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      Angiotensin-converting enzyme gene insertion/deletion polymorphism is associated with risk of oral precancerous lesion in betel quid chewers

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          Abstract

          To investigate whether angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism is related to the risk of oral precancerous lesions (OPL) in Taiwanese subjects who chew betel quid, a total of 61 betel quid chewers having OPL were compared with 61 asymptomatic betel quid chewers matched for betel quid chewing duration and dosage. The frequency of homozygote for ACE D variant is significantly higher in the case subjects than that of the controls (44.3 vs 24.6%; P=0.0108). The adjusted odds ratio of the D homozygous for the risk of OPL is 8.10 (95% confidence interval (CI)=2.04–32.19, P=0.003). In the allelic base analysis, the D allele is also significantly associated with higher risk of OPL. When grouping the study subjects by smoking status, the association between ACE I/D polymorphism and risk of OPL was only observed in nonsmokers. Our results support the theory that genetic factors may contribute to the susceptibility of OPL and suggest that smoking and genetic factors may be differently involved in the development of OPL.

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          Angiotensin II and renal fibrosis.

          J. Egido, S Mezzano, Rosa Ortega (2001)
          Angiotensin (Ang) II, the main peptide of the renin angiotensin system (RAS), is a renal growth factor, inducing hyperplasia/hypertrophy depending on the cell type. This vasoactive peptide activates mesangial and tubular cells and interstitial fibroblasts, increasing the expression and synthesis of extracellular matrix proteins. Some of these effects seem to be mediated by the release of other growth factors, such as TGF-beta. In experimental models of kidney damage, renal RAS activation, cell proliferation, and upregulation of growth factors and matrix production were described. In some of these models, blockade of Ang II actions by ACE inhibitors and angiotensin type 1 (AT(1)) antagonists prevents proteinuria, gene expression upregulation, and fibrosis, as well as inflammatory cell infiltration. Interestingly, Ang II could also be involved in the fibrotic process because of its behavior as a proinflammatory cytokine, participating in various steps of the inflammatory response: Ang II (1) activates mononuclear cells and (2) increases proinflammatory mediators (cytokines, chemokines, adhesion molecules, nuclear factor kappaB). Finally, Ang II also regulates matrix degradation. These data show that drugs controlling this complex vasoactive peptide are probably one of the best ways of avoiding fibrosis in progressive renal diseases.
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            The precancer risk of betel quid chewing, tobacco use and alcohol consumption in oral leukoplakia and oral submucous fibrosis in southern Taiwan

            C. Lee, Y C Ko, H-L Huang … (2003)
            In areas where the practise of betel quid chewing is widespread and the chewers also often smoke and drink alcohol, the relation between oral precancerous lesion and condition to the three habits is probably complex. To explore such association and their attributable effect on oral leukoplakia (OL) and oral submucous fibrosis (OSF), a gender–age-matched case–control study was conducted at Kaohsiung, southern Taiwan. This study included 219 patients with newly diagnosed and histologically confirmed OL or OSF, and 876 randomly selected community controls. All information was collected by a structured questionnaire through in-person interviews. A preponderance of younger patients had OSF, while a predominance of older patients had OL. Betel quid chewing was strongly associated with both these oral diseases, the attributable fraction of OL being 73.2% and of OSF 85.4%. While the heterogeneity in risk for areca nut chewing across the two diseases was not apparent, betel quid chewing patients with OSF experienced a higher risk at each exposure level of chewing duration, quantity and cumulative measure than those who had OL. Alcohol intake did not appear to be a risk factor. However, cigarette smoking had a significant contribution to the risk of OL, and modified the effect of chewing based on an additive interaction model. For the two oral premalignant diseases combined, 86.5% was attributable to chewing and smoking. Our results suggested that, although betel quid chewing was a major cause for both OL and OSF, its effect might be difference between the two diseases. Cigarette smoking has a modifying effect in the development of oral leukoplakia.
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              Mistyping ACE heterozygotes.

              V. Shanmugam, K Sell, Kalyan Saha (1993)
              Article 0 comments Cited 46 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Br J Cancer
                Title: British Journal of Cancer
                Publisher: Nature Publishing Group
                ISSN (Print): 0007-0920
                ISSN (Electronic): 1532-1827
                Publication date (Electronic): 05 September 2005
                Publication date (Print): 05 September 2005
                Volume: 93
                Issue: 5
                Pages: 602-606
                Affiliations
                [1 ]Department of Clinical Research, Pingtung Christian Hospital, Pingtung 900, Taiwan
                [2 ]Graduate Institute of Dental Sciences, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
                [3 ]Graduate Institute of Oral Health Sciences, College of Dental Medicine, Kaohsiung Medical University, No. 100, Shih-Chuan 1st Road, Kaohsiung 807, Taiwan
                [4 ]Statistical Analysis Laboratory, Department of Clinical Research, Kaohsiung Medical University Chung-Ho Memorial Hospital, Kaohsiung 807, Taiwan
                Author notes
                [* ]Author for correspondence: tiyush@ 123456kmu.edu.tw
                Article
                Publisher Item ID: 6602746
                DOI: 10.1038/sj.bjc.6602746
                PMC ID: 2361601
                PubMed ID: 16136034
                SO-VID: ae0598ab-56d9-42fd-afcf-68553ff7c0c3
                Copyright © Copyright 2005, Cancer Research UK
                History
                Date received : 22 April 2005
                Date revision received : 08 July 2005
                Date accepted : 13 July 2005
                Categories
                Subject: Epidemiology

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: oral precancerous lesions,betel quid,angiotensin-converting enzyme
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: oral precancerous lesions, betel quid, angiotensin-converting enzyme

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