p53 mutation hotspot in radon-associated lung cancer

Taylor, Jack A.; Watson, Mary Ann; Michels, Ruth; Saccomanno, Geno; Anderson, Marshall W.; Devereux, Theodora R.

doi:10.1016/s0140-6736(94)90818-4

Cited by 114 publications

(51 citation statements)

References 4 publications

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“…In our cases with NK/T-cell lymphoma, exon 5 is the most common site for mutations, ie, 13 of 30 (43%) mutations occurred in exon 5. Some carcinogens might cause mutation in specific codons, as was observed in the mutation of codon 249 in lung and liver cancers induced by irradiation (Anderson et al, 1995;Taylor et al, 1994). Relatively restricted distribution of mutational spots were found in our cases; codon 273, one of the so-called mutational "hot spots" (Hollstein et al, 1991), was involved in 2 cases, and codons 151, 193, and 251 were involved in 2 or 3 cases.…”

Section: Et Alsupporting

confidence: 58%

Mutations of the p53 Gene in Nasal NK/T-Cell Lymphoma

Hongyo

Syaifudin

et al. 2000

Laboratory Investigation

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SUMMARY:Mutations of the p53 tumor suppressor gene are reported in various kinds of malignancies including lymphomas.However, p53 gene mutations in nasal NK/T-cell lymphoma have not been reported because most parts of tumors are necrotic and a small amount of living tumor tissues is available for the molecular study. Expression and mutations of the p53 gene were examined in the paraffin-embedded specimens of the nasal lesions from 42 Chinese (Beijing and Chengdu) and Japanese (Okinawa and Osaka) patients with nasal NK/T-cell lymphoma by the immunohistochemistry and single strand conformation polymorphism (SSCP) analysis of polymerase chain reaction (PCR) amplified products followed by direct sequencing. Thirty single-nucleotide substitution mutations were observed in 20 of 42 cases (47.6%). Among the 30 mutations, 18 were missense (mainly G:C to A:T transitions), 9 were silent, and 1 was a nonsense mutation. The remaining 2 mutations involved intron 5 and exon 5 terminal points. Abnormal expression of the p53 protein was also observed in 19 of 42 (45.2%) cases. The incidence was significantly (4-fold) higher in the cases of Osaka than those in other areas, although the incidence of p53 mutations in the cases of Osaka was one-half to one-third of those in the other three areas. The results may suggest some racial, environmental, or lifestyle differences in the cause of nasal tumorigenesis. (Lab Invest 2000, 80:493-499).

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Section: Et Alsupporting

confidence: 58%

Mutations of the p53 Gene in Nasal NK/T-Cell Lymphoma

Hongyo

Syaifudin

et al. 2000

Laboratory Investigation

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“…At molecular level, exposure to radon and alpha particles may lead to hypoxanthineguanine phosphoribosyl transferase (hprt) gene mutations that ranged from complete deletion of the gene, partial deletions to gene rearrangements (Lutze et al 1992). Occupational studies on uranium miners also showed that about 31% of lung cancers contained the same mutation at codon 249 of the p53 gene (Vahakangas et al 1992;Taylor et al 1994). These genetic and cytogenetic changes attributed to radon have been reported to be linear and dose-dependent in many in vitro and in vivo experiments.…”

Section: Discussionmentioning

confidence: 97%

Residential Radon and Lung Cancer Risk: An Updated Meta-analysis of Case-control Studies

Zhang¹,

Sun²,

Dong³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background: Numbers of epidemiological studies assessing residential radon exposure and risk of lung cancer have yielded inconsistent results. Methods: We therefore performed a meta-analysis of relevant published casecontrol studies searched in the PubMed database through July 2011 to examine the association. The combined odds ratio (OR) were calculated using fixed-or random-effects models. Subgroup and dose-response analyses were also performed. Results: We identified 22 case-control studies of residential radon and lung cancer risk involving 13,380 cases and 21,102 controls. The combined OR of lung cancer for the highest with the lowest exposure was 1.29 (95% CI 1.10-1.51). Dose-response analysis showed that every 100 Bq/m 3 increment in residential radon exposure was associated with a significant 7% increase in lung cancer risk. Subgroup analysis displayed a more pronounced association in the studies conducted in Europe. Studies restricted to female or non-smokers demonstrated weakened associations between exposure and lung cancer. Conclusions: This metaanalysis provides new evidence supporting the conclusion that residential exposure to radon can significantly increase the risk of lung cancer in a dose-response manner.

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“…The occurrence of p53 mutations has even been associated with a shortened patient survival (Horio et al, 1994), although this finding could not be verified by other authors (Van Zandwijk et al, 1995). Certain p53 mutations appeared to be specific for radon-associated lung cancer (Taylor et al, 1994). The protein product of the p53 gene represents an important tumour suppressor protein that is also detectable in serum (Fontanini et al, 1994).…”

Section: Discussionmentioning

confidence: 97%

p53 protein, EGF receptor, and anti-p53 antibodies in serum from patients with occupationally derived lung cancer

et al. 1999

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The oncogene product epidermal growth factor receptor (EGF-R), the tumour suppressor gene product p53 and anti-p53 antibodies are detectable in the serum of certain cancer patients. Increased levels of some of these products were reported in lung cancer patients after occupational asbestos exposure and after exposure to polycyclic aromatic hydrocarbons or vinylchloride. In the first step, this study investigated the possible diagnostic value of serum EGF-R, p53-protein and anti-p53 antibodies, measured by an enzyme-linked immunosorbent assay, in lung tumour patients. In addition to being investigated on a molecular epidemiological basis, these parameters were examined as biomarkers of carcinogenesis, especially with regard to asbestos incorporation effects or of radon-induced lung cancers. Also, a possible effect of cigarette smoking and age dependence were studied. A total of 116 male patients with lung or pleural tumours were examined. The histological classification was four small-cell cancers, six large-cell cancers, 32 adenocarcinomas, 47 squamous carcinomas, 12 mixed lung carcinomas, five diffuse malignant mesotheliomas and ten lung metastasis of extrapulmonary tumours. Twenty-two lung cancers and all mesotheliomas were related to asbestos, 22 lung cancers were related to ionizing radiation and 61 patients had cigarette smoke-related lung cancer. Besides these patients 50 male patients with non-malignant lung or pleural diseases were included; of the latter eight subjects suffered from asbestosis. Controls were 129 male subjects without any lung disease. No significantly elevated or decreased serum values for p53 protein, EGF-R, or anti-p53 antibodies as a function of histological tumour type, age, or degree and type of exposure (asbestos, smoking, ionizing radiation) could be found. The utility of p53-protein, EGF-R and anti-p53 antibodies as routine biomarkers for screening occupationally derived lung cancers is limited. © 1999 Cancer Research Campaign

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p53 mutation hotspot in radon-associated lung cancer

Cited by 114 publications

References 4 publications

Mutations of the p53 Gene in Nasal NK/T-Cell Lymphoma

Mutations of the p53 Gene in Nasal NK/T-Cell Lymphoma

Residential Radon and Lung Cancer Risk: An Updated Meta-analysis of Case-control Studies

p53 protein, EGF receptor, and anti-p53 antibodies in serum from patients with occupationally derived lung cancer

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