Chromosome Instability and Risk of Squamous Cell Carcinomas of Head and Neck

Wang, Li E.; Xiong, Ping; Zhao, Hui; Spitz, Margaret R.; Wei, Qingyi

doi:10.1158/0008-5472.can-07-6568

Cited by 14 publications

(11 citation statements)

References 25 publications

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“…It has been modified with a variety of etiologically related mutagens to evaluate cancer susceptibility in association studies [29–34, 46–50]. These studies constantly showed mutagen sensitivity as a risk factor for cancer development.…”

Section: Discussionmentioning

confidence: 99%

Gamma-ray-induced mutagen sensitivity and risk of sporadic breast cancer in young women: a case–control study

Wang

Han

Xiong

et al. 2012

Breast Cancer Res Treat

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Hypersensitivity to radiation exposure has been suggested to be a risk factor for the development of breast cancer. In this case–control study of 515 young women (≤55 years) with newly diagnosed sporadic breast cancer and 402 cancer-free controls, we examined the radiosensitivity as measured by the frequency of chromatid breaks induced by gamma-radiation exposure in the G2 phase of phytohemagglutinin-stimulated and short-term cultured fresh lymphocytes. We found that the average chromatid breaks per cell from 50 well-spread metaphases were statistically significantly higher in 403 non-Hispanic White breast cancer patients (0.52 ± 0.22) than that in 281 non-Hispanic White controls (0.44 ± 0.16) (P value < 0.001), and in 60 Mexican American breast cancer patients (0.52 ± 0.19) than that in 65 Mexican American controls (0.44 ± 0.16) (P value = 0.021), but the difference was not significant in African Americans (52 cases [0.45 ± 0.16] versus 56 controls [0.47 ± 0.16], P = 0.651). The frequency of chromatid breaks per cell above the median of control subjects was associated with two-fold increased risk for breast cancer in non-Hispanic Whites and Mexican Americans. A dose–response relationship was evident between radiosensitivity and risk for breast cancer (Ptrend < 0.001) in these two ethnic groups. We concluded that gamma-ray-induced mutagen sensitivity may play a role in susceptibility to breast cancer in young non-Hispanic White and Mexican American women.

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Section: Discussionmentioning

confidence: 99%

Gamma-ray-induced mutagen sensitivity and risk of sporadic breast cancer in young women: a case–control study

Wang

Han

Xiong

et al. 2012

Breast Cancer Res Treat

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“…The study population has been described elsewhere (28). Patients with newly diagnosed, histopathologically confirmed SCCHN were recruited from The University of Texas M. D. Anderson Cancer Center between September 1998 and March 2006.…”

Section: Methodsmentioning

confidence: 99%

Reduced DNA Repair Capacity for Removing Tobacco Carcinogen–Induced DNA Adducts Contributes to Risk of Head and Neck Cancer but not Tumor Characteristics

Wang

Sturgis

et al. 2010

Clinical Cancer Research

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Purpose: Although cigarette smoking and alcohol use are known risk factors for squamous cell carcinoma of head and neck (SCCHN), only a few exposed individuals develop this disease, suggesting an individual susceptibility. In this study, we investigated the associations between genetically determined DNA repair capacity (DRC) for removing tobacco-induced DNA adducts and risk of SCCHN and tumor characteristics.Experimental Design: We measured DRC in cultured T lymphocytes using the host-cell reactivation assay in a hospital-based case-control study of 744 SCCHN patients and 753 age-, sex-, and ethnicitymatched cancer-free controls recruited from The University of Texas M.D. Anderson Cancer Center.Results: Patients with SCCHN had significantly lower mean DRC (8.84% ± 2.68%) than controls (9.97% ± 2.61%; P < 0.0001), and the difference accounted for ∼2-fold increased risk of SCCHN [adjusted odds ratio (OR), 1.91; 95% confidence interval (CI), 1.52-2.40] after adjustment for other covariates. Compared with the highest DRC quartile of controls, this increased risk was dose dependent (second highest quartile: OR, 1.40; 95% CI, 0.99-1.98; third quartile: OR, 1.87; 95% CI, 1.34-2.62; and fourth quartile: OR, 2.76; 95% CI, 1.98-3.84, respectively; P trend < 0.0001). We also assessed the performance of DRC in risk prediction models by calculating the area of under the receiver operating characteristic curve. The addition of DRC to the model significantly improved the sensitivity of the expanded model. However, we did not find the association between DRC and tumor sites and stages.Conclusion: DRC is an independent susceptibility biomarker for SCCHN risk but not a tumor marker. Clin Cancer Res; 16(2); 764-74. ©2010 AACR.

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“…This is a cytogenetic assay that quantifies chromatid breaks in cultured peripheral blood lymphocytes (PBLs) after exposure to different mutagens (31;32). Numerous studies used mutagen sensitivity assays to evaluate DNA repair capacity in patients with a variety of malignancies (including head and neck cancer, bladder cancer, breast cancer, non-small cell lung cancer, and basal cell carcinoma) and in general, showed higher mutagen sensitivity in patients with cancer to healthy controls (33-37). A strength of this assay is the reproducibility when conducted by different laboratories (38) however, a weakness is that the assay read-out does not assess the direct damage induced by the mutagen or it's repair.…”

Section: Mutagen Sensitivity Assaysmentioning

confidence: 99%

DNA Repair: From Genome Maintenance to Biomarker and Therapeutic Target

Jalal

Earley

Turchi

2011

Clinical Cancer Research

108

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A critical link exists between an individual's ability to repair cellular DNA damage and cancer development, progression and response to therapy. Knowledge gained regarding the proteins involved and types of damage repaired by the individual DNA repair pathways has led to the development of a variety of assays aimed at determining an individual's DNA repair capacity. These assays and their use in the analysis of clinical samples has yielded useful though somewhat conflicting data. In this review article, we discuss the major DNA repair pathways, the proteins and genes required for each, assays used to assess activity and the relevant clinical studies to date. With the recent results from clinical trials targeting specific DNA repair proteins for the treatment of cancer, accurate, reproducible and relevant analysis of DNA repair takes on an even greater significance. We highlight the strengths and limitations of these DNA repair studies and assays with respect to the clinical assessment of DNA repair capacity to determine cancer development and response to therapy.

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Chromosome Instability and Risk of Squamous Cell Carcinomas of Head and Neck

Cited by 14 publications

References 25 publications

Gamma-ray-induced mutagen sensitivity and risk of sporadic breast cancer in young women: a case–control study

Gamma-ray-induced mutagen sensitivity and risk of sporadic breast cancer in young women: a case–control study

Reduced DNA Repair Capacity for Removing Tobacco Carcinogen–Induced DNA Adducts Contributes to Risk of Head and Neck Cancer but not Tumor Characteristics

DNA Repair: From Genome Maintenance to Biomarker and Therapeutic Target

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