Evidence for upregulated repair of oxidatively induced DNA damage in human colorectal cancer

Kırkalı, Güldal; Keles, Didem; Canda, Aras Emre; Terzi, Cem; Reddy, P.G.; Dizdaroğlu, Miral; Oktay, Gülgün

doi:10.1016/j.dnarep.2011.08.008

Cited by 23 publications

(12 citation statements)

References 72 publications

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“…3). Kirkali et al observed higher levels of DNA damage products in rectum compared to the colon (56), which corroborates our observations of tissue-specific differences in formation or repair of DNA damage.…”

Section: )supporting

confidence: 81%

“…In peripheral blood lymphocytes of colorectal carcinoma patients, levels of etheno adducts as well as DNA repair rates were lower than in healthy subjects (54). Further, Kirkali et al observed lower levels of the purine oxidation products 4,6-diamino-5-formamidopyrimidine, 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyG), 8-oxo-dG, and (5'S)-8,5′-cyclo-2′-deoxyadenosine in tumor tissue compared to surrounding normal tissue in patients with colorectal cancer (56).…”

Section: )mentioning

confidence: 99%

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Infection-induced colitis in mice causes dynamic and tissue-specific changes in stress response and DNA damage leading to colon cancer

Mangerich

Knutson

Parry³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

208

294

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Helicobacter hepaticus -infected Rag 2 -/- mice emulate many aspects of human inflammatory bowel disease, including the development of colitis and colon cancer. To elucidate mechanisms of inflammation-induced carcinogenesis, we undertook a comprehensive analysis of histopathology, molecular damage, and gene expression changes during disease progression in these mice. Infected mice developed severe colitis and hepatitis by 10 wk post-infection, progressing into colon carcinoma by 20 wk post-infection, with pronounced pathology in the cecum and proximal colon marked by infiltration of neutrophils and macrophages. Transcriptional profiling revealed decreased expression of DNA repair and oxidative stress response genes in colon, but not in liver. Mass spectrometric analysis revealed higher levels of DNA and RNA damage products in liver compared to colon and infection-induced increases in 5-chlorocytosine in DNA and RNA and hypoxanthine in DNA. Paradoxically, infection was associated with decreased levels of DNA etheno adducts. Levels of nucleic acid damage from the same chemical class were strongly correlated in both liver and colon. The results support a model of inflammation-mediated carcinogenesis involving infiltration of phagocytes and generation of reactive species that cause local molecular damage leading to cell dysfunction, mutation, and cell death. There are strong correlations among histopathology, phagocyte infiltration, and damage chemistry that suggest a major role for neutrophils in inflammation-associated cancer progression. Further, paradoxical changes in nucleic acid damage were observed in tissue- and chemistry-specific patterns. The results also reveal features of cell stress response that point to microbial pathophysiology and mechanisms of cell senescence as important mechanistic links to cancer.

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Section: )supporting

confidence: 81%

Section: )mentioning

confidence: 99%

Infection-induced colitis in mice causes dynamic and tissue-specific changes in stress response and DNA damage leading to colon cancer

Mangerich

Knutson

Parry³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

208

294

View full text Add to dashboard Cite

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“…Several studies have inferred higher BER or NER capacity in tumors via an indirect approach of measuring the steadystate level of DNA damage, assuming that a low damage level reflects a high repair rate. All those studies reported a significantly lower level of specific damage in DNA from tumors, presumably explained by upregulation of repair (32)(33)(34). No study has found evidence for deficiency of excision repair pathways in tumors.…”

Section: Discussionmentioning

confidence: 99%

Functional, Genetic, and Epigenetic Aspects of Base and Nucleotide Excision Repair in Colorectal Carcinomas

Slyšková

Korenkova

Collins

et al. 2012

Clinical Cancer Research

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Purpose: DNA repair capacity (DRC) is a determinant not only of cancer development but also of individual response to therapy. Previously, altered base and nucleotide excision repair (BER and NER) have been described in lymphocytes of patients with sporadic colorectal cancer. We, for the first time, evaluate both excision repair capacities in human colon biopsies to study their participation in colorectal tumorigenesis.Experimental design: Seventy pairs of tumor and adjacent healthy tissues were analyzed for BER-and NER-specific DRC by a comet repair assay. Tissue pairs were further compared for expression levels of a panel of 25 BER and NER genes complemented by their promoter methylation status.

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“…Besides lipid modifications also increased leukocyte activation in carcinogenic tissue was found [34], which indicates possible contribution of inflammatory cells to a further oxidative stress [32]. It was found that the level of DNA lesions varied between colon and rectum tissues, being lower in the former than in the latter [35]. …”

Section: Oxidative Stress and Colorectal Cancermentioning

confidence: 99%

Oxidative Stress in the Pathogenesis of Colorectal Cancer: Cause or Consequence?

Perše

2013

BioMed Research International

177

137

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There is a growing support for the concept that reactive oxygen species, which are known to be implicated in a range of diseases, may be important progenitors in carcinogenesis, including colorectal cancer (CRC). CRC is one of the most common cancers worldwide, with the highest incidence rates in western countries. Sporadic human CRC may be attributable to various environmental and lifestyle factors, such as dietary habits, obesity, and physical inactivity. In the last decades, association between oxidative stress and CRC has been intensively studied. Recently, numerous genetic and lifestyle factors that can affect an individual's ability to respond to oxidative stress have been identified. The aim of this paper is to review evidence linking oxidative stress to CRC and to provide essential background information for accurate interpretation of future research on oxidative stress and CRC risk. Brief introduction of different endogenous and exogenous factors that may influence oxidative status and modulate the ability of gut epithelial cells to cope with damaging metabolic challenges is also provided.

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Evidence for upregulated repair of oxidatively induced DNA damage in human colorectal cancer

Cited by 23 publications

References 72 publications

Infection-induced colitis in mice causes dynamic and tissue-specific changes in stress response and DNA damage leading to colon cancer

Infection-induced colitis in mice causes dynamic and tissue-specific changes in stress response and DNA damage leading to colon cancer

Functional, Genetic, and Epigenetic Aspects of Base and Nucleotide Excision Repair in Colorectal Carcinomas

Oxidative Stress in the Pathogenesis of Colorectal Cancer: Cause or Consequence?

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