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Induction of osteogenic sarcomas and tumors of the hepatobiliary system in nonhuman primates with aflatoxin B1.

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The carcinogenicity of aflatoxin B1 (AFB1) has been under evaluation in nonhuman primates for the past 13 years. A total of 47 Old World monkeys, chiefly rhesus and cynomolgus, have received AFB1 i.p. (0.125 to 0.25 mg/kg) and/or p.o. (0.1 to 0.8 mg/kg) for 2 months or longer, and 12 are currently

Volume change induced in ascites sarcoma cells by aflatoxin B1.

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A diploid rat liver cell culture. IV. Malignant transformation by aflatoxin B1.

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Chronic exposure of a cloned rat hepatocyte culture (RL-PR-C) to a subtoxic, sublethal dose of aflatoxin B1 resulted in malignant transformation. Continuous exposure to aflatoxin B1 caused increasing tumorigenic potential as tested by back injection into isogenic animals. Control cultures exhibited

Carcinogenicity of aflatoxin B1 in rhesus monkeys: two additional cases of primary liver cancer.

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Three of 42 (7%) monkeys given aflatoxin B1 (AFB1) for longer than 2 years have developed primary malignant neoplasms of the liver. Liver biopsies performed at intervals during aflatoxin administration revealed that neoplasia was preceded by pathologic lesions of the liver, including toxic

Aflatoxin B1 and/or hepatitis B virus induced tumor spectrum in a genetically engineered hepatitis B virus expression and Trp53 haploinsufficient mouse model system for hepatocarcinogenesis.

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The authors investigated the spectrum of tumors and Trp53 mutations in genetically engineered models using the FVB/N mouse that expressed the hepatitis B virus genome and/or carried a Trp53 null and wildtype allele and/or were exposed to aflatoxin B1. Liver tumor incidence was increased when all

Feline sarcoma virus in vitro infection of human cells. Influence of chemical carcinogens on focus formation.

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Human fibroblast cells treated with benzo[alpha]pyrene (BP), aflatoxin B1 (AFB1) or N-acetoxy-2-fluorenylacetamide (A-AAF) inhibited Snyder-Theilen feline sarcoma virus (ST-FeSV) focus formation. Inhibition of focus formation resulting from chemical treatment was not related to cytotoxic

Effect of aflatoxin B1 on growth of normal and malignant rat fibroblasts in tissue culture (DNA synthesis).

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The effect of aflatoxin B1 on rat embryo fibroblasts WREF, the transformed line of rat fibroblasts AWRF-1 derived from WREF and the XC line of rat fibroblasts transformed by Rous sarcoma virus has been compared. By determining growth inhibition of cultured cells and inhibition of colony formation

The reactivity and carcinogenicity of aflatoxin B1-2,3-dichloride, a model for the putative 2,3-oxide metabolite of aflatoxin B1.

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Aflatoxin B1-2,3-dichloride (AFB1-Cl2) was synthesized as a model for the probable ultimate carcinogen, aflatoxin B1-2,3-oxide. As expected for aflatoxin B1-2,3-oxide, AFB1-Cl2 has an electrophilic carbon 2; it decomposed in water (half-life of 0.5 min in 10% dimethyl sulfoxide, pH 7.4) with the

Low frequency of p53 gene mutation in tumors induced by aflatoxin B1 in nonhuman primates.

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Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas from southern Africa and Qidong in China. To test this hypothesis, nine tumors induced by aflatoxin B1 in nonhuman primates were analyzed for mutations in the

Oesophageal cancer and Kaposi's sarcoma in Malawi: a comparative analysis.

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Given that oesophageal cancer (OC) is common in Malawi and its outcome is so dismal, would it be pragmatic to promptly mitigate the effects of smoking, alcohol and aflatoxins rather than seek a higher degree of local evidence for their role in OC? We retrospectively analysed a total of 13,217 OC and

Overexpression of the oncoprotein p53 in primary hepatic tumors of childhood does not correlate with gene mutations.

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High levels of expression of the p53 protein and gene mutations have been described in adult hepatocellular carcinomas. It has been postulated that specific mutations in exon 7 may be caused by aflatoxin exposure. To determine whether p53 mutations occur in childhood liver cancer unassociated with

The long-term culture of a diploid rat hepatocyte cell strain.

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We have developed a cell culture system of cloned rat hepatocytes which is named RL-PR-C. This culture has been grown in culture for over 150 passages (560 p.d.). It remains diploid by modal number count for over 50 passages (183 p.d.) after which there is a variation in the modal number between 41

Part II: Cancer in Indigenous Africans--causes and control.

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Africa has contributed substantial knowledge to the understanding of certain risk factors for cancer, such as the role of several infectious agents (eg, viruses, bacteria, and parasites), aflatoxins, and certain lifestyle factors. Although the relative importance of many lifestyle factors is

Urinary catabolites of ribonucleic acid as cancer markers: a preliminary report of their use in patients with lung cancer.

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Rats with aflatoxin-B1-induced hepatomas and dimethylnitrosamine-induced nephroblastomas excreted greater than normal amounts of urinary modified nucleosides and bases, catabolites of ribonucleic acid (RNA). Although both neoplasms caused increased excretions of the same catabolites, their

Mutational hotspot in the p53 gene in human hepatocellular carcinomas.

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Human hepatocellular carcinomas (HCC) from patients in Qidong, an area of high incidence in China, in which both hepatitis B virus and aflatoxin B1 are risk factors, were analysed for mutations in p53, a putative tumour-suppressor gene. Eight of the 16 HCC had a point mutation at the third base

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