DNA repair in lymphoblastoid cell lines from patients with head and neck cancer

Objective: To analyze and compare components of the 3 primary DNA repair pa thways of Epstein-Barr virus-transformed lymphocyte (lymphoblastoid) cell l ines derived from 9 patients with squamous cell carcinoma of the head and n eck and Il cancer-free controls. These cell lines were previously character ized by using an established cytogenetic marker of cancer susceptibility (m utagen sensitivity assay). Design: To evaluate nucleotide excision repair (NER), we measured the react ivation level of a tobacco carcinogen-damaged plasmid containing a bacteria l reporter gene transfected into these cells. To assess mismatch repair (MM R) and recombinational repair, selected gene transcript levels were quantif ied by using a multiplex reverse transcriptase-polymerase chain reaction as say. The results of these DNA repair assays were correlated with the previo usly measured mutagen sensitivity values. Results: The NER capacities of the 2 groups were similar: 25.1% (range, 14. 3%-33.3%) for the patient cell lines and 26.0% (range, 9.4%-47.7%) for the control lines. Transcriptase levels for 6 MMR genes (hMSH3, hMSH2, hPMS2, G TBP, hMLH1, and hPMS1) did not differ in the 2 groups. Transcript levels fo r 4 of 6 recombinational repair genes (XRCC7, XRCC6, XRCC1, and RAD51) were higher in the patient cell lines, though this difference was significant o nly for XRCC7 (P = .003). The mutagen sensitivity values correlated with th e NER capacity (P = .05) and the expression of XRCC4 (P = .01) and RAD51 (P = .06) genes. Conclusions: As revealed by the above-named assays, these lymphoblastoid ce ll lines derived from patients with head and neck cancer had minor alterati ons in DNA repair function. However, these differences in DNA repair do app ear to affect the cytogenetic marker of cancer susceptibility, mutagen sens itivity.