Functional polymorphism in manganese superoxide dismutase and antioxidant status: Their interactions on the risk of cervical intraepithelial neoplasia and cervical cancer

Tong, Seo Yun; Lee, Jong Min; Song, Eun Seop; Lee, Kwang Beom; Kim, Mi Kyung; Lee, Jae Kwan; Son, Soo Chang; Lee, Jung Pil; Kim, Jae Hoon; Kwon, Young Jun

doi:10.1016/j.ygyno.2009.07.032

Cited by 26 publications

(24 citation statements)

References 29 publications

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“…Cervical cancer patients however, are fewer in number compared with other types of cancer, and therefore we were limited as to the number of patients we could recruit to our study. Our study of 154 patients (82 carcinomas and 72 CINs) compares favorably with other recently published case-control studies in the same geographical area (38)(39)(40), but clearly there is a need for further research with larger sample sizes across diverse populations.…”

Section: Cin Scc Cin Scc --------------------------------------------supporting

confidence: 75%

Single nucleotide polymorphisms in DNA repair genes and risk of cervical cancer: A case-control study

et al. 2011

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Abstract. In this report, we describe a case control study in a Chinese population aimed at identifying possible associations between susceptibility to cervical cancer and single nucleotide polymorphisms in XRCC1 194C>T, XRCC1 280G>A, XRCC1 399G>A, ERCC2 751A>C , ERCC2 156C>A, ERCC1 118C>T, PARP1 762T>C , RAD51 135G>C and HER2 655A>G. The cases comprised 154 patients: 80 cervical squamous cell carcinomas (SCCs), 2 adenocarcinomas and 72 cervical intraepithelial neoplasias (CINs). A total of 177 healthy women were recruited as the controls. A significant association was found between ERCC1 118C>T and SCC in the additive genetic model [odds ratio (OR)=1.711; 95% confidence interval (CI), 1.089-2.880; p=0.021] and the dominant genetic model (OR=1.947; 95% CI, 1.056-3.590; p=0.033). Among women with a smoking family member, ERCC1 118C>T increased SCC risk in the additive model (OR=2.800; 95% CI, 1.314-5.968; p= 0.008). For women who had first intercourse before 22 years of age, XRCC1 280G>A was found to act as a protective factor for SCC under the additive model (OR=0.228; 95% CI, 0.058-0.900; p=0.035), while RAD51 135G>C was a risk factor for CIN (OR=4.246; 95% CI, 1.335-13.502; p=0.014). For women who had first intercourse after 22 years of age, the additive genetic model showed RAD51 135G>C (OR=0.359; 95% CI, 0.138-0.934; p=0.036) and HER2 655A>G (OR=0.309; 95% CI, 0.098-0.972; p=0.045) to be protective factors for SCC. XRCC1 399G>A increased CIN risk among women who first gave birth before the age of 22 in the additive genetic model (OR=4.459; 95% CI, 1.139-17.453; p=0.032). For those who first gave birth after age 22, ERCC1 118C>T was found to be a risk factor for SCC in the additive genetic model (OR=1.884; 95% CI, 1.088-3.264; p=0.024). A significant interaction was observed between RAD51 135G>C and age at first intercourse (p interaction =0.033 for SCC, p interaction =0.021 for CIN), as well with sexual partner number (p interaction =0.001 for SCC). The interaction between HER2 655A>G and age at first intercourse, ERCC2 156C>A and family smoking status and XRCC1 280G>A and alcohol consumption were significant, with p interaction =0.023 for SCC, p interaction =0.021 for CIN and p interaction =0.025 for SCC, respectively.

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Section: Cin Scc Cin Scc --------------------------------------------supporting

confidence: 75%

Single nucleotide polymorphisms in DNA repair genes and risk of cervical cancer: A case-control study

et al. 2011

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“…SCCA1 and SCCA2, known clinical biomarkers of SCC, (18) were observed overexpressed in both cervical SCC specimens. Aberrant expression of ENO1, (19) Maspin, (20) PKM2, (21) MnSOD, (22) PRDX isoforms (23) and TPM2 (24) in cervical cancer have been reported. The present study supports the notion that these proteins are involved in cervical cancer and were also observed in our database.…”

Section: Discussionmentioning

confidence: 99%

Glucose‐regulated protein 58 modulates cell invasiveness and serves as a prognostic marker for cervical cancer

Liao

Huang

et al. 2011

Cancer Science

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Human papilloma virus infection is critical but not sufficient to cause cervical cancer. Molecular markers of cervical carcinogenesis are essential. The aim of this study was to identify aberrantly expressed proteins in cervical cancer and determine their clinical significance. A two-dimensional polyacrylamide gel electrophoresis (2-DE) proteomic strategy was used for screening candidate proteins. Immunoblotting and immunohistochemical (IHC) analyses were performed to confirm the results of 2-DE, and the clinical significance was estimated. Glucose-regulated protein 58 (Grp58) was overexpressed in 73% of cancers. The IHC staining showed that the Grp58 histoscore was significantly higher in patients with adenocarcinoma (AD) compared with squamous cell carcinoma (P < 0.05). Grp58 staining was intense in AD with a penetration depth greater than half of the cervical stroma (P = 0.033). High Grp58 expression was associated with low overall survival and recurrence-free survival (RFS) rates (P = 0.007 and P = 0.013, respectively). In multivariate analysis, high Grp58 expression (P = 0.042) and lymph node metastasis (P = 0.026) were determined as independent prognostic factors for RFS. Patients exhibiting both high Grp58 expression and lymph node metastasis displayed poorer outcomes than the other patient groups. In functional studies, knockdown of Grp58 in HeLa cells led to decreased cell invasiveness and inhibition of lung metastasis in a xenograft mouse model. In conclusion, Grp58 serves as a potent prognostic factor of cervical AD. Estimation of the Grp58 index in conjunction with the lymph node metastasis status might aid in predicting the prognosis of cervical AD. (Cancer Sci 2011; 102: 2255-2263 C ervical cancer is one of the most common cancers among women worldwide. Approximately 500 000 diagnoses of cervical cancer are made each year, leading to 274 000 deaths, although the incidence and death rate have declined markedly in the past three decades because of effective screening.(1) Human papillomaviruses (HPV) are the causative agents of over 99% of cervical cancers containing viral sequences. Infection by highrisk HPV types is necessary but not sufficient for progression to cancer. Most HPV infections are transient without clinical manifestation and are cleared naturally; <1% of women become HPV carriers and remain at high risk of developing cervical cancer.(2)The mechanisms underlying the progression and regression of lesions caused by HPV infection are unknown, and further investigation of the molecular alterations in cervical cancer is needed.Glucose-regulated protein 58 (Grp58) is a glycoprotein-specific thiol-oxidoreductase belonging to the disulfide isomerase family of proteins. Grp58 is a multifunctional protein.(3) Recent studies suggest that Grp58 plays a role in cancer, although related information is limited. Hirano et al.(4) demonstrated that enhanced expression of Grp58 was associated with oncogenic transformation in normal rat kidney cells. Grp58 overexpression modulates STAT3 signaling in cancer...

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“…This polymorphism has also been extensively investigated in diseases associated with oxidative stress, such as cancer, with several studies further examining potential modulation by the diet [23]. For example, diet has been shown to modify the relationship between the MnSOD Val16Ala polymorphism and cervical intraepithelial neoplasia (CIN, subdivided into CIN1 and CIN2/3 based on histology) and cervical cancer [24]. In this case-control study, C allele carriers showed a 57.3% reduced risk of CIN1, but no association with CIN2/3 or cervical cancer; however, several significant interactions were noted with serum levels of dietary antioxidants on CIN1, CIN2/3, and cervical cancer risk including β-carotene, lycopene, zeaxanthin/lutein, retinol, and α- and γ-tocopherol.…”

Section: Superoxide Dismutasementioning

confidence: 99%

“…In this case-control study, C allele carriers showed a 57.3% reduced risk of CIN1, but no association with CIN2/3 or cervical cancer; however, several significant interactions were noted with serum levels of dietary antioxidants on CIN1, CIN2/3, and cervical cancer risk including β-carotene, lycopene, zeaxanthin/lutein, retinol, and α- and γ-tocopherol. For example, the reduced risk of CIN1 associated with the C allele was only seen among those with above median levels of serum β-carotene [>0.205 µg/ml; odds ratio (OR): 0.286, 95% confidence interval (CI): 0.086–0.953; interaction p = 0.002] and γ-tocopherol (>0.30 µg/ml; OR: 0.272, 95% CI: 0.079–0.944; interaction p = 0.033) [24]. Two recent meta-analyses have also examined the association between the MnSOD Val16Ala polymorphism and breast cancer risk with modification by vitamin C, vitamin E, and carotenoid [25] and fruit and vegetable consumption [19].…”

Section: Superoxide Dismutasementioning

confidence: 99%

Nutrigenetics and Modulation of Oxidative Stress

2012

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Oxidative stress develops as a result of an imbalance between the production and accumulation of reactive species and the body’s ability to manage them using exogenous and endogenous antioxidants. Exogenous antioxidants obtained from the diet, including vitamin C, vitamin E, and carotenoids, have important roles in preventing and reducing oxidative stress. Individual genetic variation affecting proteins involved in the uptake, utilization and metabolism of these antioxidants may alter their serum levels, exposure to target cells and subsequent contribution to the extent of oxidative stress. Endogenous antioxidants include the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, paraoxanase, and glutathione S-transferase. These enzymes metabolize reactive species and their by-products, reducing oxidative stress. Variation in the genes coding these enzymes may impact their enzymatic antioxidant activity and, thus, the levels of reactive species, oxidative stress, and risk of disease development. Oxidative stress may contribute to the development of chronic disease, including osteoporosis, type 2 diabetes, neurodegenerative diseases, cardiovascular disease, and cancer. Indeed, polymorphisms in most of the genes that code for antioxidant enzymes have been associated with several types of cancer, although inconsistent findings between studies have been reported. These inconsistencies may, in part, be explained by interactions with the environment, such as modification by diet. In this review, we highlight some of the recent studies in the field of nutrigenetics, which have examined interactions between diet, genetic variation in antioxidant enzymes, and oxidative stress.

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Functional polymorphism in manganese superoxide dismutase and antioxidant status: Their interactions on the risk of cervical intraepithelial neoplasia and cervical cancer

Cited by 26 publications

References 29 publications

Single nucleotide polymorphisms in DNA repair genes and risk of cervical cancer: A case-control study

Single nucleotide polymorphisms in DNA repair genes and risk of cervical cancer: A case-control study

Glucose‐regulated protein 58 modulates cell invasiveness and serves as a prognostic marker for cervical cancer

Nutrigenetics and Modulation of Oxidative Stress

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