancer.

206 alteration and role of MEG3 in environmental carcinogen-induced lung tumorigenesis.

207 ic predisposition of these mice to increased carcinogen-induced lung tumorigenesis.

208 l-oestradiol (EE2)-supplemented diet affects carcinogen-induced mammary cancer risk in daughters, gra

209 rs of overweight fathers had higher rates of carcinogen-induced mammary tumors which were associated

210 ach carcinogenesis, we firstly constructed a carcinogen-induced mouse gastric tumor model combined wi

211 Carcinogen-induced mouse models of cancer have shown tha

212 We have shown that cured meat promotes carcinogen-induced preneoplastic lesions and increases s

213 d that STING-deficient mice are resistant to carcinogen-induced skin cancer, similar to myeloid diffe

214 nmt3a-but not Dnmt3b-increases the number of carcinogen-induced squamous tumors, without affecting tu

215 pression of DNMT3b increased and accelerated carcinogen-induced transformation.

216 increases susceptibility to spontaneous and carcinogen-induced tumor development.

217 tor E2-related factor-2 (Nrf2) protects from carcinogen-induced tumorigenesis, underlying the rationa

218 sions and showed increased susceptibility to carcinogen-induced tumorigenesis.

219 polyphenols on the development and growth of carcinogen-induced tumors in experimental animal models,

220 The exome-wide mutation spectra in carcinogen-induced tumours overwhelmingly display signat

221 nd copy number alterations compared with the carcinogen-induced tumours, suggesting that carcinogen-i

222 Ionizing radiation is a potent carcinogen, inducing cancer through DNA damage.

223 ir links to tissues of origin, environmental/carcinogen influences, and DNA repair defects.

224 showed that cadmium [Cd(II)], a known human carcinogen, inhibited all activity of hUNG at 100 muM.

225 ntains very high levels of the non-threshold carcinogen inorganic arsenic (i-As), at concentrations a

226 sulted in the release of known and suspected carcinogens into the environment.

227 Arsenic, a human carcinogen, is a high-affinity MRP1 substrate as arsenic

228 ght exposure at night, a recently recognized carcinogen, is associated with an increased risk of canc

229 by H. pylori, the gastric cancer associated carcinogen, leads to the ubiquitination and reduction of

230 is one of the most widespread environmental carcinogens, methods of remediation are still limited.

231 er, which were induced either by exposure to carcinogens (methyl-nitrosourea (MNU) and urethane) or b

232 highly tumor prone when challenged with the carcinogen methylcholanthrene (MCA).

233 alterations, and underline the importance of carcinogen models for understanding the complex mutation

234 Oxidation of the carcinogen-modified SA with m-chloroperoxybenzoic acid (

235 cal evidence from NGS data that well-defined carcinogen mutational signatures are indeed present in t

236 Treatment of Lzts2-deficient mice with a carcinogen, N-butyl-N-(4-hydroxybutyl) nitrosamine, incr

237 our knowledge, discovered that environmental carcinogen nickel exposure led to MEG3 downregulation, c

238 0.5% O2) and concurrent treatment with metal carcinogen (nickel) to evaluate the passage-dependent re

239 Glycidol is a probable carcinogen not previously identified in the vapor, and a

240 ecently been implicated as a potential major carcinogen of smoking-related lung cancer.

241 s with hypermutation caused by chemotherapy, carcinogens, or germline alterations.

242 into CSCs by nearby MECs is dependent on the carcinogen originally used to malignantly transform the

243 (n) method to measure DNA adducts of several carcinogens originating from well-done cooked meats, tob

244 ) exposure to the rodent liver non-genotoxic carcinogen, phenobarbital (PB).

245 The food-derived carcinogen PhIP (2-amino-1-methyl-6-phenylimidazo[4,5-b]

246 cts derived from four other classes of human carcinogens: polycyclic aromatic hydrocarbons (PAHs), ar

247 s to DNA that are derived from environmental carcinogens present in tobacco smoke, automobile exhaust

248 , which constitute a family of known bladder carcinogens present in tobacco smoke.

249 e major deoxyguanosine (dG) adducts of these carcinogens ranged between 1.3 and 2.2 adducts per 10 (9

250 yonic fibroblasts (MEFs) exposed in vitro to carcinogens recapitulate key features of mutational sign

251 e models and in vitro studies, tobacco smoke carcinogens reduced expression of Fzd9 while prostacycli

252 ould lead to chemical detoxification of food carcinogens, reducing the cancer risk associated with me

253 UVR, as one of the most ubiquitous carcinogens, represents both a challenge and an enormous

254 ory tumour microenvironments correlates with carcinogen resistance and immune regulation mediated by

255 he population exposure to both toxicants and carcinogens resulting from tobacco use.

256 The current single-chemical-as-carcinogen risk assessment paradigm might underestimate

257 Here we show that a spectrum of carcinogen-specific mutational and epigenetic alteration

258 The use of the AOM as colon specific carcinogen substance altered the liver and lung architec

259 Chemical carcinogens such as benzo[a]pyrene (BaP) and 2-amino-1-m

260 Remarkably, the pattern of carcinogen susceptibility across the genome of primary c

261 Furthermore, they identify carcinogen susceptibility as an origin of genome instabi

262 r driver genes have an intrinsic increase in carcinogen susceptibility, including the BRAF oncogene t

263 Alcohol is a carcinogen suspected of increasing lung cancer risk.

264 electronic cigarettes generate less tar and carcinogens than combustible cigarettes, use of electron

265 ional Agency for Research on Cancer) Group 1 carcinogen that causes hepatocellular carcinoma (HCC).

266 Acetaldehyde is an ethanol-derived definite carcinogen that causes oesophageal squamous cell carcino

267 g 4-hydroxy-2-nonenal (4-HNE), an endogenous carcinogen that contributes to colorectal carcinogenesis

268 rodiol-t-9,10-epoxide (anti-BPDE) is a known carcinogen that damages DNA, and this damage is influenc

269 l epoxide (BPDE) is a potent cigarette smoke carcinogen that forms guanine adducts at TP53 CpG mutati

270 and treated them with azoxymethane (AOM), a carcinogen that induces sporadic colorectal cancer.

271 show that UVB radiation, a known human skin carcinogen that operates by causing DNA damage, induced

272 s (HAAs) are a class of structurally related carcinogens that are formed during the combustion of tob

273 N-Nitrosamines are potent mutagens and carcinogens that can be formed during oxidative water tr

274 kely to be due to second-hand smoke or other carcinogens that cause oxidative DNA damage, implying th

275 N-nitrosamines (NAms) are highly active carcinogens that have been detected in food and beverage

276 Nickel compounds are well-established human carcinogens that induce tumorigenesis partly through the

277 Although asbestos is a well-known lung carcinogen, the pleural plaque-lung cancer link remains

278 As possible carcinogens, their chronic ingestion in food preparation

279 ct target of STAT3 and is induced by tobacco carcinogens through STAT3 pathway.

280 cancer risk from one of strict avoidance of carcinogens to one of adherence to exposure limits deeme

281 monstrate that next-generation sequencing of carcinogen-transformed HBECs treated with the demethylat

282 The multiplicity of gastric tumor in carcinogen-treated mice was significantly increased by c

283 Carcinogen-treated RDEB mice developed invasive tumors p

284 ion of 1-fluoro-2,4-dinitrobenzene (DNFB) to carcinogen-treated skin led to the development of papill

285 uted and represented a minor fraction of the carcinogen-treated skin surface (10.3% of the imaging ar

286 tumors occurring with increased incidence in carcinogen-treated subjects.

287 Epidermal proliferation was reduced in the carcinogen-treated transgenic skin, whereas epidermal ke

288 hydroxamic acids and polyhalogenated quinoid carcinogens, two important classes of compounds of major

289 allele and expose the resultant mice to the carcinogen urethane, which induces Kras mutation-positiv

290 in mice before cancer induction by the smoke carcinogen, urethane, resulted in increased lung tissue

291 e to lung tumorigenesis induced by the smoke carcinogen, urethane.

292 amage caused by environmental and endogenous carcinogens using a set of low-fidelity translesion synt

293 is (2-chloroethyl) phosphate (TCEP), a known carcinogen, was found in the V6 commercial mixture (14%

294 A (OTA) is a fungal metabolite and putative carcinogen which can contaminate a variety of foods such

295 lmingly display signatures of the initiating carcinogen, while adenocarcinomas acquire additional C >

296 urce and precursor of NDMA, a probable human carcinogen, while chemical disinfection can produce CNTs

297 Arsenic (As(3+)) is a carcinogen with considerable environmental and occupatio

298 Sex differences in associations of tobacco carcinogens with lung cancer risk have been hypothesized

299 UV light is an established carcinogen, yet evidence suggests that UV-seeking behavi

300 When challenged with carcinogens, zebrafish developed liver cancer that resem