8‐Hydroxy‐2′‐deoxyguanosine (8‐OH‐dG) as a potential survival biomarker in patients with nonsmall‐cell lung cancer

Shen, Jie; Deininger, Prescott L.; Hunt, Jay D.; Zhao, Hua

doi:10.1002/cncr.22417

Cited by 78 publications

(58 citation statements)

References 35 publications

(37 reference statements)

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“…Our findings relating to colorectal cancer have not been described earlier, but high levels of 8-oxo-dG have been associated with poor outcome in non small cell lung cancer and renal cell carcinoma (Miyake et al, 2004;Shen et al, 2007) whereas oxidative damage in non-cancerous liver tissues also appears to predict recurrence of hepatocellular cancer (Matsumoto et al, 2003).…”

Section: Discussionsupporting

confidence: 58%

Nuclear oxidative damage correlates with poor survival in colorectal cancer

Sheridan

Tosetto

et al. 2008

Br J Cancer

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Oxidative DNA damage results from DNA adducts such as 8-oxo-7, 8 dihydro-2 0 -deoxyguanosine (8-oxo-dG), which is a pro-mutagenic lesion. No known association between 8-oxo-dG, disease progression and survival exists in colorectal cancer (CRC). We examined levels of 8-oxo-dG in sporadic CRC to determine its relationship with pathological stage and outcome. A total of 143 CRC patients and 105 non-cancer patients were studied. Nuclear and cytoplasmic 8-oxo-dG was assessed using immunohistochemistry. Double immunofluorescence using 8-oxo-dG and manganese superoxide dismutase (MnSOD) antibodies localised cytoplasmic 8-oxo-dG. Apoptosis was detected using TUNEL. Nuclear staining levels were similar in tumour tissue and matched normal mucosa in both epithelial (P ¼ 0.22) and stromal (P ¼ 0.85) cells. Epithelial cytoplasmic staining was greater in tumour tissue (Po0.001). Double immunofluorescence localised cytoplasmic 8-oxo-dG to mitochondria. Epithelial and stromal nuclear 8-oxo-dG decreased with local disease spread, but highest levels were found in distant disease (Po0.01). Survival was related to epithelial nuclear and stromal staining in normal mucosa (Po0.001) and tumour (Po0.01) but was unrelated to cytoplasmic staining. Normal control cells in tissue from cancer patients with high levels of 8-oxo-dG failed to undergo cell death. 8-oxo-dG may be an important biomarker of disease risk, progression and survival for CRC patients. British Journal of Cancer (2009) Colorectal cancer is one of the commonest cancers in the Western World (Ferlay et al, 2007) and genetic events associated with tumour initiation and progression have been extensively studied (Fearon and Vogelstein, 1990). The majority of mutations found in sporadic colorectal cancer are due to single-base substitutions (Sjoblom et al, 2006) such as GC to TA transversions.Oxidative stress is defined as a disturbance in the balance between the production of reactive oxygen species and antioxidant defences. It is associated with aging and implicated in a variety of disease processes including atherosclerosis, diabetes mellitus and cancer (Pacifici and Davies, 1991;Maritim et al, 2003;Valko et al, 2004;Minuz et al, 2006). Endogenous sources of reactive oxygen species production include oxidative phosphorylation and inflammatory cell activation, and despite multiple conserved redox modulating systems, a proportion of reactive oxygen species continuously escape the mitochondrial respiratory chain. The significance of reactive oxygen species within antioxidant systems and its role in carcinogenesis is not fully understood. Enhanced antioxidant mechanisms in gastrointestinal tumour cells in vivo are associated with chemo-resistance, metastasis and poor prognosis, whereas many in vitro studies suggest that antioxidant enzymes have tumour-suppressing properties (Janssen et al, 1998;Toh et al, 2000), although the majority of conflicting results may be explained by reference to the net redox status of malignant cells (Kinnula and Crapo, 2004).The DNA adduct, 8-oxo-7,...

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Section: Discussionsupporting

confidence: 58%

Nuclear oxidative damage correlates with poor survival in colorectal cancer

Sheridan

Tosetto

et al. 2008

Br J Cancer

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“…In a study by Dincer et al (2007), the 8-oxodG plasma levels were significantly higher in controls than in gastric and colon carcinoma patients, which is also in line with our results. However, high 8-oxodG levels from tumour tissue DNA have also been reported as an independent prognostic factor of poor survival in lung cancer and hepatocellular carcinoma (Matsumoto et al, 2003;Shen et al, 2007). This emphasizes the diverse prognostic function of 8-oxodG in different malignancies.…”

Section: Discussionmentioning

confidence: 99%

“…For example, in studies on breast carcinomas, the 8-oxodG levels have been reported as being 8 to 17 times higher in comparison with those in healthy breast tissue (Matsui et al, 2000). Elevated levels of 8-oxodG from cancer patients compared with healthy subjects have also been observed in lung cancer (Vulimiri et al, 2000;Shen et al, 2007), basal cell carcinoma (Nishigori et al, 2005), bladder cancer (Kaczmarek et al, 2005), acute lymphoblastic leukaemia (Sentürker et al, 1997), colorectal cancer (Oliva et al, 1997), high grade cervical dysplasia (Romano et al 2000), renal cell carcinoma (Okamoto et al, 1994), prostate cancer (Miyake et al, 2004), gastric intestinal metaplasia (Farinati et al, 2008) and gastric adenocarcinoma (Lee et al, 1998). Evidence from these studies suggests that elevated 8-oxodG levels in these malignant or premalignant diseases compared with healthy individuals would be a sign of increased oxidative stress, impaired antioxidant defence or inadequate repair of oxidatively damaged DNA.…”

Section: Discussionmentioning

confidence: 99%

8-Hydroxydeoxyguanosine: a new potential independent prognostic factor in breast cancer

et al. 2010

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BACKGROUND: is the commonly used marker of oxidative stress-derived DNA damage. 8-OxodG formation is regulated by local antioxidant capacity and DNA repair enzyme activity. Earlier studies have reported contradictory data on the function of 8-oxodG as a prognostic factor in different cancer types. METHODS: We assessed pre-operative serum 8-oxodG levels with an enzyme-linked immunosorbent assay in a well-defined series of 173 breast cancer patients. 8-OxodG expression in the nuclei of cancer cells from 150 of these patients was examined by immunohistochemistry. RESULTS: The serum 8-oxodG levels and immunohistochemical 8-oxodG expression were in concordance with each other (Po0.05). Negative 8-oxodG immunostaining was an independent prognostic factor for poor breast cancer-specific survival according to the multivariate analysis (Po0.01). This observation was even more remarkable when ductal carcinomas only (n ¼ 140) were considered (Po0.001). A low serum 8-oxodG level was associated statistically significantly with lymphatic vessel invasion and a positive lymph node status. CONCLUSIONS: Low serum 8-oxodG levels and a low immunohistochemical 8-oxodG expression were associated with an aggressive breast cancer phenotype. In addition, negative 8-oxodG immunostaining was a powerful prognostic factor for breast cancer-specific death in breast carcinoma patients.

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“…Increased levels of 8-OH-dG are associated with the aging process as well as with a number of pathological conditions including cancer, diabetes, and hypertension. 28,45 Oxaliplatin neurotoxicity is described to be localized at dorsal root ganglia level. 47 As reported by Jacobs et al 22 concentration in CSF is limited.…”

Section: Discussionmentioning

confidence: 99%

Oxaliplatin-Induced Neuropathy: Oxidative Stress as Pathological Mechanism. Protective Effect of Silibinin

Mannelli

Zanardelli

Failli

et al. 2012

The Journal of Pain

151

120

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Oxaliplatin is the standard treatment for advanced colorectal cancer. Its dose-limiting toxicity is the development of a painful neuropathic syndrome sustained by unclear mechanisms. Although the oxidative hypothesis is a matter of debate, direct data about oxidative damage induced in vivo by anticancer agents are lacking and the efficacy of the available antioxidant compounds are unsatisfactory. In a rat model of painful oxaliplatin-induced neuropathy (2.4 mgkg À1 i.p., daily for 21 days), we described an important component of oxidative stress. In the plasma of oxaliplatin-treated rats, the increases in carbonylated protein and thiobarbituric acid reactive substances were the index of the resultant protein oxidation and lipoperoxidation, respectively. The same pattern of oxidation was revealed also in the sciatic nerve, and in the spinal cord where the damage reached the DNA level. The antioxidant compound silibinin (100 mgkg À1 per os), administered once a day, starting from the first day of oxaliplatin injection until the 20th, prevented oxidative damage as did a-tocopherol. Repetitive administration of silibinin, as well as a-tocopherol, reduced oxaliplatin-dependent pain induced by mechanical and thermal stimuli. Antioxidants were also able to improve motor coordination. The antineuropathic effect of both molecules improved by about 50% oxaliplatin-induced behavioral alterations.Perspective: This study characterizes oxidative stress parameters in a rat model of oxaliplatininduced neuropathy. A relationship between the improvement of oxidative alterations and pain relief is established in rats treated with natural antioxidant compounds like a-tocopherol and silibinin. Silibinin could be a valid therapeutic option for chemotherapy-induced neuropathy.

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8‐Hydroxy‐2′‐deoxyguanosine (8‐OH‐dG) as a potential survival biomarker in patients with nonsmall‐cell lung cancer

Cited by 78 publications

References 35 publications

Nuclear oxidative damage correlates with poor survival in colorectal cancer

Nuclear oxidative damage correlates with poor survival in colorectal cancer

8-Hydroxydeoxyguanosine: a new potential independent prognostic factor in breast cancer

Oxaliplatin-Induced Neuropathy: Oxidative Stress as Pathological Mechanism. Protective Effect of Silibinin

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