|1.||Wu, Xifeng: 12 articles (09/2008 - 01/2002)|
|2.||Spitz, Margaret R: 11 articles (06/2008 - 01/2002)|
|3.||Wei, Qingyi: 7 articles (01/2012 - 10/2003)|
|4.||Wang, Li-E: 7 articles (01/2012 - 10/2003)|
|5.||Cheng, Ya-Wen: 4 articles (01/2013 - 01/2006)|
|6.||Lee, Huei: 4 articles (01/2013 - 01/2006)|
|7.||Dinney, Colin P: 4 articles (09/2008 - 04/2003)|
|8.||Sturgis, Erich M: 4 articles (08/2008 - 06/2007)|
|9.||Singh, Shivendra V: 4 articles (11/2007 - 02/2003)|
|10.||Grossman, H Barton: 4 articles (03/2006 - 04/2003)|
09/16/1997 - "The results of the present study suggest that differences in the ability of OSCs to modulate GST activity toward anti-BPDE may, at least in part, account for their differential chemopreventive efficacy against BP-induced cancer in mice."
08/01/2008 - "This study evaluated the hypothesis that common genetic variation in CSA and CSB is associated with mutagen sensitivity induced by BPDE in 276 cancer-free smokers. "
01/01/2014 - "As expected, BPDE caused significant DNA fragmentation in tumor compared to negative control tissues. "
07/01/2010 - "DNA damage in macroscopically healthy pharyngeal mucosal tissue of 30 patients with (15) and without cancer (15) of the oropharynx was evaluated after incubation with Benz[a]pyren-7,8-diol-9,10-epoxid (BPDE), a tobacco-associated carcinogen. "
10/01/2007 - "Chronic exposure of wild-type (Cdc25B+/+) MEFs to anti-BPDE (0.1 micromol/L) caused neoplastic transformation characterized by colony formation in culture and tumor production in nude mice. "
|2.||Lung Neoplasms (Lung Cancer)
07/15/2007 - "In conclusion, the present study points towards an important role of p53 in regulation of cellular responses to BPDE in human lung cancer cells."
01/01/2012 - "These results strongly suggest an important role for EGFR in BPDE-induced transformation, and substantiate that MUC1 is involved in lung cancer development, at least partly through mediating carcinogen-induced activation of the EGFR-mediated cell survival pathway that facilitates cell transformation."
07/15/2007 - "The H460 human lung cancer cell line (wild-type p53) was relatively more sensitive to BPDE-mediated growth inhibition and enrichment of sub-diploid apoptotic fraction compared with H1299 cells. "
07/01/2004 - "The predicted BPDE spectrum strongly resembles the G-->T mutation spectrum compiled from known lung cancer mutation data from smokers and further supports evidence that BPDE contributes to the overall smoking-related mutation distribution in lung cancer. "
10/01/2003 - "After exposing the cells to 4 microM BPDE for 5 h, we observed a significantly lower AC in lung cancer patients (155.2+/-143.9%) than in the controls (216.6+/-184.6%) (P<0.05). "
|3.||Xeroderma Pigmentosum (Kaposi's Disease)
01/01/1986 - "Xeroderma pigmentosum fibroblasts, complementation group A (XP12BE) had 20-25% more ESS at each dose than the BPDE-treated normal (HSBP) cells. "
01/01/2002 - "First, we treated apparently normal and xeroderma pigmentosum lymphoblastoid cell lines with various doses of benzo(a)pyrene diol epoxide (BPDE) and harvested cells at different time points. "
05/15/1991 - "We have now determined the kinds and location of independent mutations induced by BPDE in the coding region of the hypoxanthine (guanine) phosphoribosyltransferase gene of synchronized repair-deficient xeroderma pigmentosum cells (XP12BE, complementation group A), treated at S or in G1. "
06/01/1982 - "The cytotoxic and mutagenic effect of (+/-)-7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti BPDE) in normally excising diploid human cells treated just prior to onset of S was compared with that of cells allowed approximately 16 h for excision repair before onset of S and with that observed in excision-deficient xeroderma pigmentosum (XP12BE) cells. "
12/01/1987 - "Results of the studies in diploid human cells indicated that when compared on the basis of equal numbers of DNA adducts, BPDE is more effective than 1-NOP in inducing mutations in DNA repair-proficient cells, but when compared in repair-deficient xeroderma pigmentosum human cells that do not remove such adducts from their DNA, the frequency of mutants induced per adduct is equal. "
04/01/2008 - "In this study, we have characterized the effect of the ultimate carcinogenic DEs, (+)-anti-BPDE and (-)-anti-DBPDE following short exposure times, on Mdm2 and p53 pathway in A549 human lung epithelial carcinoma cells. "
02/01/2012 - "Here, we studied the role of p53 and the pro-apoptotic protein BAX in BPDE-induced cell death by using wild-type- or knock-out-human colon carcinoma cells. "
07/01/2010 - "BPDE caused significant DNA damage compared to the negative control in oropharyngeal mucosa cells of patients with- and without carcinoma. "
09/01/2009 - "BPDE caused significant DNA damage compared to the negative control in oropharyngeal mucosa cells of patients with and without carcinoma. "
10/01/2005 - "These expression data provide a clue to further cloning novel genes and studying functions in BPDE-induced carcinoma."
|5.||Genetic Predisposition to Disease (Genetic Predisposition)
08/01/2002 - "Our hypothesis is that the presence of BPDE-induced 3p21.3 aberrations is a biomarker of an individual's genetic susceptibility and that individuals with these aberrations are at an increased risk for HNSCC. "
07/01/1998 - "These findings suggest that high BPDE-induced b/c values in lymphocytes are an independent risk factor for SCCHN and a marker for genetic susceptibility to tobacco-induced carcinogenesis."
09/01/1996 - "The BPDE mutagen sensitivity assay will facilitate epidemiological studies of genetic susceptibility to smoking-related cancers."
08/01/2002 - "The results from this study demonstrated that 3p21.3 may be a specific molecular target of tobacco carcinogens and that BPDE sensitivity at this locus may reflect an individual's genetic susceptibility to HNSCC."
06/01/2008 - "This study demonstrates that chromosome 3p may be a specific molecular target of cigarette carcinogens and BPDE sensitivity in chromosome 3p may reflect the genetic susceptibility of an individual to renal cell carcinoma."
|2.||DNA (Deoxyribonucleic Acid)
|5.||Glutathione (Reduced Glutathione)
|8.||amsonic acid (DAS)