2010
DOI: 10.1016/j.oraloncology.2010.08.009
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Influence of genetic polymorphisms on frequency of micronucleated buccal epithelial cells in leukoplakia patients

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Cited by 36 publications
(24 citation statements)
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“…However, contrary to our results, some studies reported that CYP1A1 m1 and m2 variants did not show any effect on DNA damage among coke-oven and graphide electrode workers (Marczynski et al, 2002;Chen et al, 2006;Moretti et al, 2007). Mahimkar et al (2010) found no association of CYP1A1 gene polymorphism with MN in exfoliated buccal cells in leukoplakia patients.…”
Section: Discussioncontrasting
confidence: 99%
“…However, contrary to our results, some studies reported that CYP1A1 m1 and m2 variants did not show any effect on DNA damage among coke-oven and graphide electrode workers (Marczynski et al, 2002;Chen et al, 2006;Moretti et al, 2007). Mahimkar et al (2010) found no association of CYP1A1 gene polymorphism with MN in exfoliated buccal cells in leukoplakia patients.…”
Section: Discussioncontrasting
confidence: 99%
“…Several cytogenetic endpoints have been extensively used for bio-monitoring of human exposure to carcinogenic substances [26,29], with the increase in MNC being considered as predictive of an elevated cancer risk [15][16][17]30]. According to Holland et al [11], buccal epithelial cells represent a recognized target site for early genotoxic events induced by carcinogenic substances that enter the body via inhalation or ingestion.…”
Section: Discussionmentioning
confidence: 99%
“…Micronuclei in exfoliated buccal epithelial cells emerge during mitosis of the basal layers of the epithelium as extra-chromosomal DNA particles, when chromosome fragments or whole chromosomes lag behind and fail to be included in the main nuclei of the daughter cells, as a result of a clastogenic or aneugenic events [11,12]. Micronuclei in epithelial cells reflect genotoxic events occurring in the dividing basal cell layer of the putative target organ 1-3 weeks earlier [13,14], which allows for cytogenetic surveillance of groups at high risk of developing organ-specific cancer (e.g., upper aerodigestive tract) or oral premalignant lesions [15][16][17]. Chromosomal damage in epithelial cells also leads to nuclear anomalies other than micronuclei, such as karyorrhexis, karyolysis, pyknosis, condensed chromatin, 'broken eggs' and bi-nucleated cells [11,18].…”
Section: Introductionmentioning
confidence: 99%
“…Several cytogenetic endpoints have been extensively used for biomonitorization of human exposure to carcinogenic substances (Ceppi et al, 2010;Knudsen and Hansen, 2007), being the increase in MNC considered predictive of elevated cancer risk (Bloching et al, 2000;Bonassi et al, 2007;Mahimkar et al, 2010;Saran et al, 2008). According to Holland et al (2008), buccal epithelial cells represent a recognized target site for early genotoxic events induced by carcinogenic substances that enter the body via inhalation or ingestion.…”
Section: Discussionmentioning
confidence: 99%
“…Micronuclei in exfoliated buccal epithelial cells emerge during mitosis of the basal layers of the epithelium as extra chromosomal DNA particles, when chromosome fragments or whole chromosomes lag behind and fail to be included in the main nuclei of the daughter cells, as a result of a clastogenic or aneugenic events (Holland et al, 2008;Tolbert et al, 1992). Micronuclei in epithelial cells reflect genotoxic events occurring in the dividing basal cell layer 1-3 weeks earlier of the putative target organ (Stich et al, 1983;Tolbert et al, 1991), which allows for cytogenetic surveillance of groups at high risk of developing organ-specific cancer (e.g., upper aerodigestive tract) or oral premalignant lesions (Bloching et al, 2000;Mahimkar et al, 2010;Saran et al, 2008). Chromosomal damage in epithelial cells also leads to nuclear anomalies other than micronuclei, such as karyorrhexis, karyolysis, pyknosis, condensed chromatin, broken eggs and binucleated cells (Holland et al, 2008;Thomas et al, 2009).…”
Section: Introductionmentioning
confidence: 99%