Cigarette smoking and p53 mutations in lung cancer and bladder cancer.

Husgafvel‐Pursiainen, Kirsti; Kannio, Annamaria

doi:10.1289/ehp.96104s3553

Cited by 31 publications

(24 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, a few studies showed no obvious correlation between the types and/or frequencies of p53 mutations in bladder tumors and the patients' smoking history (52,53). In lines with several previous findings (5,(10)(11)(12)(13)50,54), the majority of p53 mutations in our study were G:C-A:T transitions (62.9%), followed by transversions (34.3%), and occurred throughout exons 4 to 8. Furthermore, eight of the mutations in our study occurred at the same codons as those reported by Stern et al (50), including a CGG-TGG transition at codon 282 and a CGG-CAG transition at codon 248 that were identified in both studies.…”

Section: ------------------------------------------------------------supporting

confidence: 93%

“…There have been several studies investigating the relationship between polymorphisms of DNA repair genes, specifically XPD and XRCC1 (28,29,(31)(32)(33)(34)(35)46,47), and the role of p53 mutations (10)(11)(12) in bladder cancer. Given the lack of direct functional measures of DNA repair capacity associated with the different polymorphisms, it is difficult to integrate the sometime divergent results of the existing studies on XPD and XRCC1.…”

Section: ------------------------------------------------------------mentioning

confidence: 99%

“…Within bladder tumors, the frequency of p53 mutations is between 15 and 60% (11)(12)(13)(14). The origin(s) and mechanism of formation of these mutations in bladder cancer are unclear.…”

Section: Introductionmentioning

confidence: 99%

“…There have been a number of studies investigating the prevalence of p53 mutations and their role in bladder cancer risk (10)(11)(12). A few studies have reported the relationship between polymorphisms of DNA repair genes, specifically XPD and XRCC1, and bladder cancer risk (28,29,(31)(32)(33)(34)(35)38,39).…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Genetic polymorphisms in the DNA repair genes XPD and XRCC1, p53 gene mutations and bladder cancer risk

Gao

Romkes²,

Zhong³

et al. 2010

Oncol Rep

View full text Add to dashboard Cite

Abstract. Previous studies have suggested that certain genetic polymorphisms, specifically the Xeroderma pigmentosum group D (XPD) gene codon 751 and the X-ray repair crosscomplementing group 1 (XRCC1) gene codon 399 polymorphisms, were associated with an increased risk of lung cancer, and, in some studies, with a greater risk for mutations in the p53 tumor suppressor gene in lung tumors. To evaluate whether these gene polymorphisms may be associated with an increased risk for bladder cancer or in association with p53 mutation status in bladder tumors, we screened for polymorphisms at XPD codons 751 and XRCC1 codon 399 in DNA isolated from blood of 194 bladder cancer patients and 313 healthy controls and for mutations in exons 4 to 8 of the p53 gene in bladder tumor DNA from 174 bladder cancer patients. There was a significantly higher prevalence of the XPD 751 Gln allele among the bladder cancer group, compared with the control group. No association was found between bladder cancer risk and the XRCC1 399 polymorphism. p53 mutations were found in 20.1% (35/174) patients. There was no difference in p53 mutation status among individuals with different genotypes. These results suggest that individuals who have the XPD 751 Gln allele may be at an increased risk for bladder cancer, although this may not lead to an increased risk for mutations in the p53 gene.

show abstract

Section: ------------------------------------------------------------supporting

confidence: 93%

Section: ------------------------------------------------------------mentioning

confidence: 99%

“…Within bladder tumors, the frequency of p53 mutations is between 15 and 60% (11)(12)(13)(14). The origin(s) and mechanism of formation of these mutations in bladder cancer are unclear.…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Genetic polymorphisms in the DNA repair genes XPD and XRCC1, p53 gene mutations and bladder cancer risk

Gao

Romkes²,

Zhong³

et al. 2010

Oncol Rep

View full text Add to dashboard Cite

show abstract

“…Their potent carcinogenic capability is primarily mediated by imposing genotoxic stress and damage in host cells. For example, formation of DNA adducts is frequently induced, which results in loss-of-function mutation in tumor suppressor genes, such as p53 (39,(45)(46)(47)(48). p53 is a well-established master regulator for the DNA repair response, cell cycle checkpoint and apoptosis, and numerous studies have implicated a long-standing association between the high incidence of its perturbed expression or function and the development of various types of cancer (49,50).…”

Section: Discussionmentioning

confidence: 99%

Pathogenic mechanisms of lung adenocarcinoma in smokers and non-smokers determined by gene expression interrogation

Chen

2015

Oncology Letters

View full text Add to dashboard Cite

Abstract. Cigarette smoking is the leading risk factor for lung cancer, which accounts for the highest number of cancer-related mortalities worldwide in men and women. Individuals with a history of smoking are 15-30 times more likely to develop lung cancer compared with those who do not smoke. However, our understanding of the underlying molecular mechanisms that contribute to lung tumorigenesis in smokers versus non-smokers remains incomplete. In order to investigate such mechanisms, the present study aimed to systemically interrogate microarray datasets from tumor biopsies and matching normal tissues from stage I and II lung adenocarcinoma patients who had never smoked or were current smokers. The gene expression analysis identified 422 (99 upregulated and 323 downregulated) and 534 (174 upregulated and 360 downregulated) differentially-expressed genes from the never-smokers and current smokers, respectively, and the two groups shared 277 genes that exhibited similar trends of alteration. These genes encode regulators that are involved in a variety of cellular functions, including collagen metabolism and homeostasis of caveolae plasma membranes. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes characterization indicated that biological pathways, including extracellular matrix-receptor interaction and cell migration and proliferation, were all affected in the lung cancer patients regardless of the smoking status. However, smoking induced a unique gene expression pattern characterized by upregulation of cell cycle regulators (CDK1, CCNB1 and CDC20), as well as significantly affected biological networks, including p53 signaling pathways. Taken together, these findings suggest novel mechanistic insights, and provide an improved understanding of the smoking-induced molecular alterations that contribute to the pathogenesis of lung adenocarcinoma.

show abstract

TSLP and TSLP receptors variants are associated with smoking

Semlali

Almutairi

Azzi

et al. 2019

Molec Gen & Gen Med

View full text Add to dashboard Cite

Background To search for new prevention markers for early detection of the diseases caused by tobacco, we aimed to investigate the polymorphisms in TSLP and TSLPRs associated with cigarette smoking in the Saudi population. Materials and methods Samples were collected from 177 smokers and 126 healthy controls. Three TSLP SNPs [rs3806933, rs2289276, and rs10043985], three TSLPR SNPs [rs36133495, rs36177645, and rs36139698], and two IL7R SNPs rs1053496 and rs12516866 were analyzed by genotyping. Results Two TSLP SNPs (rs10043985 and rs3806933) and one TSLPR SNP (rs36139698) showed significant correlations with smoking behavior, but not IL7R rs12516866 and rs1053496. rs10043985 showed a clear association with long‐term smoking regardless of daily cigarette consumption. rs2289276 was associated with short‐term smoking but not with daily cigarette consumption. rs3806933 was highly associated with different smoker subgroups. Rs36139698 was highly associated with long‐term smokers who consumed ≥20 cigarettes/day, and the “T” allele was associated only with individuals who smoked ≤20 cigarettes/day. Rs36139698 corresponds to a P195L substitution and produces a TSLPR mutant with a predicted ΔΔG increase of 2.15 kcal/mol and has a more stable structure than the wild‐type variant. Conclusions Investigating TSLP and TSLPR polymorphisms is crucial for elucidating the mechanisms underlying tobacco‐induced diseases.

show abstract

Cigarette smoking and p53 mutations in lung cancer and bladder cancer.

Cited by 31 publications

References 22 publications

Genetic polymorphisms in the DNA repair genes XPD and XRCC1, p53 gene mutations and bladder cancer risk

Genetic polymorphisms in the DNA repair genes XPD and XRCC1, p53 gene mutations and bladder cancer risk

Pathogenic mechanisms of lung adenocarcinoma in smokers and non-smokers determined by gene expression interrogation

TSLP and TSLP receptors variants are associated with smoking

Contact Info

Product

Resources

About