The p53 network in lung carcinogenesis

Robles, Ana I.; Linke, Steven P.; Harris, Curtis C.

doi:10.1038/sj.onc.1205563

Cited by 134 publications

(99 citation statements)

References 104 publications

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“…Experimental and molecular epidemiological studies have provided evidence for a link between exposure to some carcinogens and a development of cancers harbouring characteristic TP53 mutations (Nagao, 1999;Hussein & Harris, 2000;Hollstein et al 1994;Robles et al 2002;Chan et al 2003). However, the majority of factors causing TP53 mutations remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Geographical Variations in TP53 Mutational Spectrum in Ovarian Carcinomas

Dansonka-Mieszkowska

Ludwig

Kraszewska

et al. 2006

Annals of Human Genetics

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SummaryThe TP53 gene mutational spectrum in human tumours shows variations related to tissue of origin, carcinogen exposure or molecular background. We have compared TP53 mutations in ovarian carcinomas from different geographical regions; this study was based on data extracted and verified from the IARC database (R10, 2005), and on our results from 127 carcinomas. In total 873 mutations were evaluated. Tumours from Japan and Korea had a higher frequency of exon 7 mutations (38% vs 25%, p = 0.011) and lower frequency of exon 8 mutations (11% vs 29%, p = 0.0003) than those from Western countries; they were particularly different from Norwegian tumours which showed the lowest proportion of exon 7 (19%, p = 0.001) and highest proportion of exon 8 (37%, p < 0.0001) mutations. There were also differences in the profile of TP53 hotspots. The third hotspot in tumours from Poland was amino acid (AA) 176 (8.2% of substitutions vs 1.7% in other countries, p < 0.001), while in tumours from the UK it was AA 220 (8.9% vs 2.3%, p < 0.001). Codon 273 was the only apparent hotspot in the Norwegian tumours, while it was rarely mutated in Polish and Asian tumours. In contrast to other data tumours from Norway presented with 273 HIS codon (82% of mutations at AA 273, p = 0.002), while tumours from the UK shared the 273 CYS codon (80%, p < 0.001). Further analysis of TP53 gene mutations in ovarian cancer by geography could provide greater insights.

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Section: Introductionmentioning

confidence: 99%

Geographical Variations in TP53 Mutational Spectrum in Ovarian Carcinomas

Dansonka-Mieszkowska

Ludwig

Kraszewska

et al. 2006

Annals of Human Genetics

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“…Mutations in human cancer are the most frequent in the p53 gene (19). Mutation in the p53 gene is found in 50 % of non-small cell lung cancers and in 90 % of small cell lung cancers (20).…”

Section: Discussionmentioning

confidence: 99%

Chronic effects of environmental biomass smoke on lung histopathology in turkish non-smoking women: a case series

Günbatar

Sertoğullarından

Özbay

et al. 2012

Archives of Industrial Hygiene and Toxicology

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Biomass is widely used for fuel in developing countries. Particles and gases of biomass burning may cause changes in the lung. In this prospective study we investigated histopathological changes in the lungs of 42 non-smoking women [mean age (59±10) years] caused by biomass smoke. We valuated exposure to biomass smoke, case histories, and the fi ndings of physical examination, radiology, bronchoscopy, and lung histopathology. Mean exposure to biomass smoke was (28±9) hour-year (1 hour-year equals 365 hours of exposure per year with average exposure of 1 hour a day). The radiological fi ndings were mass (42 %), reticulonodular opacities (31 %), mediastinal lymphadenopathy (26 %), pleuro-parenchymal fi brotic banding (19 %), widening of the pulmonary artery (14 %), ground glass (11 %), mosaic perfusion (9 %), consolidation (9 %), segmental or subsegmental atelectasis (7 %), and bronchiectasis (7 %). The patients were diagnosed with lung cancer (35 %), interstitial lung disease (31 %), sarcoidosis (9 %), tuberculosis (9 %), chronic obstructive pulmonary disease (4 %), chronic bronchitis (9 %), and metastasis (4 %). Bronchoscopy showed pilies, oedema, erythema, bronchus narrowing, endobronchial tumour, mucosal irregularity, increased vascularisation, blue-black anthracotic plaques, mucosal oedema, and purulent secretion. Transbronchial biopsies revealed neutrophil and lymphocyte leucocytes in the perivascular, peribronchiolar, and interalveolar septa, slightly enlarged connective tissue, thickening of the basal membrane, thickening of interalveolar septa, intimal and medial thickening of the vascular wall and vascular lumen narrowing, anthracosis between the cells and in the bronchiole epithelium. These fi ndings confi rm that biomass smoke has important toxic effects on the lung parenchyma, interstitium, and pulmonary vessels that may result in malignancies.

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“…The precise mechanism underlying the worse OS with the T/T genotype being associated with p53 status remains unknown [32]. However, tumors of MDM2 T/T patients tended to be positive in LVI and pleural invasion (Table 3), which have been reported to be worse prognostic factors associated with tumor proliferation and aggressiveness [33,34].…”

Section: Mdm2 Snp309 and Lung Cancer Prognosesmentioning

confidence: 99%

Prognostic potential of the MDM2 309T>G polymorphism in stage I lung adenocarcinoma

et al. 2016

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The MDM 2 protein plays an important role in the regulation of cell proliferation and apoptosis via ubiquitination and proteasome‐mediated degradation of p53. The genetic polymorphism rs2279744 (c.309T>G) of the MDM 2 gene is reportedly associated with susceptibility and/or prognosis in various cancers. In this study, we investigated the risk factors for worse survival in patients with lung adenocarcinoma ( AC ). We examined the association between c.309T>G and the prognosis of lung cancer by retrospectively reviewing 453 lung cancer patients. We studied both, clinicopathological and genetic characteristics, including the c.309T>G, p53 Arg72Pro, EGFR , KRAS , and p53 mutations. Associations between these factors and survival outcome were analyzed using Cox proportional hazards models. The frequencies of MDM 2 polymorphisms were T/T, 20.8%; T/G, 48.6%, and G/G, 30.7%. The overall survival ( OS ) of AC patients with pathological stage I disease and the MDM 2 T/T genotype was significantly shorter than that of those with the T/G or G/G genotypes ( P = 0.02). Multivariate analysis revealed that the MDM 2 T/T genotype was an independent, significant prognostic factor (hazard ratio [ HR ] = 2.23; 95% confidence interval [ CI ]: 1.07–4.65; P = 0.03). The MDM 2 T/T genotype was predictive of poorer survival in a Japanese population. Genotyping for this polymorphism might predict the clinical outcomes of stage I AC patients.

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The p53 network in lung carcinogenesis

Cited by 134 publications

References 104 publications

Geographical Variations in TP53 Mutational Spectrum in Ovarian Carcinomas

Geographical Variations in TP53 Mutational Spectrum in Ovarian Carcinomas

Chronic effects of environmental biomass smoke on lung histopathology in turkish non-smoking women: a case series

Prognostic potential of the MDM2 309T>G polymorphism in stage I lung adenocarcinoma

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