Gamma radiation–induced apoptosis, G2 delay, and the risk of salivary and thyroid carcinomas—a preliminary report
✍ Scribed by Rong Zheng; Kristina R. Dahlstrom; Qingyi Wei; Erich M. Sturgis
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 348 KB
- Volume
- 26
- Category
- Article
- ISSN
- 1043-3074
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✦ Synopsis
Abstract
Background.
While radiation has been the only well‐established risk factor for salivary and thyroid cancers, the exact mechanisms remain unknown. We hypothesized that individuals with altered apoptotic response to γ irradiation may be susceptible to salivary and thyroid cancers.
Methods.
We tested our hypothesis in a pilot case‐control study of 29 patients with neoplasms of the salivary and thyroid glands and 29 cancer‐free control subjects. Patients and control subjects were matched on age, sex, and ethnicity. In vitro γ radiation–induced apoptosis in lymphocytes was quantified utilizing the TUNEL assay and flow cytometry.
Results.
The mean apoptotic capacity was 13.55 ± 10.54 for control subjects, 5.75 ± 4.96 for patients with salivary gland carcinomas (p = .003), and 6.87 ± 4.45 for patients with thyroid carcinomas (p = .006). These differences were associated with a 10‐fold increased risk of salivary gland carcinoma (odds ratio [OR] = 10.71; 95% confidence interval [CI], 1.21–94.86) and a four‐fold increased risk of thyroid carcinoma (OR = 3.93; 95% CI, 0.90–17.08).
Conclusions.
Our data suggests that γ radiation–induced apoptosis may serve as a biomarker of genetic susceptibility to salivary and thyroid carcinoma, and further confirmatory studies with larger sample size are warranted. © 2004 Wiley Periodicals, Inc. Head Neck 26: 612–618, 2004