Strong association between the GSTM1-null genotype and lung cancer in a Turkish population

Pınarbaşı, Hatice; Siliğ, Yavuz; Çetinkaya, Öge; Seyfıklı, Zehra; Pınarbaşı, Ergün

doi:10.1016/s0165-4608(03)00059-1

Cited by 35 publications

(25 citation statements)

References 15 publications

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“…In a Japanese population, the GSTM1 null genotype was positively correlated with squamous cell carcinoma of the lung, although not with adenocarcinoma (Kihara et al, 1993). Similar analysis in a Finnish population again demonstrated a correlation of the GSTM1 null genotype with squamous cell cancer, as well as in Scottish, Norwegian, and Turkish populations (Zhong et al, 1991;Hirvonen et al, 1993;Ryberg et al, 1997;Pinabasi et al, 2003). However, data are not consistent and some studies have shown a lack of significant association between the GSTM1 null genotype and lung cancer risk for both squamous cell carcinoma and overall lung cancer (London et al, 1995;Rebbeck, 1997).…”

Section: Carcinogen Metabolismmentioning

confidence: 80%

Genetic susceptibility to tobacco-related cancer

et al. 2004

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Although cigarette smoking is the dominant risk factor for several epithelial cancers, only a small fraction of individuals with tobacco exposure develop cancer. The underlying hypothesis is that genetic factors may render certain smokers more susceptible to cancer than others. Genetic alterations in critical regulatory pathways may predispose cells to carcinogenesis. These pathways include regulation of xenobiotic metabolism; control of genomic stability, including DNA repair mechanisms, cell-cycle checkpoints, apoptosis and telomere length; and control of microenvironmental factors, such as matrix metalloproteinases, inflammation and growth factors. In addition, epigenetic events, such as promoter hypermethylation and loss of imprinting, are also involved in carcinogenesis. In this review, we will summarize recent advances in genetic susceptibility to tobacco-related cancer. Emphasizing on risk assessment, we will describe how genetic variations in the above-mentioned genetic pathways modify the tobacco-related cancer risk. In addition, we will discuss how genetic variations may assist in predicting clinical outcome, such as the natural history of cancer and treatment response. The measurements of genetic susceptibility by both genotypic and phenotypic assays are covered in the text. Finally, we present a number of current concerns that need to be addressed as the exciting field of molecular cancer epidemiology advances rapidly.

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Section: Carcinogen Metabolismmentioning

confidence: 80%

Genetic susceptibility to tobacco-related cancer

et al. 2004

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“…Several case-control studies conducted in countries of diverse ethnicities were published later. Four in 10 found an overall positive association with lung cancer (29,(32)(33)(34), whereas the others were negative for an association (23,(35)(36)(37)(38)(39)(40). When exposure to environmental carcinogens was taken into account, effect modification was found in some but not all studies.…”

Section: Discussionmentioning

confidence: 99%

GSTM1andCYP1A1Polymorphisms, Tobacco, Air Pollution, and Lung Cancer: A Study in Rural Thailand

Pisani

Srivatanakul

Randerson-Moor

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Objectives: The Lampang Province is situated in the northern region of Thailand. Incidence rates of lung cancer are high for Asian standards, particularly in women. This study was conducted to quantify the risk of lung cancer associated with exposures prevalent in the area and to investigate possible interactions with genetic susceptibility. The presence of several large open-cast coal mines from 1955 close to electricity-generating plants was a particular focus of concern. Methods: Two-hundred and eleven cases of primary lung cancers diagnosed in 1993 to 1995 and residents in the province were recruited at the Lampang Provincial Hospital (main referral center for treatment of the disease). Two sets of controls, frequency-matched to the cases by sex and age, were recruited (a) from the resident population (202 interviewed) and (b) from patients admitted to the hospital for diseases predominantly unrelated to tobacco smoking (211 interviewed). Sociodemographic information, complete residential history, and characteristics of the household (place of cooking, cooking fuel, and heating fuels), occupational history, and history of tobacco smoking were obtained by interview. Cases and controls (f50% of the populationbased series) provided a blood sample. A point source air pollution exposure index was calculated for each village/ township reported in residential histories based on the linear distance from the Mae Moh Center (the area of the electricity-generating plants), the year-specific gaseous (SO 2 and NO 2 ) or total suspended particulate emissions from the Mae Moh Power Plant, and the percentage of wind from the center. Odds ratios (OR) for the disease associated with categorical variables were estimated within unconditional logistic regression. Extraction of genomic DNA and genotyping of variants in CYP1A1 and GSTM1 were conducted to assess the extent of modification of risk by these genes that are involved in the metabolism of polycyclic aromatic hydrocarbons, a common component of the exposures. Results: Overall, there was no evidence of relevant differences in the socioeconomic level of the three groups. The two control sets were similar with respect to lifelong tobacco habit and were subsequently pooled in analyses. Neversmokers were 7% of men and 33% of women. Smoking of local traditional products unfiltered and high in tar content is a common habit in the rural female population. ORs associated with smoking increased with duration of the habit and average daily amount, being 4.9 [95% confidence interval (95% CI), 2.5-9.7] for smokers of z7 cigarettes/d and 3.3 (95% CI, 1.7-6.2) for duration of 41 years or longer compared with nonsmokers. Smoking of local products was associated with an independent OR of 3.1 (95% CI, 1.7-5.6) adjusted for lifelong cumulative amount of tobacco smoked. Although most smokers had the habit for at least 16 years, the daily consumption was low compared with Western standards. Other potential sources of exposure to lung carcinogens (emission from the power-generating pla...

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“…In addition to bladder cancer, increased risk of other tumors including those of the esophagus, lung, and prostate (40)(41)(42)(43)(44) have been associated with polymorphisms in these genes. These findings would agree with the notion that susceptibility alleles may increase the risk of different types of cancer within families.…”

Section: Discussionmentioning

confidence: 99%

Risk of Bladder Cancer Associated with Family History of Cancer: Do Low-Penetrance Polymorphisms Account for the Increase in Risk?

Murta-Nascimento

Silverman

Kogevinas

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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The relationship between family history of cancer in firstdegree relatives and risk of bladder cancer was examined in the Spanish Bladder Cancer Study. Information on family history of cancer was obtained for 1,158 newly diagnosed bladder cancer cases and 1,244 controls included in 18 hospitals between 1998 and 2001. A total of 464 (40.1%) cases and 436 (35.1%) controls reported a family history of cancer in z1 relative [odds ratio (OR), 1.32; 95% confidence interval (95% CI), 1.11-1.59]; the OR was 1.23 (95% CI, 1.01-1.50) among those with only one relative affected and 1.67 (95% CI, 1.23-2.29) among those with z2 affected relatives (P trend = 0.0004). A greater risk of bladder cancer was observed among those diagnosed at age V45 years (OR, 2.67; 95% CI, 1.10-6.50) compared with those diagnosed over age 45 years (OR, 1.27; 95% CI, 1.06-1.52). The OR of bladder cancer among subjects reporting a family history of cancer of the bladder was 2.34 (95% CI, 0.95-5.77). Statistically significant associations emerged between bladder cancer risk and family history of cancer of the esophagus, lung, prostate, and brain. The OR of bladder cancer for those reporting family history of bladder cancer was 4.76 (95% CI, 1.25-18.09) among NAT2-slow acetylators and 1.17 (95% CI, 0.17-7.86) among NAT2-rapid/ intermediate acetylators (P interaction = 0.609). Among individuals with GSTM1 null and present genotypes, the corresponding ORs were 2.91 (95% CI, 0.44-19.09) and 4.21 (95% CI, 1.26-14.14), respectively (P interaction = 0.712). Limitations of our study are small sample size in subgroup analyses, reliability of family history data, and possible residual confounding by shared environmental exposures. Overall, our findings support the hypothesis that genetic factors play a role in bladder cancer etiology. Whether these correspond to low-penetrance cancer-predisposing polymorphisms acting together and/or interacting with environmental factors warrants further research. (Cancer Epidemiol Biomarkers Prev 2007;16(8):1595 -600)

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Strong association between the GSTM1-null genotype and lung cancer in a Turkish population

Cited by 35 publications

References 15 publications

Genetic susceptibility to tobacco-related cancer

Genetic susceptibility to tobacco-related cancer

GSTM1andCYP1A1Polymorphisms, Tobacco, Air Pollution, and Lung Cancer: A Study in Rural Thailand

Risk of Bladder Cancer Associated with Family History of Cancer: Do Low-Penetrance Polymorphisms Account for the Increase in Risk?

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