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Propensity for DNA Damage in Psoriasis Patients Genotyped for Two Candidate Genes | OMICS International | Abstract
ISSN: 2157-2518

Journal of Carcinogenesis & Mutagenesis
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Case Report

Propensity for DNA Damage in Psoriasis Patients Genotyped for Two Candidate Genes

G. Gandhi1*, Premjot Singh Girgila2, Ramesh K. Aggarwal3 and Brinderjit Singh Buttar1

1Department of Human Genetics, Guru Nanak Dev University, Amritsar, Punjab, India

2Formerly at Skin and T.B. Ward, Sri Guru Ram Das Charitable Hospital, Amritsar, Punjab, India

3Molecular Genetics Lab., Centre for Cellular and Molecular Biology, Hyderabad, India

*Corresponding Author:
Dr. G. Gandhi
Department of Human Genetics
Guru Nanak Dev University
Amritsar 143 005, India
Tel: +91-183-2258802-09 Extn. 3444
Fax: +91-183-2258820
Email: [email protected]

Received date: November 13, 2010; Accepted date: December 04, 2010; Published date: December 06, 2010

Citation: Gandhi G, Girgila PS, Aggarwal RK, Buttar BS (2010) Propensity for DNA Damage in Psoriasis Patients Genotyped for Two Candidate Genes. J Carcinogene Mutagene 1:112 doi: 10.4172/2157-2518.1000112

Copyright: © 2010 Gandhi G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Studies assessing genetic damage and its association with disease-candidate genes in patients belonging to geographically distinct populations are scanty. The present study evaluated DNA damage using the alkaline Single Cell Gel Electrophoresis assay in peripheral blood leukocytes of Psoriasis Punjabi Patients on systemic-topical therapy who had been genotyped for two disease-candidate genes (HLA-C, human leukocyte antigen and the coiled-coil alpha-helical rod protein 1(CCHCR1). Genetic damage was disease gene-influenced as homozygous mutants for CCHCR1 Exon 4 site 386* (C→T) and heterozygous mutants for 404* (C→T) alleles had significantly more damage (p<0.05) compared to respective homozygous wild types. The arginine to tryptophan substitution alters the protein, triggering keratinocyte proliferation and probably inflammation/ oxidative stress. This along with drug-treatment probably caused the observed DNA damage. Population sub-groups had no within group differences but larger sizes can explore this possibility. Studies of this type can provide disease-gene-damage prone information for exploring DNA- safe therapeutics.