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The CYP2A13 Arg257Cys Polymorphism and its Relationship to Lung Cancer
Published in Cut Adeya Adella, Stem Cell Oncology, 2018
N.N. Soeroso, B.Y.M. Sinaga, R. Zain-Hamid, A.H. Sadewa, E. Syahruddin
This research failed to confirm the association between genetic polymorphism of CYP2A13 Arg257Cys and lung cancer susceptibility. Of all 25 cases and 25 controls, the combined genotype frequency of CT and TT was found to be 32% and 24% respectively (Table 2). Chi-square analysis revealed that there was no significant association between genetic polymorphism CYP2A13 Arg257Cys and lung cancer susceptibility (OR 0.67; 95% CI 0.19-2.32; p = 0.52). Figure 1 shows that the Arg257Cys mutation eliminates an Hhal cleavage site (Cheng et al., 2004).
Respiratory Tract Cancer
Published in Peter G. Shields, Cancer Risk Assessment, 2005
So far the polymorphic genes most studied in lung cancer include CYP1A1, CYP2E1, CYP2D6 (Table 1), and the phase II genes GSTM1, GSTP1, NAT2 and EPHX (Table 2). At least four polymorphic variants of the CYP1A1 gene have been identified, two of which are thought to result in increased enzyme activity. Japanese studies have shown that high susceptibility to lung cancer is associated with CYP1A1 gene polymorphisms (homozygosity for the rare MspI allele (m2 variant), and exon 7 substitution (Val allele) (34). The association has not been confirmed in European and North American studies. The CYP1A1 genotype frequencies like many other genes show inter-ethnic differences. The frequency of the m2 and Val variant is much less in Caucasians and it will require about 500–1000 cases to study the association in this ethnic population. This lung cancer susceptibility is dependent on the cigarette dose, showing a high relative risk at low dose level of cigarette smoking for individuals with susceptible genotypes (35,36). However, further studies are required in this area since the MspI and the exon 7 polymorphisms are not strictly linked and large differences in catalytic activities for these different alleles have not been shown.
Molecular Biology of Lung Cancer as the Basis for Targeted Therapy
Published in Kishan J. Pandya, Julie R. Brahmer, Manuel Hidalgo, Lung Cancer, 2016
Oliver Gautschi, Philip C. Mack, Jim Heighway, Paul H. Gumerlock, David R. Gandara
Only a relatively low percentage (10–20%) of smokers develop lung cancer, suggesting the presence of genetic factors that modify individual susceptibilities to various carcinogens. The aforementioned TP53 is frequently somatically mutated in lung cancer, but lung cancer only occasionally occurs in families with the Li–Fraumeni syndrome (the majority of which are segregating constitutional TP53 mutations), suggesting that TP53 is not a high penetrance lung cancer susceptibility gene (37). On the other hand, several low penetrance single nucleotide polymorphisms (SNPs) of genes involved in DNA repair and detoxification have been shown to alter lung cancer risk in smokers, including the cytochrome, gluta-thione S-transferase and nicotinamide adenine dinucleotide (NADH)-transferase genes, MGMT, XPD, and XRCC1 (38). SNPs of genes involved in cell cycle control and mitosis have also been reported in this context. The CCND1 A870G gene polymorphism has been correlated with the early onset of lung cancer, as described in our work on smoking-induced lung cancer risk (39). The CCND1 polymorphism modulates alternative splicing of the primary CCND1 transcript, which leads, on translation, to two different CCND1 proteins (CCND1a and CCND1b) (40). CCND1 is frequently overexpressed in tumor cells. CCND1a transfers from the cytoplasm to the nucleus upon activation by CDKs. CCND1b, however, is constitutively nuclear in localization because it lacks a residue that is required for nuclear export (41). As demonstrated in model systems, CCND1b has increased oncogenic potential and this may explain why the A870G genotype modifies disease risk and/or clinical outcome across a range of malignancies, including lung cancer.
Vitamin D and Lung Cancer; Association, Prevention, and Treatment
Published in Nutrition and Cancer, 2021
Weijie Wang, Wentao Hu, Shihang Xue, Qi Chen, Yongsheng Jiang, Haina Zhang, Wei Zuo
Lung cancer is the most prevalently diagnosed type of malignancy in the general population and the leading cause of cancer-related mortality all over the globe (1, 2). That notwithstanding, there are distinct diversities in the onset or incidence of lung cancer as well as related mortality in accordance with geographical region (3). Currently, the precise etiopathogenesis of lung cancer is obscure; nonetheless, several environmental, genetic, and epigenetic factors have been implicated in lung cancer as well as a wide range of diseases (4–9). As an environmental factor, epidemiological studies have reported that smoking is the most strongly associated element in the development of lung cancer (10, 11). In addition, several predisposing factors of lung cancer to enumerate are air pollutions, infections, environmental carcinogens, and even dietary deficiencies (12, 13). Genetic risk factors have also been associated with susceptibility to lung cancer, as big genome-wide association studies (GWAS) have recognized many genetic risk loci in association with increased risk of lung cancer susceptibility (14, 15).
Genetic polymorphism of Arg213His variant in the SULT1A1 gene is associated with reduced susceptibility to lung cancer in North Indian population
Published in Xenobiotica, 2021
Harleen Kaur Walia, Navneet Singh, Siddharth Sharma
Tobacco smoking is considered a noteworthy risk factor for the development of lung cancer. 90% of lung cancer cases diagnosed are solely ascribed due to smoking (de Groot et al. 2018). SULT1A1, a phase II detoxification enzyme, plays a vital role in the detoxification of carcinogens present in cigarettes and hazardous chemicals (Wang et al. 2008). It has been postulated that polymorphism in the genes that code for carcinogen metabolizing enzymes might affect the individual’s susceptibility towards initiation of cancer. In this North Indian case-control study, we evaluated if there might be a correlation between SULT1A1 Arg213His polymorphism and risk of lung cancer in North Indian patients undergoing platinum based-doublet chemotherapy. In our study, the three different genetic models (co-dominant, dominant and recessive) were used to explore the correlations between SULT1A1 variants towards lung cancer susceptibility.
High diagnostic value of miRNAs for NSCLC: quantitative analysis for both single and combined miRNAs in lung cancer
Published in Annals of Medicine, 2021
Minhan Yi, Zexi Liao, Langmei Deng, Li Xu, Yun Tan, Kun Liu, Ziliang Chen, Yuan Zhang
Lung cancer (LC) is a type of malignant neoplasm arising from bronchial mucosa or glands which accounts for the largest proportion of cancer globally in consideration of patient quantity as well as mortality [1, 2]. Histologically, LC is categorized as small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC) which is further classified as adenocarcinoma (AD), squamous cell carcinoma (SCC) and large cell carcinoma (LCC) [3]. NSCLC, accounting for 80–85% of LC, harbours specific molecular and genetic characteristics [4], indicating the likelihood to distinguish NSCLC from other subtypes of LC under the help of particular biomarkers. We have identified the association between interleukin polymorphisms and protein levels with lung cancer susceptibility as well as phenotypes in our previous study [5]. Current challenges lying on its early diagnosis: lung tissue biopsy, being regarded as “gold standard”, has to be done through invasive bronchoscopy or surgical excision [4]; CT [6] as well as PET-CT [7] are widely applied in the definition of TNM stage in NSCLC, which still lacks specific diagnostic directivity towards NSCLC. Novel diagnostic methods such as the detection of circulating tumour cells or other circulating biomarkers [8] need further confirmation [9]. Among all possible biomarkers under research, microRNAs (miRNAs) are considered to be one of the most promising objects in terms of early detection of NSCLC [10].