Apoptotic capacity and risk of squamous cell carcinoma of the head and neck.

Published

Journal Article

BACKGROUND: Tobacco smoke and alcohol drinking are the major risk factors for squamous cell carcinoma of the head and neck (SCCHN). Smoking and drinking cause DNA damage leading to apoptosis, and insufficient apoptotic capacity may favour development of cancer because of the dysfunction of removing damaged cells. In the present study, we investigated the association between camptothecin (CPT)-induced apoptotic capacity and risk of SCCHN in a North American population. METHODS: In a case-control study of 708 SCCHN patients and 685 matched cancer-free controls, we measured apoptotic capacity in cultured peripheral blood lymphocytes in response to in vitro exposure to CPT by using the flow cytometry-based method. RESULTS: We found that the mean level of apoptotic capacity in the cases (45.9 ± 23.3%) was significantly lower than that in the controls (49.0 ± 23.1%) (P = 0.002). When we used the median level of apoptotic capacity in the controls as the cutoff value for calculating adjusted odds ratios, subjects with a reduced apoptotic capacity had an increased risk (adjusted odds ratio = 1.42, 95% confidence interval = 1.13-1.78, P = 0.002), especially for those who were age ≥57 (1.73, 1.25-2.38, 0.0009), men (1.76, 1.36-2.27, <0.0001) and ever drinkers (1.67, 1.27-2.21, 0.0003), and these variables significantly interacted with apoptotic capacity (Pinteraction = 0.015, 0.005 and 0.009, respectively). A further fitted prediction model suggested that the inclusion of apoptotic capacity significantly improved in the prediction of SCCHN risk. CONCLUSION: Individuals with a reduced CPT-induced apoptotic capacity may be at an increased risk of developing SCCHN, and apoptotic capacity may be a biomarker for susceptibility to SCCHN.

Full Text

Duke Authors

Cited Authors

  • Liu, Z; Liu, H; Han, P; Gao, F; Dahlstrom, KR; Li, G; Owzar, K; Zevallos, JP; Sturgis, EM; Wei, Q

Published Date

  • February 2017

Published In

Volume / Issue

  • 72 /

Start / End Page

  • 166 - 176

PubMed ID

  • 28033527

Pubmed Central ID

  • 28033527

Electronic International Standard Serial Number (EISSN)

  • 1879-0852

Digital Object Identifier (DOI)

  • 10.1016/j.ejca.2016.11.018

Language

  • eng

Conference Location

  • England