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  • American Association for Cancer Research (AACR)  (57)
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  • 1
    Online Resource
    Online Resource
    Abstract A40: The enhancement of p53 stability via the inhibition of JNK-modulated ubiquitination with the activation of redox factor 1 (Ref-1) in response to non-genotoxic antioxidant selenomethionine (semet)
    American Association for Cancer Research (AACR) ; 2008
    In:  Cancer Prevention Research Vol. 1, No. 7_Supplement ( 2008-11-01), p. A40-A40
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 1, No. 7_Supplement ( 2008-11-01), p. A40-A40
    Abstract: A40 p53 has been known to play an important role as an tumor suppressor gene for the maintaining of genome stability. In the field of cancer prevention study, p53 has been issued to clarify the mechanism of activation under the non-genotoxic cancer preventive agents containing antioxidant selenium. In previous our study, p53 has been reported to be the function of transcriptional activation activated without the genotoxicity through the redox modulation in response to selenomethionine (SeMet). In this study, we investigated that the mechanism of p53 protein stabilization enhanced by SeMet. Our data showed that the ubiquitinated p53 was decreased in the cells exhibiting the downregulation of JNK which is one of E3-ubiquitin ligases compared with in mock-treated cells suggesting that the JNK-modulated p53 ubiquitination might be inhibited by SeMet. To define the mechanism of the enhanced p53 stability in the presence of SeMet, redox factor 1 (Ref-1) which has been documented as one of the factors modulating the redox status in response to antioxidants was downregulated using siRNA. Our data showed the first time that the interaction of JNK and p53 was increased in Ref-1 siRNA-treated cells in the presence of SeMet implicating that the Ref-1 activated by SeMet might be involved in the inhibition of JNK-mediated p53 ubiquitination. Our study suggested that the enhancement of p53 stabilization in response to SeMet might provide an important clue for the cancer prevention. Citation Information: Cancer Prev Res 2008;1(7 Suppl):A40.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-08-A40
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
    detail.hit.zdb_id: 2422346-3
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  • 2
    Online Resource
    Online Resource
    Abstract LB-167: Identification of ionizing radiation (IR)-responsive mRNA in p53-deficient human non-small cell lung cancer (NSCLC) grown in three-dimensional cell culture system
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. LB-167-LB-167
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. LB-167-LB-167
    Abstract: Non-small cell lung cancer (NSCLC) has been known as the most common human malignancy. The p53 tumor suppressor gene is mutated in approximately 50 % of NSCLC. For treatment of lung cancer, radiotherapy using -ray is general treatment. However, many patients suffer from recurred disease. Therefore, the definite mechanism of radiation based on in vivo mimic system is required for effective remedical value to NSCLC. Most of radiation biology studies were performed in conventional monolayer culture system which can not represent in vivo tumor environment. Hence, study applying in vivo mimic three-dimensional culture system is necessary to elucidate the molecular mechanism of solid tumor. Here, we analyzed gene expression profile induced by ionizing radiation (IR) in H1299 cells grown as spheroid in three-dimensional cell culture system. Our data showed that different gene expression profiles among monolayer culture system, three-dimensional small spheroid and three-dimensional large spheroid system. Particularly, genes related with microenvironment including adhesion junction and hypoxia had different expression level in three-dimensional spheroid system compare with monolayer culture system. This study suggested that in vivo mimic three-dimensional cell culture engineering approach might provide critical clues for understanding of cellular responses in p53 mutated or deleted lung cancer cells against IR. (* This work was supported by Nuclear Research Development Program of the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korean government (MEST). (Grand code: 2007-2001431, 2008-2001694, 2009-0078295) from Korea Science and Engineering Foundation) Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-167.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-LB-167
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
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    Online Resource
    Abstract 1236: Interferon consensus sequence binding protein (ICSBP)-induced cell proliferation mediated by TGF-β signaling pathway and MAPKs activation in HL-60 cells
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1236-1236
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1236-1236
    Abstract: Interferon consensus sequence binding protein (ICSBP), also known as IRF-8, is a member of the interferon (IFN)- regulatory factors (IRFs) induced by IFN-γ. ICSBP is mostly associated with differentiation of hematopoietic cells and known as a tumor suppressor. ICSBP contains the conserved transactivation domain which is shared by Smad4, suggesting a possible connection of IRF and TGF-β signaling. To test this connection, ICSBP was stably expressed in acute promyelocytic leukemia cell line, HL-60, that expresses little ICSBP. Although TGF-β receptor expression was undetectable in HL-60 cells, the expression of ICSBP in HL-60 (ICSBP-HL-60) resulted in an increased TGF-β receptor expression. Interestingly, even without TGF-β stimulation, both Smad and non-Smad pathways were activated in ICSBP-HL-60 cells compared with Mock-HL-60 cells, indicating ligand-independent activation of TGF-β receptor signaling. In addition, ICSBP expression augmented cell growth and suppression of ICSBP using siRNA specific for ICSBP abolished TGF-β receptor expression and attenuated cell growth. Consistently, reduction of TGF-βRI using siRNA or TGF-β receptor inhibitor, SB431542, also attenuated growth of ICSBP-HL-60 cells compared with Mock cells. Furthermore, MAPK pathways appeared to be involved in ICSBP-mediated cell growth because MAPKs are activated in ICSBP-HL-60 cells and specific inhibitor of this pathway was able to decrease the growth of ICSBP-HL-60 cells more sensitively than Mock-HL-60 cells. Suppression of ICSBP by siRNA effectively inhibited phosphorylation of MAPKs. All these data suggest that ICSBP up-regulates TGF-β receptor, activates ligand-independent TGF-β mediated signaling pathways, such as MAPKs activation, leading to cell proliferation. This study provides a new function of ICSBP in the regulation of cell proliferation Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1236.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-1236
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
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    Abstract 4996: Interferon consensus sequence binding protein (ICSBP) promotes epithelial to mesenchymal transition (EMT)-like phenomena, cell motility, and invasion via TGF-β signaling in U2OS cells
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 4996-4996
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 4996-4996
    Abstract: Interferon consensus sequence binding protein (ICSBP) is a transcription factor induced by interferon gamma (IFN-γ) and a member of the interferon regulatory factor (IRF) family. ICSBP is predominantly expressed in hematopoietic cells and regulates the immune response and cell growth and differentiation. However, little is known about its function in non-hematopoietic cells. Here we show a novel function for ICSBP in epithelial to mesenchymal transition (EMT)-like phenomena (ELP), cell motility, and invasion in human osteosarcoma cell lines, including U2OS cells. IFN-γ treatment induced ICSBP expression and EMT-like morphological change in U2OS cells, which were suppressed by ICSBP knock-down. To further investigate the role of ICSBP in ELP, we established a stable U2OS cell line that overexpresses ICSBP. ICSBP expression caused U2OS cells to have a more elongated shape and an increased vimentin and fibronectin expression. ICSBP expression also promoted adhesiveness, motility, and invasiveness of U2OS cells. ICSBP up-regulated transforming growth factor (TGF)-β receptors and activated TGF-β signaling cascades, which were responsible for ELP as well as increased cell motility and invasion. In addition, ICSBP-induced TGF-β receptor activation resulted in the up-regulation of Snail. Knock-down of Snail attenuated the ICSBP-induced augmentation of cell motility and invasion. Up-regulation of Snail, ELP, and increased invasion by ICSBP expression were also observed in other osteosarcoma cell lines, such as Saos-2 and 143B. Furthermore, ICSBP and TGF- β receptor I were expressed in 45/54 (84%) and 47/54 (87%) of human osteosarcoma tissues, respectively, and showed significant correlation (r= 0.47, p= 0.0007) with respect to their expression levels. Taken altogether, these data demonstrate a novel function for ICSBP in ELP, cell motility, and invasion through the TGF-β and Snail signaling pathways Citation Format: Jee Young Sung, Seog-Yun Park, June Hyuk Kim, Hyun Guy Kang, Jong Hyung Yoon, Yoon Sook Na, Yong-Nyun Kim, Byung-Kiu Park. Interferon consensus sequence binding protein (ICSBP) promotes epithelial to mesenchymal transition (EMT)-like phenomena, cell motility, and invasion via TGF-β signaling in U2OS cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4996. doi:10.1158/1538-7445.AM2014-4996
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-4996
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 5
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    Abstract 2208: Interferon Consensus Sequence-Binding Protein (ICSBP) regulates the transforming growth factor-beta type I receptor expression in osteosarcoma cells
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 2208-2208
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 2208-2208
    Abstract: Transforming growth factor-beta (TGF-β), known as a tumor suppressor, may exert tumor promoting activity in the advanced stage of cancer. Previously, we reported that interferon consensus sequence-binding protein (ICSBP), also known as interferon regulatory factor-8, up-regulates TGF-β type I receptor (TGF-βR I), and augments growth in HL-60 leukemic cells. In the current study, we demonstrate that ICSBP expression up-regulates TGF-βR I and increase in cell growth in U2OS human osteosarcoma cells. To further investigate the mechanism of TGF-βR I up-regulation by ICSBP, we tested the possibility that ICSBP regulates promoter activity of TGF-βR I gene. We analyzed the promoter region of the human TGF-βR I gene in U2OS cells to find putative transcription elements regulated by ICSBP. Luciferase reporter gene assays indicated that ICSBP expression could enhance TGF-βR I gene expression, and by promoter deletion analysis we identified a functional ICSBP-dependent region located at nucleotides -220 to +5 in the TGF-βR I promoter. We also performed EMSA (Electro Mobility Shift Assay) using probe and found that there are putative ICSBP binding sites between -222 to -204 regions. In conclusion, ICSBP increased TGF-βR I expression by binding to TGF-βR I promoter (-220/218) regions in U2OS cells. Note: This abstract was not presented at the meeting. Citation Format: Jee Young Sung, Hyeryeong Kim, Kyung-Sil Yoon, Yong-Nyun Kim, Byung-Kiu Park. Interferon Consensus Sequence-Binding Protein (ICSBP) regulates the transforming growth factor-beta type I receptor expression in osteosarcoma cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2208. doi:10.1158/1538-7445.AM2015-2208
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-2208
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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    detail.hit.zdb_id: 410466-3
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  • 6
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    Abstract LB157: Cereblon inhibits prostate cancer progression and metastasis by negatively regulating 6PGD
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 8_Supplement ( 2023-04-14), p. LB157-LB157
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 8_Supplement ( 2023-04-14), p. LB157-LB157
    Abstract: As the third enzyme of the pentose phosphate pathway (PPP), abnormally elevated levels of 6-phosphogluconate dehydrogenase (6PGD) have been documented in various human cancers. We demonstrate that reduced cereblon (CRBN) protein expression is the underlying mechanism of elevated 6PGD expression in metastatic prostate cancer cells. We establish 6PGD as a new endogenous substrate for CRBN by demonstrating that it interacts directly with CRBN and is ubiquitinated by CRL4CRBN. In addition, CRBN negatively regulates prostate cancer cell progression and metastasis, as abnormally high 6PGD, in the absence of sufficient CRBN, enhances the metastatic potential of prostate cancer in vitro and in vivo. Our findings show convincingly that carbohydrate metabolism regulated by 6PGD is linked to prostate cancer metastasis via CRBN. Based on these data, we propose that the 6PGD-CRBN axis may be a suitable target for further research into new therapeutics for mitigating prostate cancer metastasis. Citation Format: Koushik Guchhait, Hyeon Seung Yoon, Seungheon Shin, Hyun-Su An, Hye Seung Nam, Francisco D. Yanqui-Rivera, Samara M. Oña, Miguel Á. Mendez, Seokjae Park, Eun-Kyoung Kim, Jong Yeon Hwang, Jee-Young Han, Doo Yong Chung, Daeho Park, Su-Geun Yang, Chul-Seung Park, Steve K. Cho. Cereblon inhibits prostate cancer progression and metastasis by negatively regulating 6PGD [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 2 (Clinical Trials and Late-Breaking Research); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(8_Suppl):Abstract nr LB157.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-LB157
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 7
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    Abstract 475: Preoperativechemoradiation increases levels of immune system modulators in tumor tissue in locally advanced rectal cancer
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 16_Supplement ( 2020-08-15), p. 475-475
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 475-475
    Abstract: Purpose: Neoadjuvant chemoradiation therapy (CRT) is a widely and effectively used preoperative treatment strategy in locally advanced rectal cancers. However, little research has been done to characterize the molecular changes caused by neoadjuvant CRT in these cancer tissues. The purpose of this study was to investigate the effects of preoperative CRT on tumor gene expression in Korean patients with colorectal cancer (CRC). Materials and methods: We included 11 paired human rectal cancer tissues before and after irradiation between August 2016 and December 2017, and performed RNA sequencing analysis. Principal component analysis of CRC demonstrated strong similarity in respective groups of CRC tissues before and after CRT from CRC patients at the transcriptome level. Results: Volcano plot filtering identified 3325 differentially expressed genes (DEGs) in CRC tissues after CRT, compared to CRC tissues before CRT. Gene set enrichment analysis with DEGs revealed 45 signaling pathways associated with down-regulated target genes, significantly including the mismatch repair signaling pathway. CRT significantly increased tumor mutation burden (TMB) in CRC tissues. Notably, preoperative CRT increased immune signature scores including interferon-gamma, immune cytolytic score, and immune signature. Conclusion: Neoadjuvant CRT modulates immune-related characteristics of CRC, including increasing TMB and various immune signature scores, suggesting that neoadjuvant CRT has potential to improve responsiveness to immunotherapy. Citation Format: SungUk Bae, Shin Kim, Hye Won Lee, Sang Jun Byun, Jee Young Park, Hyeonji Min. Preoperativechemoradiation increases levels of immune system modulators in tumor tissue in locally advanced rectal cancer [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 475.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2020-475
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
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    Smoking Status and Occupational Exposure Affects Oxidative DNA Injury in Boilermakers Exposed to Metal Fume and Residual Oil Fly Ash
    American Association for Cancer Research (AACR) ; 2004
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 13, No. 3 ( 2004-03-01), p. 454-460
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 13, No. 3 ( 2004-03-01), p. 454-460
    Abstract: Epidemiologic studies demonstrate increased cancer incidence among workers exposed to polycyclic aromatic hydrocarbons (PAH) and metals, probably through cumulative oxidative DNA damage in response to carcinogens. Boilermakers are exposed to particulates of residual oil fly ash (ROFA) and metal fume that contain carcinogenic PAH and metals. We conducted a repeated-measures cohort study in boilermakers during the overhaul of an oil-fired boiler to determine a possible association between the level of 8-hydroxy-2′-deoxyguanosine (8-OH-dG; an oxidative injury biomarker) and biomarkers of PAH (1-hydroxypyrene; 1-OHP) and metal exposure. Preshift and postshift urine samples were analyzed for 8-OH-dG, cotinine, 1-OHP, and metals. Generalized estimating equations were used to model the multivariate relationship of 8-OH-dG to the explanatory variables of interest. Biomarker levels were determined for 181 urine samples from 20 male subjects (mean age 45 years, 50% smokers). Metal and 1-OHP levels increased cross-week and were affected by smoking status. Levels of 8-OH-dG were higher in nonsmokers at the start of the workweek yet declined after occupational exposure to similar levels as in smokers. Multivariate analysis indicated that metal × cotinine interaction terms for nickel, vanadium, chromium, and copper were significantly associated with the 8-OH-dG level, but there were differential effects depending on the metal. This study suggests that oxidative DNA damage in boilermakers is influenced by the interaction between occupational exposures and smoking status. In addition, boilermakers may have reduced ability to repair damaged DNA after ROFA and metal fume exposure. This finding has clinical relevance because these exposures may increase the cancer susceptibility of boilermakers.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.454.13.3
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2004
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 9
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    A Urinary Metabolite of Phenanthrene as a Biomarker of Polycyclic Aromatic Hydrocarbon Metabolic Activation in Workers Exposed to Residual Oil Fly Ash
    American Association for Cancer Research (AACR) ; 2005
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 14, No. 3 ( 2005-03-01), p. 687-692
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 14, No. 3 ( 2005-03-01), p. 687-692
    Abstract: Residual oil fly ash is a chemically complex combustion product containing a significant component of potentially carcinogenic transition metals and polycyclic aromatic hydrocarbons (PAH). Various biomarkers of PAH exposure have been investigated previously, most notably 1-hydroxypyrene (1-OHP), in urine. In this study, we assessed the utility of r-1,t-2,3,c-4-tetrahydroxy-1,2,3,4-tetrahydrophenanthrene (trans, anti-PheT), a metabolite of phenanthrene, to detect occupational PAH exposure. Urine samples collected across the workweek were analyzed for 1-OHP and trans, anti-PheT in boilermakers (n = 20) exposed to residual oil fly ash. Median baseline urinary trans, anti-PheT concentrations were 0.50 μg/g creatinine in current tobacco smokers and 0.39 μg/g creatinine in nonsmokers. Median baseline urinary 1-OHP concentrations in smokers and nonsmokers were 0.31 and 0.13 μg/g creatinine, respectively. To study further the effect of smoking exposure on the urinary PAH markers, urinary cotinine was used. Although urinary trans, anti-PheT and 1-OHP concentrations were correlated (Spearman r = 0.63; P & lt; 0.001) for all subjects, the regression coefficient between log-transformed trans, anti-PheT and log 1-OHP was statistically significant only for subjects with low levels of urinary cotinine or for nonsmokers. Each 1-unit increase in log 1-OHP was associated with a 0.77-unit increase (95% confidence interval, 0.45-1.09) in log trans, anti-PheT in subjects with low levels of urinary cotinine (P & lt; 0.001). In these subjects, dichotomized occupational exposure status was a significant predictor of log trans, anti-PheT (P = 0.02) but not of log 1-OHP (P = 0.2). In conclusion, we found that urinary trans, anti-PheT was detected in levels comparable with 1-OHP in occupationally exposed workers, particularly nonsmokers. This study shows that urinary trans, anti-PheT may be an effective biomarker of uptake and metabolic activation of PAHs.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-04-0428
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2005
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  • 10
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    Abstract 3065: Interferon consensus sequence-binding protein (ICSBP) regulates the transforming growth factor-beta type I receptor expression in osteosarcoma cells
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 3065-3065
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 3065-3065
    Abstract: Transforming growth factor-beta (TGF-β), known as a tumor suppressor, may exert tumor promoting activity in the advanced stage of cancer. Previously, we reported that interferon consensus sequence-binding protein (ICSBP), also known as interferon regulatory factor-8, up-regulates TGF-βtype I receptor (TGF-βR I), and augments growth in HL-60 leukemic cells. In the current study, we demonstrate that ICSBP expression up-regulates TGF-βR I and increase in cell growth in U2OS human osteosarcoma cells. To further investigate the mechanism of TGF-βR I up-regulation by ICSBP, we tested the possibility that ICSBP regulates promoter activity of TGF-βR I gene. We analyzed the promoter region of the human TGF-βR I gene in U2OS cells to find putative transcription elements regulated by ICSBP. Luciferase reporter gene assays indicated that ICSBP expression could enhance TGF-βR I gene expression, and by promoter deletion analysis we identified a functional ICSBP-dependent region located at nucleotides −300 to −1 in the TGF-βR I promoter. We also performed chromatin immunoprecipitation using anti-ICSBP and found that there are putative ICSBP binding sites in −300 to −1 region. In conclusion, ICSBP increased TGF-βR I expression by binding to TGF-βR I promoter (−300/−1) in U2OS cells. Exploration for the specific ICSBP binding sequences within TGF-βR I promoter (−300/−1) is under way, which may be helpful in understanding the regulatory mechanism involved in TGF-βR I expression by ICSBP. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3065. doi:1538-7445.AM2012-3065
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-3065
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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