ライフサイエンスコーパス: carcinogen

1 sed sucrose to be scrutinized as a potential carcinogen.

2 spontaneous cancers not driven by a specific carcinogen.

3 Rice contains arsenic, a known skin carcinogen.

4 s an environmental and occupational chemical carcinogen.

5 n normal epithelial cells exposed to a major carcinogen.

6 Arsenic is a well-documented human carcinogen.

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

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

9 Ionizing radiation is a well known human carcinogen.

10 nated solvent classified as a probable human carcinogen.

11 Ionising radiation is a potent human carcinogen.

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

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

14 or influences on the extreme tropism of this carcinogen.

15 zed microcystins as a kind of neurotoxin and carcinogen.

16 s enhanced sensitivity to a bladder-specific carcinogen.

17 t risk factor for cancer and classified as a carcinogen.

18 rsenic, a ubiquitous environmental toxin and carcinogen.

19 hane is a known toxicant and suspected human carcinogen.

20 ning of fuel for heating or cooking releases carcinogens.

21 sing health risks accompanied by exposure to carcinogens.

22 the circadian influence on the metabolism of carcinogens.

23 clearance of the lung airway epithelium from carcinogens.

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

25 r fluke species are recognised as biological carcinogens.

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

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

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

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

30 enitor cells simultaneously with exposure to carcinogens.

31 ions regarding human hazard from exposure to carcinogens.

32 t contributions to protection from cutaneous carcinogens.

33 ation in the joint effects of common dietary carcinogens.

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

35 sreplication of DNA damage caused by tobacco carcinogens.

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

37 are commonly exhibited by established human carcinogens.

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

39 dentification and hazard evaluation of human carcinogens.

40 DNA lesions caused by UV light and chemical carcinogens.

41 f the formation of tumors induced by tobacco carcinogens.

42 ) before treatment with low doses of tobacco carcinogens.

43 a variety of tumorigenic effects induced by carcinogens.

44 mples and liver samples exposed to genotoxic carcinogens.

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

46 early three-quarters of these rodent mammary carcinogens.

47 to be specifically up-regulated by genotoxic carcinogens.

48 damage to the epithelium by UVR or chemical carcinogens.

49 cytoplasmic signaling pathways, as potential carcinogens.

50 and identifying potential drug and chemical carcinogens.

51 pment of dysplasia in the setting of dietary carcinogens.

52 posed to 79 known or suspected environmental carcinogens.

53 ted by children and adolescents' exposure to carcinogens.

54 n numerous toxic substances, including known carcinogens.

55 halomethanes, are possible or probable human carcinogens.

56 evelops HCC without the addition of specific carcinogens.

57 atural product streptozotocin, are prominent carcinogens(1,2) and important cancer chemotherapeutics(

58 e were intranasally treated with the tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanon

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

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

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

62 Wild-type mice were exposed to the carcinogen, 4-nitroquinoline 1-oxide (4NQO).

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

64 ma, in which tumorigenesis is initiated by a carcinogen 7,12-dimethylbenz[alpha]anthracene, and then

65 e infection with S. haematobium as a group 1 carcinogen, a definitive cause of cancer.

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

67 pyrolysis of vitamin E acetate also produces carcinogen alkenes and benzene for which the negative lo

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

69 sk much later, our understanding of EBV as a carcinogen and a possible target for therapeutic interve

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

71 cles coated by organic compounds, is a known carcinogen and mutagen.

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

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

74 cellular transformation induced by chemical carcinogens and identified a subset of cell transformati

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

76 the lung associated with exposure to tobacco carcinogens and inflammation, A/J mice were intranasally

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

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

79 rizes the recent advances on tissue-specific carcinogens and their complex crosstalk with the comprom

80 PCBs are classified as xenoestrogens and carcinogens and their health risks may be sex-specific.

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

82 The reliable identification of carcinogens and understanding of carcinogenicity has bec

83 T1, which are required for detoxification of carcinogens and whose low expression levels are associat

84 1,4-Dioxane is a likely human carcinogen, and an excess 10(-6) cancer risk is associat

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

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

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

88 ism of many commonly prescribed medications, carcinogens, and endogenous compounds.

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

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

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

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

93 erapeutic/chemotherapeutic drugs, nutrients, carcinogens, and toxins.

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

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

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

97 Red and processed meat, recognized carcinogens, are risk factors for colorectal neoplasia,

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

99 y linking increased exposure to IARC group 1 carcinogens (As, Cd, Cr, Ni) and group 2 carcinogens (V,

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

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

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

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

104 rp53DeltaIECAktE17K) upon challenge with the carcinogen azoxymethane.

105 Here we report that cigarette smoke and the carcinogen benzo(a)pyrene (BaP) induce PD-L1 expression

106 s) including naphthalene (NAP) and the known carcinogen benzo(a)pyrene (BaP), sulfur dioxide (SO(2)),

107 genic, genotoxic, teratogenic, and potential carcinogens both in vitro and in vivo.

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

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

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

111 It is deemed as a potential human carcinogen by IARC and classified under class 2B.

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

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

114 Many carcinogens damage both DNA and protein constituents of

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

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

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

118 , high-fat diet of AN people and exposure to carcinogens derived from diet or environment are associa

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

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

121 in HCC using mouse models of HCC induced by carcinogen diethylnitrosamine (DEN).

122 WT and Nod2(-/-) mice were treated with the carcinogen dimethylbenz[a]anthracene (DMBA) and maintain

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

124 development after administration of chemical carcinogens (dimethylbenzanthrazene).

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

126 sed susceptibility to mutations from tobacco carcinogen DNA adducts.

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

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

129 investigate the effects of papillomavirus on carcinogen-driven skin cancer, we colonized several stra

130 adolescence exposure to multiple industrial carcinogens during critical periods of development.

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

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

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

134 Whether tobacco carcinogens enable exposed cells immune escape resulting

135 Among all of the known biological carcinogens, Epstein-Barr virus (EBV) and Kaposi's sarco

136 lls deprived of IL-22 signals and exposed to carcinogens escaped DDR-controlled apoptosis, contained

137 cause of the typically long interval between carcinogen exposure and cancer diagnosis.

138 e would be sentinels for monitoring personal carcinogen exposure and might drive direct changes in ce

139 We measured urinary concentrations of eight carcinogen exposure biomarkers (heavy metals and polycyc

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

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

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

143 rformed to identify pathways associated with carcinogen exposure.

144 ny sporadic cancers is directly initiated by carcinogen exposure.

145 valuating human health risks associated with carcinogen exposure.

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

147 activated oncogene, less than a month after carcinogen exposure.

148 ations and to form lung tumors after tobacco carcinogen exposure.

149 etabolites and biological mechanisms linking carcinogens exposure with early health effects.

150 e of cancer risk in the absence of continued carcinogen exposures is simply a function of stochastica

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

152 With recurring carcinogen exposures, individual tumors develop in a fie

153 field" persists in the absence of continued carcinogen exposures, resulting in a sustained risk for

154 the environmental and occupational chemical carcinogen FA.

155 g chromatin against damage by the endogenous carcinogen FA.

156 d in the oxidations of most drugs, steroids, carcinogens, fat-soluble vitamins, and natural products.

157 Helicobacter pylori infection is a proven carcinogen for gastric cancer.

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

159 contaminant in the environment and a serious carcinogen for the human being.

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

161 ntly exposed to acrylamide, a probable human carcinogen found in commonplace sources such as most hea

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

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

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

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

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

167 stics approach similar to that pioneered for carcinogen hazard identification to female reproductive

168 re playing an increasingly important role in carcinogen hazard identification.

169 of gastric epithelial cells to the bacterial carcinogen Helicobacter pylori causes DNA double strand

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

171 log of 1,3-butadiene and is a possible human carcinogen (IARC Group 2B).

172 s an environmental and occupational chemical carcinogen implicated in the damage of proteins and nucl

173 e possibility that ECS is a lung and bladder carcinogen in addition to nicotine.

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

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

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

177 mplicate ECS as a lung and potential bladder carcinogen in mice.

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

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

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

181 adolescents (aged 9-15) exposed to multiple carcinogens in a polluted area surrounding the largest p

182 3), a process that is driven by more than 60 carcinogens in cigarette smoke that directly damage and

183 utagenic activity of the SN2-type alkylating carcinogens in cigarettes.

184 re able to detect mutations induced by three carcinogens in five tissues of two strains of mice withi

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

186 P1 axis has synergistic effect with chemical carcinogens in promoting malignant transformation of uro

187 ganic arsenic oxides have been identified as carcinogens in several human tissues, including epidermi

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

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

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

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

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

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

194 Carcinogens induce malignancies by creating DNA lesions

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

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

197 Carcinogen-induced apoptosis may trigger escape from dor

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

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

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

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

202 r eicosanoid blockade is unlikely to prevent carcinogen-induced cancer progression.

203 X-2/sEH inhibition is an approach to prevent carcinogen-induced cancer.

204 Carcinogen-induced cancers typically have high mutation

205 of the impact of immune cells on viral- and carcinogen-induced cancers.

206 uppresses hepatocarcinogenesis by inhibiting carcinogen-induced compensatory hepatocyte proliferation

207 This includes the potentiation of the carcinogen-induced DNA damage response, at the tumor ini

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

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

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

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

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

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

214 e and dampened therapeutic responses against carcinogen-induced neoplasias and transplantable tumors.

215 ted mechanical allodynia in female mice with carcinogen-induced OSCC.

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

217 educed body size but were also less prone to carcinogen-induced skin tumours, in part due to reduced

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

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

220 conferring resistance and susceptibility to carcinogen-induced tumorigenesis is frequently studied i

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

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

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

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

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

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

227 ould be altered to reduce the content of the carcinogen inorganic arsenic.

228 can arise when metabolic enzymes convert pro-carcinogens into a highly DNA reactive products.

229 The most prevalent human carcinogen is sunlight-associated ultraviolet (UV), a ph

230 al epidermal cells that have been exposed to carcinogens is unknown.

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

232 Atrazine, a class 3a carcinogen, is a pesticide of chloro triazine family and

233 Acrylamide a neurotoxin and strong carcinogen, is found in various thermally processed food

234 iAs is a class I carcinogen known to target the skin, lungs, bladder, and

235 les and over-representation of environmental carcinogen-like mutational signatures in older females.

236 Although silica is a confirmed human lung carcinogen, little is known regarding the cancer risks a

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

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

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

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

241 inbred BD strains postnatally exposed to the carcinogen N-ethyl-N-nitrosourea developed PTMCs, which

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

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

244 tations and cancer and results from external carcinogens or endogenous cellular processes.

245 CC) arises through exposure to environmental carcinogens or malignant transformation by human papillo

246 cerization field in the absence of exogenous carcinogens or promoters requires a two-field composite

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

248 rols the growth of distinct (transplantable, carcinogen- or oncogene induced) orthotopic NSCLC models

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

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

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

252 Toxic environmental carcinogens promote cancer via genotoxic and nongenotoxi

253 Ten key characteristics of carcinogens provide a valuable tool for organizing and a

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

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

256 ive organs, but its role as a primary breast carcinogen remains controversial.

257 posure to arsenic (As), a human toxicant and carcinogen, remains a global public health problem.

258 Ionising radiation (IR) is a recognised carcinogen responsible for cancer development in patient

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

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

261 dence for potential listing in the Report on Carcinogens (RoC).

262 lternative for addressing the limitations in carcinogen screening.

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

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

265 Here, we demonstrate that carcinogens, such as aflatoxin B(1) (AFB(1)), induce apo

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

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

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

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

270 The de facto gold-standard approach to carcinogen testing adopts the 2-y rodent bioassay, a tim

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

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

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

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

275 g tumorigenesis induced by benzo[a]pyrene, a carcinogen that induces mutations in Kras.

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

277 chlorinated biphenyls (PCBs) are known human carcinogens that are byproducts of pigment manufacturing

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

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

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

281 nvironmental factors are well established as carcinogens, there remains a large knowledge gap of othe

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

283 Carcinogen-treated RDEB mice developed invasive tumors p

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

285 number of epidermal papillomas formed after carcinogen treatment.

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

287 The environmental carcinogen urethane exhibits a profound specificity for

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

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

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

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

292 by work to improve hazard identification of carcinogens using key characteristics (KCs), we have dev

293 p 1 carcinogens (As, Cd, Cr, Ni) and group 2 carcinogens (V, Hg, PAHs) with elevated oxidative stress

294 with significant levels of volatile organic carcinogens (VOCs), such as formaldehyde, benzene, and c

295 exposed to 1 of 20 known or suspected human carcinogens, we reveal that most agents do not generate

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

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

298 and, potentially, dimethyl arsenic acid are carcinogens widely elevated in rice.

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

300 (FF) are exposed to recognized and probable carcinogens, yet there are few studies of chemical expos