DNA damage in peripheral blood leukocytes in tobacco users

Guttikonda, Venkateswara Rao; Patil, Rekha; Kumar, GS

doi:10.4103/0973-029x.141329

Cited by 5 publications

(7 citation statements)

References 6 publications

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“…Similar results were obtained by Rawat et al 26 on comparing the mean tail length of PBLs in different habit groups with the control group with no habit and obtained highly significant results. Similar results have been stated by other authors also 28 . Many other investigators have investigated the effect of habit on mean tail length and have obtained comparable results 11,35 .…”

Section: Discussionsupporting

confidence: 93%

“…The generation of ROS and exposure to genotoxins causes DNA breaks, reduced DNA repair capacity and oxidation of purines or pyrimidines. These genotoxins attack different sites on the DNA leading to the accumulation of DNA damage which increases the risk of cancer 18,[28][29] . They also observed that the amount of DNA damage was greatest in OSCC patients as this group had the maximum mean tail length followed by leukoplakia and OSMF.…”

Section: Discussionmentioning

confidence: 99%

“…The formation of DNA adducts and the resulting mutations are responsible for oncogene activation and inactivation of tumor suppressor genes, leading to cancer. Few authors have reported presence of these DNA adducts in smokers 28,[33][34] .…”

Section: Discussionmentioning

confidence: 99%

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DNA damage in buccal cells in oral PMDs and malignant disorders by comet assay

Rawat¹,

Urs

Chakravarti

et al. 2019

Braz. J. Oral Sci.

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Aim: DNA damage associated with Oral Squamous Cell Carcinoma (OSCC) and potentially malignant disorders (PMDs) is produced due to carcinogenic agents or increased oxidative stress. Comet assay can assist in early detection and evaluation of the amount of DNA damage; lymphocytesare the most commonly used cells for performing comet assay. Utilisation of buccal epithelial cells in comet assay can be a minimally invasive and rapid method. The present study compared the efficacy of comet assay in assessing DNA damage in buccal cells over peripheral blood leucocytes (PBLs) in oral potentially malignant and malignant disorders. Methods: The study included fifty five patients each of Leukoplakia, Oral Submucous Fibrosis (OSMF) and OSCC along with fifty five healthy individuals as control. Buccal epithelial cells were collected from all the selected subjects. DNA damage was evaluated bymeasuring the mean tail length (µm). Results: A significantly increased mean tail length (µm) and higher DNA damage were found in OSCC (26.1096 + 1.84355) and there was a progressive stepwise increase in mean tail length from control(8.4982 + 0.93307) to PMD [leukoplakia (14.6105 + 0.71857); OSMF (12.5009 + 1.12694)] to OSCC.The mean tail length in different habit groups was greater than controls, though no significant difference was noted between habit groups. The mean tail length of buccal cells was significantly greater than the mean tail length of PBLs in all study groups and controls. Conclusion: Hence, use of comet assay on buccal epithelial cells can prove to be beneficiary for evaluation of DNA damage.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

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DNA damage in buccal cells in oral PMDs and malignant disorders by comet assay

Rawat¹,

Urs

Chakravarti

et al. 2019

Braz. J. Oral Sci.

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“…Oxidative stress is increased and antioxidant defences are decreased in patients with oral cancer [ 59 ]. There is DNA damage produced by free radicals generated by the use of tobacco [ 60 ], and this damage plays a significant role in oral carcinogenesis [ 60 ]. Nitrosative stress has also been implicated in DNA damage.…”

Section: Inflammation-related Mechanisms In Cancer Pathogenesis Wmentioning

confidence: 99%

Role of COX-2/PGE2 Mediated Inflammation in Oral Squamous Cell Carcinoma

Nasry

Rodríguez-Lecompte

Martin

2018

Cancers

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A significant amount of research indicates that the cyclooxygenase/prostaglandin E2 (PGE2) pathway of inflammation contributes to the development and progression of a variety of cancers, including squamous cell carcinoma of the oral cavity and oropharynx (OSCC). Although there have been promising results from studies examining the utility of anti-inflammatory drugs in the treatment of OSCC, this strategy has been met with only variable success and these drugs are also associated with toxicities that make them inappropriate for some OSCC patients. Improved inflammation-targeting therapies require continued study of the mechanisms linking inflammation and progression of OSCC. In this review, a synopsis of OSCC biology will be provided, and recent insights into inflammation related mechanisms of OSCC pathobiology will be discussed. The roles of prostaglandin E2 and cluster of differentiation factor 147 (CD147) will be presented, and evidence for their interactions in OSCC will be explored. Through continued investigation into the protumourigenic pathways of OSCC, more treatment modalities targeting inflammation-related pathways can be designed with the hope of slowing tumour progression and improving patient prognosis in patients with this aggressive form of cancer.

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“…Guttikonda et al [17] evaluated DNA damage levels in the PBLs of tobacco-habituated individuals with clinically normal mucosa and patients with oral carcinoma and compared with a control group of healthy volunteer using SCGE and fluorescent ethidium bromide stain. They found that the mean DNA damage levels in normal subjects, tobacco users with normal mucosa, and tobacco users with oral cancer patients increased significantly.…”

Section: Projects For the Apoptosis And Buccal Cell Micronuclei Assaymentioning

confidence: 99%

Emergence of micronuclei and apoptosis as potential biomarker of oral carcinogenesis: An updated review

Patil¹

2018

ASJO

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More than 95% cancers of oral cavity are squamous cell carcinoma. They contribute major health problems in developing countries like India. The critical etiological factor for oral squamous cell carcinoma (OSCC) is the consumption of tobacco in various forms. OSCC results from alterations in genes that control the cell cycle or that are involved in deoxyribonucleic acid repair and are characterized by the loss of ability of cells to evolve to death when genetic damage occurs. The occurrence of chromosomal damage can be evaluated by counting micronuclei (MNs) and degenerative alterations, indicative of apoptosis such as karyorrhexis, pyknosis, and condensed chromatin. Apoptosis has been associated with the elimination of potentially malignant cells, hyperplasia, and tumor progression. Hence, reduced apoptosis or its resistance plays a vital role in carcinogenesis. MNs are one of such biomarkers that are cytoplasmic chromatin masses with the appearance of small nuclei that arise from lagging chromosomes at anaphase or from acentric chromosome fragments. They are induced in the cells by numerous genotoxic agents that damage the chromosome. Bigger MNs result from exclusion of whole chromosome following damage to the spindle apparatus of the cell (aneugenic effect), whereas smaller MNs result from structural aberrations causing chromosomal fragments (clastogenic effect). Thus, MN count and apoptosis can be a useful biomarker, and it can be used as a screening test for patients with habit of tobacco consumption and patients with manifestations of oral lesion including premalignant and malignant conditions.

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DNA damage in peripheral blood leukocytes in tobacco users

Cited by 5 publications

References 6 publications

DNA damage in buccal cells in oral PMDs and malignant disorders by comet assay

DNA damage in buccal cells in oral PMDs and malignant disorders by comet assay

Role of COX-2/PGE2 Mediated Inflammation in Oral Squamous Cell Carcinoma

Emergence of micronuclei and apoptosis as potential biomarker of oral carcinogenesis: An updated review

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