Cigarette smoking, genetic polymorphisms and colorectal cancer risk: the Fukuoka Colorectal Cancer Study

Nisa, Hoirun; Kono, Suminori; Yin, Guang; Toyomura, Kengo; Nagano, Jun; Mibu, Ryuichi; Tanaka, Masao; Kakeji, Yoshihiro; Maehara, Yoshihiko; Okamura, Tomonori; Izutsu, Koji; Futami, Kitaroh; Maekawa, Takafumi; Yasunami, Yohichi; Takenaka, Katsuto; Ichimiya, Hitoshi; Terasaka, Reiji

doi:10.1186/1471-2407-10-274

Cited by 50 publications

(46 citation statements)

References 38 publications

(60 reference statements)

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“…Nisa et al showed that lifestyle and genetic factors have played in the role in colorectal carcinogenesis. They studied in comparison genetic of smoker and non-smoker colorectal cancer patients in Fukuoka, Japan used RFLP-MspI PCR Method [6]. CYP genes are member of large families of endoplasmic and cytosolic enzyme genes.…”

Section: B Methods: Pcr-rflpmentioning

confidence: 99%

“…Studies in Japan and other country showed the gene has been associated with a risk of colorectal cancer [6,14,18,19,20,21]. The other researcher was reported that CYP1A1 MspI was contributed to increased cancer susceptibility among Asians.…”

Section: B Methods: Pcr-rflpmentioning

confidence: 99%

“…Epidemiological studies in Europe, Asia, and America have shown this disease is more prevalent in adults aged 45 to 50 years. Furthermore, there is still lack of information about colorectal cancer in Indonesia [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

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Genetic pattern of CYP1A1*2A (T>C) gene in patients with colorectal cancer in South Jakarta – Indonesia

Adhiyanto¹,

Ardini²,

Nisa³

et al. 2017

Proceedings of the 1st International Integrative Conference on Health, Life and Social Sciences (ICHLaS 2017)

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Abstract-The information of relationship between genetics and cancer in Indonesia, especially colon cancer, is still limited. This study aimed to determine the genetic pattern of colon cancer allele in Fatmawati Hospital, Jakarta -Indonesia. We conducted a case-control study of 40 colorectal cancer patients and 133 volunteers as controls. We observed CYP1A1*2A alleles using RFLP-PCR method. Three milliliters of blood was used to isolate DNA. Our observation showed of the genetic patterns CYP1A1*2A with the incidence of colorectal cancer showed 17 patients were variant-type homozygote and 12 patients were heterozygote type. In this research shown the common of genotyping type CYP1A1*2A of colorectal cancer from the patients are a homozygous variant type.

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Section: B Methods: Pcr-rflpmentioning

confidence: 99%

Section: B Methods: Pcr-rflpmentioning

confidence: 99%

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Genetic pattern of CYP1A1*2A (T>C) gene in patients with colorectal cancer in South Jakarta – Indonesia

Adhiyanto¹,

Ardini²,

Nisa³

et al. 2017

Proceedings of the 1st International Integrative Conference on Health, Life and Social Sciences (ICHLaS 2017)

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“…All these compounds are metabolized by microsomal enzymes of phase 1 and 2 of cytochrome P450 (CYP1A), NADPH quinine oxidoreductase-1 (NQO-1), glutathione S-transferase (GST), and sulfotransferases. It has been reported that different expression levels of CYP1A, due to several polymorphisms in this gene, are important criteria in determining a person's risk of lung cancer (54). In India, Shah and colleagues (55) reported that smokers with heterozygous genotypes TG and/or homozygous genotype CC are more prone to develop lung cancer than those with TT genotype.…”

Section: Tobacco and Lung Cancermentioning

confidence: 99%

“…Nicotine, as the main component of cigarette, is found in the urine of smokers (58). The most important and the most abundant gene abnormalities involved in the pathogenesis of bladder cancer are mutations in the FGFR3 and TP53 genes, both of them have been reported to be strongly associated with smoking (54). In addition, XRCC1 gene polymorphism is also regarded as one of the most common genetic changes in bladder cancer associated with smoking (59).…”

Section: Tobacco and Bladder Cancermentioning

confidence: 99%

The Molecular Mechanisms of Tobacco in Cancer Pathogenesis

et al. 2017

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Context: Studies have shown that cancer is a multi-factorial disease in its pathogenesis, in addition to genetic disorders, the effect of environmental factors can also be pointed. Among all environmental factors, tobacco that is considered as the leading cause of respiratory and cardiovascular disease plays a key role in cancer pathogenesis and progression. More than 5,000 chemicals and 62 carcinogenes have been detected in tobacco, which could contribute to tumorgenesis through activating oncogenes, inhibition of tumor suppressor genes, genetic and epigenetic changes, alteration of growth pathways, angiogenesis and metastasis. Evidence Acquisition: To access the articles, we used valid external and internal databases. In order to set the search formula with maximum collectivity, at the first step, the main keywords were characterized and then equivalent terms were identified using various sources. In order to retrieve the last research papers, searches were conducted constantly from 1970 until 2015. The obtained results were screened in terms of relevance and quality indicators such as proper research design, control groups, inclusion and exclusion criteria, and also the statistical analysis. Accordingly, 150 articles were obtained and finally 64 articles which were eligible and had high relevance to the topic were selected and reviewed. Results: This review explains the association between tobacco smoking and the incidence of different human cancers; also it focuses on molecular mechanisms through which carcinogenic chemicals in tobacco smoke promote cancer progression. Among multiple components of tobacco smoke, three carcinogens, including polycyclic aromatic hydrocarbons (PAH), nictotine and nicotin-derived nitrosamine ketone (NNK) convincingly play major roles in the pathogenesis of a wide range of cancers. In fact, these toxic and carcinogenic agents alter the expression of oncogenes, tumor suppressors, DNA repair, and last but not least, apoptosis-related genes through several mechanisms, such as point mutations, deletions, translocations and gene recombination. Moreover, implication of different tumorgenic signal transduction pathways, such as PI3K/AKT, STAT3, ERK1/2 and COX-2 in tobacco-induced tumorgenesis should not be underestimated. Conclusions: Although many facts about the carcinogenic character of tobacco are yet unknown, understanding the molecular mechanisms of cancer development associated with smoking could be promising for early detection, treatment, and reducing metastasis of tobacco-related cancers.

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Copy number variations of GSTT1 and GSTM1, colorectal cancer risk and possible effect modification of cigarette smoking and menopausal hormone therapy

Rudolph¹,

Hein²,

Hoffmeister³

et al. 2012

Intl Journal of Cancer

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Copy number variations (CNVs) of the glutathione-S-transferase y-1 (GSTT1) and glutathione-S-transferase l-1 (GSTM1) gene loci can lead to complete lack of enzyme and have been associated with colorectal cancer (CRC) risk. As GSTs are involved in the detoxification of xenobiotics, CNVs may modify CRC risk associated with smoking exposure and menopausal hormone therapy (MHT) use. We investigated CRC risk associated with GSTT1 and GSTM1 CNVs and their interaction with smoking in 1,796 cases and 1,806 age-, sex-and residence-matched controls from a German population-based case-control study (DACHS). The interaction with MHT was assessed in the subset of 684 postmenopausal female cases and 681 controls. Trimodular genotypes (0/0, 1/0 and 1/1) were determined with relative quantification based on multiplex real-time polymerase chain reaction. The associations with CRC risk as well as possible effect modifications were evaluated using conditional logistic regression analysis. CNVs of GSTT1 and GSTM1 were not significantly associated with CRC risk. Compared to the 1/1 genotype, odds ratios (ORs) for the 0/1 genotype and the 0/0 genotype were 0.89 [95% confidence interval (CI): 0.77-1.04] and 0.97 (95% CI: 0.80-1.18) for GSTT1, and 0.99 (95% CI: 0.78-1.27) and 1.03 (95% CI: 0.81-1.31) for GSTM1. Compared to the nonnull genotype, ORs for the null-genotype were 1.04 (95% CI: 0.87-1.23) for GSTT1 and 1.03 (95% CI: 0.91-1.18) for GSTM1. No significant interaction with smoking and MHT use was observed. Our study does not provide evidence for a strong association between CRC risk and CNVs of GSTT1 or GSTM1 or for an effect modification of smoking or MHT use.Glutathione transferases (GSTs) are a family of enzymes that catalyze the conjugation of glutathione with charged compounds, which leads to detoxification and neutralization of various exogenous and endogenous substances.1 Copy number variations (CNVs), which can lead to decreased enzyme activity and also result in gene deletion and consequently complete lack of enzyme, exist in the glutathione S-transferase l-1 (GSTM1) and glutathione S-transferase y-1 (GSTT1) gene loci. 2,3 . Polymorphisms in the respective genes have been linked to altered cancer susceptibility and drug resistance. 4 In comparison to having at least one gene copy, meta-analyses found for Caucasians an increased risk by 15% and 32% for colorectal cancer (CRC) associated with the null genotype of GSTM1 and GSTT1, respectively. 5-7 However, when differentiated by study design, no association was observed for GSTT1 in population-based studies.6 The majority of the published studies on GSTM1 and GSTT1 polymorphisms and CRC risk used genotyping methods, which were incapable of distinguishing between individuals with one or two copies of the respective genes.8 As trimodular genotype-phenotype correlations for GSTM1 and GSTT1 genes have been observed, 2,3 this is a potential source for inconsistencies. 8 The genetic variation of the GSTs might affect genetic susceptibility for CRC, for example, by modifying the...

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Cigarette smoking, genetic polymorphisms and colorectal cancer risk: the Fukuoka Colorectal Cancer Study

Cited by 50 publications

References 38 publications

Genetic pattern of CYP1A1*2A (T>C) gene in patients with colorectal cancer in South Jakarta – Indonesia

Genetic pattern of CYP1A1*2A (T>C) gene in patients with colorectal cancer in South Jakarta – Indonesia

The Molecular Mechanisms of Tobacco in Cancer Pathogenesis

Copy number variations of GSTT1 and GSTM1, colorectal cancer risk and possible effect modification of cigarette smoking and menopausal hormone therapy

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