Risk Factors and Gene Expression in Esophageal Cancer

Xu, Xiao Chun

doi:10.1007/978-1-59745-416-2_17

Cited by 38 publications

(42 citation statements)

References 117 publications

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“…Therefore, aberrant methyl transfer caused by the inhibition of SAM synthesis may be important for alcohol-mediated carcinogenesis [3]. Retinoic acid (RA) regulates the transcription of many genes that are important for cellular growth and differentiation by signaling through its nuclear receptors (RARs) [7]. Chronic alcohol consumption decreases RA concentrations in the liver by inducing CYP2E1 [33].…”

Section: Well-established Carcinogens In Alcohol and Its Metabolitesmentioning

confidence: 99%

“…Cigarette smoking and alcohol consumption are considered to be significant risk factors for esophageal squamous cell carcinoma (ESCC) [7][8][9]. Various kinds of genetic abnormalities have been investigated in ESCC, including the activation of oncogenes and inactivation of tumor-suppressor genes, and a large body of knowledge has been obtained concerning esophageal carcinogenesis [10,11].…”

Section: Introductionmentioning

confidence: 99%

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Alcohol drinking, cigarette smoking, and the development of squamous cell carcinoma of the esophagus: molecular mechanisms of carcinogenesis

et al. 2010

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Esophageal cancer is the eighth most common incident cancer in the world and ranks sixth among all cancers in mortality. Esophageal cancers are classified into two histological types; esophageal squamous cell carcinoma (ESCC), and adenocarcinoma, and the incidences of these types show a striking variety of geographic distribution, possibly reflecting differences in exposure to specific environmental factors. Both alcohol consumption and cigarette smoking are major risk factors for the development of ESCC. Acetaldehyde is the most toxic ethanol metabolite in alcohol-associated carcinogenesis, while ethanol itself stimulates carcinogenesis by inhibiting DNA methylation and by interacting with retinoid metabolism. Cigarette smoke contains more than 60 carcinogens and there are strong links between some of these carcinogens and various smoking-induced cancers; these mechanisms are well established. Synergistic effects of cigarette smoking and alcohol consumption are also observed in carcinogenesis of the upper aerodigestive tract. Of note, intensive molecular biological studies have revealed the molecular mechanisms involved in the development of ESCC, including genetic and epigenetic alterations. However, a wide range of molecular changes is associated with ESCC, possibly because the esophagus is exposed to many kinds of carcinogens including alcohol and cigarette smoke, and it remains unclear which alterations are the most critical for esophageal carcinogenesis. This brief review summarizes the general mechanisms of alcohol- and smoking-induced carcinogenesis and then discusses the mechanisms of the development of ESCC, with special attention to alcohol consumption and cigarette smoking.

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Section: Well-established Carcinogens In Alcohol and Its Metabolitesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Alcohol drinking, cigarette smoking, and the development of squamous cell carcinoma of the esophagus: molecular mechanisms of carcinogenesis

et al. 2010

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“…More than 80% of EC cases in China are squamous cell carcinoma, but the majority in the West are adenocarcinoma (Lambert et al, 2007). The risk factors for EC in Chaoshan are smoking, alcohol consumption, and drinking or eating at high temperatures (Xu et al, 2009;Lin et al, 2011). The risk factors for EC in the West are gastroesophageal reflux disease and Barrett's esophagus (Rastogi et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Saliva Supernatant miR-21: a Novel Potential Biomarker for Esophageal Cancer Detection

Xie¹,

Chen²,

Zhang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Objective: To identify whether saliva supernatant miR-21 can serve as a novel potential biomarker in patients with esophageal cancer (EC). Methods: 32 patients with EC and 16 healthy controls were recruited in this study. Total RNA was extracted from saliva supernatant samples for measurement of miR-21 levels using RT-qPCR and relationships between miR-21 levels and clinical characteristics of EC patients were analyzed. Results: miR-21 was significantly higher in the EC than control groups. The sensitivity and specificity were 84.4% and 62.5% respectively. Supernatant miR-21 levels showed no significant correlation with cancer stage, differentiation and nodal metastasis. Conclusions: Saliva supernatant miR-21 may be a novel biomarker for EC.

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“…In addition to nAchR, nicotine could also bind to EGFR and AR-β and acts as a growth factor. Epidermal growth factor receptor (EGFR) is a tyrosine kinase receptor and plays an important role in growth, development, and tumorgenesis (40). NNK contributes to cancer cell proliferation not only by synthesis of thromboxane A2 (TXA2), but also by activating TXA2 receptor, as well.…”

Section: Tobacco and Growth Signaling Pathwaysmentioning

confidence: 99%

“…It seems that cyclooxygenase-2 (COX-2) elevates both angiogenesis and aggressive potential of tumor cells by increasing the production of prostaglandins and converting the pre-cancerous agents to carcinogens. It is demonstrated that nicotine increases metastasis of esophageal carcinoma by up-regulating and enhancing the activity of both MMP-2 and COX-2 (40). In another study, it is shown that nicotine plays an important role in migration of tumor cells mostly via increasing the expression of several chemokines/chemokine receptors, such as CXCR2, CXCR3, CXCR4 and CCL12 (50).…”

Section: The Impact Of Tobacco On Angiogenesis and Cancer Metastasismentioning

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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Risk Factors and Gene Expression in Esophageal Cancer

Cited by 38 publications

References 117 publications

Alcohol drinking, cigarette smoking, and the development of squamous cell carcinoma of the esophagus: molecular mechanisms of carcinogenesis

Alcohol drinking, cigarette smoking, and the development of squamous cell carcinoma of the esophagus: molecular mechanisms of carcinogenesis

Saliva Supernatant miR-21: a Novel Potential Biomarker for Esophageal Cancer Detection

The Molecular Mechanisms of Tobacco in Cancer Pathogenesis

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