p53 mutation pattern in hepatocellular carcinoma in workers exposed to vinyl chloride

Weihrauch, Markus; Lehnert, G.; Köckerling, F.; Wittekind, Christian; Tannapfel, Andrea

doi:10.1002/(sici)1097-0142(20000301)88:5<1030::aid-cncr12>3.3.co;2-w

Cited by 5 publications

(7 citation statements)

References 3 publications

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“…However, leaving aside the controversy about epidemiological results, the pathology reports should be appreciated, indicating that VC does not cause cirrhosis but periportal fibrosis and steatohepatitis …”

Section: Discussionmentioning

confidence: 99%

Do occupational exposures to vinyl chloride cause hepatocellular carcinoma and cirrhosis?

Lotti

2017

Liver International

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Controversy exists about the association between occupational exposures to vinyl chloride and hepatocellular carcinoma and cirrhosis. Two large multicentre mortality cohort studies, one American and another European, reported higher mortality for primary cancer of liver and biliary tract. However, the American study was not able to rule out misclassification, because based on death certificates and under the heading primary liver cancers, some angiosarcomas, the typical neoplasia associated with vinyl chloride, may have been included. The American study does not report on cirrhosis mortality. The European study also reports higher mortality of primary liver cancer, but contrary to the American study in a further analysis based on 10 verified cases of hepatocellular carcinoma, an exposure‐response trend with duration of employment and with cumulative exposure to vinyl chloride was detected. A smaller cohort belonging to this multicentre cohort confirmed these results. Meta‐analyses based on the two large cohorts concluded for a small excess of primary liver cancer, although misclassification could not be ruled out. Excess risk of cirrhosis was reported in the European cohort, in a subcohort and in a cross‐sectional study. However, a meta‐analysis did not confirm this excess. Several critical appraisals of the literature reached antithetical conclusions about hepatocellular carcinoma, cirrhosis and occupational exposures to vinyl chloride. For both hepatocellular carcinoma and cirrhosis, a study suggests an additive and multiplicative effect of vinyl chloride exposure with viral hepatitis and alcohol consumption respectively. Pathology reports seem to indicate a possible development of hepatocellular carcinoma but not of cirrhosis after high exposures to vinyl chloride.

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Section: Discussionmentioning

confidence: 99%

Do occupational exposures to vinyl chloride cause hepatocellular carcinoma and cirrhosis?

Lotti

2017

Liver International

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“…The presence of this "hotspot" mutation in patients with HCC who are from Europe, the United States, Japan, and Australia is extremely low; only three mutations (one in Europe and two in Japan) have been identified among 664 patients with HCC analyzed [1,45,53]. Generally, patients who have not been exposed to aflatoxin B 1 or hepatitis virus have a lower prevalence of p53 gene mutations, indicating that other genes involved in the process of hepatocarcinogenesis [56].…”

Section: P53 and Homologuesmentioning

confidence: 99%

Genes involved in hepatocellular carcinoma: deregulation in cell cycling and apoptosis

Tannapfel

Wittekind

2002

Virchows Arch

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Hepatocellular carcinoma (HCC) accounts for 80-90% of liver cancers and is one of the most frequent carcinomas throughout the world. The disease is more prevalent in parts of Africa and Asia than in North and South America and Europe, with a strong etiological association with viral hepatitis, hemochromatosis, known liver (hepatic) carcinogens, and toxins (mycotoxins). Clinical and molecular medical analyses have yielded a considerable amount of information about liver carcinogenesis. Many genes undergo somatic aberrations, with a tendency to cluster at genes involved in cell cycle regulation, in the p53 and Wnt/catenin pathways of signal transduction and cellular adhesion, and in the TGF-beta/IGF axis. Since HCC may arise both in liver cirrhosis and in noncirrhotic liver, one may speculate that different hepatocarcinogenetic pathways exist. Recent results of high-output gene analysis using cDNA microarrays support the idea of different genetic alterations in HCC with or without cirrhosis.

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“…The major etiologies of HCC are now well‐defined and include chronic viral hepatitis B and C, toxins and metabolic liver diseases. Previous studies have reported that the p53 tumor suppressor gene is involved in hepatocarcinogenesis, and that p53 mutation sites and specific DNA base changes differ between the various types of tumors 3,4 . For instance, a unique mutational spectrum in HCC tumors has provided a strong molecular link between carcinogen exposure and cancer development 4,5 .…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies have reported that the p53 tumor suppressor gene is involved in hepatocarcinogenesis, and that p53 mutation sites and specific DNA base changes differ between the various types of tumors 3,4 . For instance, a unique mutational spectrum in HCC tumors has provided a strong molecular link between carcinogen exposure and cancer development 4,5 . The most striking example of a specific mutation in the p53 gene is a G to T transversion in the third base of codon 249, which has been detected in patients with HCC from different geographic areas, such as China and sub‐Saharan Africa, where AFB1 dietary exposure is highly prevalent 5,6 …”

Section: Introductionmentioning

confidence: 99%

The Pro variant of the p53 codon 72 polymorphism is associated with hepatocellular carcinoma in Moroccan population

Ezzikouri

Feydi

Chafik

et al. 2007

Hepatology Research

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p53 mutation pattern in hepatocellular carcinoma in workers exposed to vinyl chloride

Cited by 5 publications

References 3 publications

Do occupational exposures to vinyl chloride cause hepatocellular carcinoma and cirrhosis?

Do occupational exposures to vinyl chloride cause hepatocellular carcinoma and cirrhosis?

Genes involved in hepatocellular carcinoma: deregulation in cell cycling and apoptosis

The Pro variant of the p53 codon 72 polymorphism is associated with hepatocellular carcinoma in Moroccan population

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