Xeroderma pigmentosum cells

P., Hubert, M., Decroix, Y. and Sarasin, A. (1986). Deficiency in the catalase activity of Xeroderma pigmentosum cells and simian virus 40 transformed human cell extracts. Cancer Res. 46, 538-544. 

Stich, H.F. and San, R.H.C., Reduced DNA repair synthesis in Xeroderma pigmentosum cells exposed to the oncogenic 4-nitroquinoline 1-oxide and 4-hydroxayminoquinoline 1-oxide, Mutat. Res., 13,279,1971. 

Maher, V., Rowan, L.A., Silinskas, K., Kateley, S., and McCormick, J. (1982). Frequency of UV-induced neoplastic transformation of diploid human fibroblasts is higher in xeroderma pigmentosum cells than in normal cells, Proc. Natl. Acad Sd. 79,2613. 

Peak, J.G, Pilas, B., Dudek, E.J. Peak, M.J. (1991) DNA breaks caused by monochromatic 365 nm ultraviolet-A radiation or hydrogen peroxide and their repair in human epithelioid and xeroderma pigmentosum cells. Photochem. Photobiol., 54, 197-203... 

Wolff, S., Bodycote, J., Thomas, G.H., Cleaver, J.E. (1975). Sister chromatid exchanges in xeroderma pigmentosum cells that are defective in DNA excision repair or post-replication repair. Genetics 81,349-355. 

Park, S.D., and J.E. Cleaver. Postreplication repair Questions of its definicition and possible alteration in xeroderma pigmentosum cell strains. 

S.M. Protic, K.H. Kraemer (1985). One pyrimidine dimer inactivates expression of a transfected gene in Xeroderma pigmentosum cells. Proc. Natl. Acad. Sci. U.S.A., 82, 6622-6626. 

C.F., Paterson, M.C., Lohman, P.H., de Weerd-Kastelein, E.A., and Bootsma, D. (1975) Xeroderma pigmentosum cells with normal levels of excision repair have a defect in DNA synthesis after... 

Berger NA, Sikorski GW (1981) Poly (adenosine diphosphoribose) synthesis in ultra-violet irradiated Xeroderma Pigmentosum cells reconstituted with micrococcus luteus UV endonuclease. Biochemistry 20 3610-3614... 

Response to UVC Radiation and Bz. Similar features of the cellular response were examined after UVC + Bz treatm t as in the case of X or y rays + Bz (5). The results are summarized in Table 2. In contrast with LY-R cells and numerous other cell lines, LY-S cells were sensitized to UVC radiation by Bz. As in the case of X or y + Bz treatment, die distinct features of LY-S cell response to UVC + Bz treatment can be explained by low ligase I activity and hence, the necessity to activate ligase n. In LY-R cells, as in xeroderma pigmentosum cells (15), the rate of DNA incisions seems too low to activate poly(ADP-ribose) polymerase. On the other hand, LY-R cells may synthesize NAD+ more efficiently than LY-S cells (Table 1), and be able to maintain a stable NAD+ level in spite of poly(ADP-ribose) polymerase activation. In fact, when a double-labelling modification of the DNA unwinding method was used to examine the difference in sb frequency between Bz-treated and untreated UVC irradiated cells, the results were identical for LY-R and LY-S cells. We interpreted this as an indication of a Bz-sensitive base excision repair system (16,17) operating in both cell strains (in contrast with a nucleotide excision functional only in LY-S strain). Lack of nucleotide excision presumably makes LY-R cells sufficiently sensitive to UVC radiation that the base excision repair is not limiting for survival. 

E. A. de Weerd-Kastelein, W. Keijzer, G. Rainaldi, and D. Bootsma, Induction of sister chromatid exchanges in xeroderma pigmentosum cells after exposure to ultraviolet light, Mutat. Res. 45, 253-261 (1977). 

S. Wolff, B. Rodin, and J. E. Cleaver, Sister chromatid exchanges induced by mutagenic carcinogens in normal and xeroderma pigmentosum cells. Nature London) 265, 347-349... 

J. E. Cleaver, Repair replication and sister chromatid exchanges as indicators of excisable and nonexcisable damage in human (xeroderma pigmentosum) cells, J. Toxicol. Environ. Health 2, 1387-1394 (1977). 

H. F. Stich, R. H. San, J. A. Miller, and E. C. Miller, Various levels of DNA repair synthesis in xeroderma pigmentosum cells exposed to the carcinogens, V-hydroxy and V-acetoxy-2-acetylaminofluorene, Nature London) New Biol. 238, 9-10 (1972). 

Cleaver, J.E., DNA repair with purines and pyrimidines in radiation- and carcinogen-damaged normal and Xeroderma pigmentosum human cells, Cancer Res., 33, 362,1972. 

Theron T, Fousteri MI, Volker M, Harries LW, Botta E, Stefanini M, Fujimoto M, Andressoo JO, Mitchell J, Jaspers NG, McDaniel LD, Mullenders LH, Lehmann AR (2005) Transcription-associated breaks in xeroderma pigmentosum group D cells from patients with combined features of xeroderma pigmentosum and Cockayne syndrome. Mol Cell Biol 25(18) 8368-8378 Thiriet C, Hayes JJ (2005) Chromatin in need of a fix phosphorylation of H2AX connects chromatin to DNA repair. Mol Cell 18(6) 617-622... 

Investigations by Yarosh over almost two decades have proven that liposomal carriers allow uptake of a DNA repair enzyme into the skin [57], This uptake significantly reduces the number of new actinic keratoses and new lesions of basal cell carcinoma in patients with xeroderma pigmentosum who were treated for 12 months [58], Moreover, in a mice model, transdermal vaccination by antigen incorporation into liposomes has also been demonstrated [59,60],... 

Basal cell nevus syndrome or xeroderma pigmentosum The efficacy and safety of imiquimod cream have not been established for patients with basal cell nevus syndrome or xeroderma pigmentosum. 

Natarajan, A.T., Verdegaal-lmmerzeel, E.A.M., Ashwood-Smifh, M.J. and Poulton, G.A. (1981) Chromosomal damage induced hy furocoumarins and UVA in hamster and human cells including cells from patients with ataxia telangiectasia and xeroderma pigmentosum. Mutation Research, 84, 113-124. 

The specific interaction of chemicals or radiation with DNA activate cdlular DNA repair processes which appear to play an important role in carcinogenesis. Eukaryotic cells show enhanced repair capacity for repair of viral nucleic add if the host cells are first damaged by chemicals or irradiation. The ihanced susceptibility to cancer of patients with defective repair systems, such as those with xeroderma pigmentosum, suggests that intact repair mechanisms are protective... 

In the rare genetic disease xeroderma pigmentosum, the cells cannot repair the damaged DNA, resulting in extensive accumulation of mutations and, consequently, skin cancers (Figure 29.28). The most common form of this disease is caused by the absence of the UV-specific excinuclease. 

De Weerd-Kastelein, E.A., Keijzer, W., Bootsma, D. (1972). Genetic heterogeneity of xeroderma pigmentosum demonstrated by somatic cell hybridization. Nature New Biol. 238, 80-83. 

E. coli bacteria4S) and in cultured human cells. In Fig. 21 the survival curves are given for human fibroblasts after treatment with various cispiatin concentrations50 The curves obtained for cells of patients suffering from inherited DNA repair deficiencies, such as xeroderma pigmentosum and Fanconi s anemia, clearly indicate that these cells are more susceptible to the cytotoxic activity of cispiatin than the same type of cells obtained from normal , healthy persons. 

XPA -/- (deletion across exons 3 and 4 of both XPA alleles, rendering cells totally defective in nucleotide excision DNA repair animals comparable to human xeroderma pigmentosum)... 

---