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DNA‐damage processing in blood lymphocytes of head‐and‐neck‐squamous‐cell‐carcinoma patients is dependent on tumor site
Author(s) -
Cloos Jacqueline,
Steen Ivar,
Timmerman Arie J.,
van der Schans Govert P.,
Snow Gordon B.,
Braakhuis Boudewijn J.M.
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19960927)68:1<26::aid-ijc5>3.0.co;2-z
Subject(s) - dna damage , chromatid , bleomycin , dna repair , head and neck cancer , dna , carcinoma , epidermoid carcinoma , biology , cancer , pathology , cancer research , medicine , immunology , genetics , chromosome , chemotherapy , gene
It has been reported that an intrinsic susceptibility to cancer is related to the way an individual responds to DNA‐damaging agents. The aim of this study was to evaluate whether, in addition to bleomycin‐induced chromosomal instability, radiation‐induced initial DNA damage and subsequent repair is associated with the development of head‐and‐neck squamous‐cell carcinoma. In this study, 2 assays were performed to measure DNA damage in human peripheral‐blood lymphocytes. One was a chromosomal aberration assay which determines sensitivity to chromatid breaks induced by bleomycin, the other an elegant immunochemical assay which measures the level of radiation‐induced strand breaks as well as subsequent repair. Age, smoking and alcohol‐drinking behavior did not influence the number of chromatid breaks, initial DNA damage or repair capacity. As has been found in previous studies, the mean number of chromatid breaks per cell was significantly different between patients (n = 18) and control persons (n = 19), whereas the amount of initial DNA damage was not. No correlation was found between the outcome of the 2 assays in the subject groups. In contrast to laryngeal‐carcinoma patients, oral‐cavity‐carcinoma patients showed significantly slower repair capacity than controls. Our hypothesis is that the way DNA damage is processed by the patients determines at which site cancer develops in the head and neck area. © 1996 Wiley‐Liss, Inc.