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  • American Association for Cancer Research (AACR)  (16)
  • 2015-2019  (16)
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  • American Association for Cancer Research (AACR)  (16)
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  • 2015-2019  (16)
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  • 1
    Online Resource
    Online Resource
    The Effects of Physical Activity and Body Fat Mass on Colorectal Polyp Recurrence in Patients with Previous Colorectal Cancer
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Prevention Research Vol. 10, No. 8 ( 2017-08-01), p. 478-484
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 10, No. 8 ( 2017-08-01), p. 478-484
    Abstract: We aimed to identify the effects of physical activity and body composition on colorectal polyp recurrence in patients with previous colorectal cancer. A total of 300 patients were selected randomly from the colorectal cancer survivor cohort of Severance Hospital (Seoul, Korea). Patients reported various recreational physical activities and received surveillance colonoscopy. Body composition was measured with a body composition analyzer. We compared patients who exercised for at least 1 hour/week (active) with those who exercised less frequently or not at all (sedentary). The active exercise group (n = 203) had a lower recurrence of advanced adenoma than the sedentary group (n = 97; 6.4% vs. 14.4%, P = 0.023). The prevalence of advanced adenoma recurrence decreased in an exercise dose-dependent manner (Ptrend = 0.019). In multivariate logistic analysis, the independent factors associated with advanced polyp recurrence were body fat mass [OR, 7.601; 95% confidence interval (CI), 1.583–36.485; P = 0.011] and active exercise (OR, 0.340; 95% CI, 0.143–0.809; P = 0.015). In Cox proportional hazards models, body fat mass (HR, 5.315; 95% CI, 1.173–24.083; P = 0.030) and active exercise (HR, 0.367; 95% CI, 0.162–0.833; P = 0.017) were the independent factors associated with cumulative advanced adenoma recurrence. In conclusion, exercising for at least 1 hour/week and low body fat mass were found to be related to lower rates of colorectal polyp recurrence in the surveillance of colorectal cancer survivors. Cancer Prev Res; 10(8); 478–84. ©2017 AACR.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.CAPR-17-0065
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
    detail.hit.zdb_id: 2422346-3
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  • 2
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    Abstract 3057: Synthetic novel Psammaplin A derivatives enhance radiation lethality in human cancer cells
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 3057-3057
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 3057-3057
    Abstract: DNA methyltransferase (DNMT) inhibitors show not only anticancer effects but radiosensitization activity. Psammaplin A (PsA), a known DNMT inhibitor, enhances radiation lethality of human cancer cells, but the chemical instability hampers in vivo application of PsA. The purpose of the present study was to synthesize novel radiosensitizers using PsA as the backbone structure. Eight novel PsA-based derivatives (MA2, MA3, MA5, MA6, MA7, MA8, MA9 and MA5M) were synthesized. They were tested for in vitro cytotoxicity and radiosensitizing effects in A549 (lung cancer) and U373MG (glioblastoma) cells using a clonogenic assay. A paired ratio t-test was used to test a statistical significance of sensitizer enhancement ratios of the compounds. All 8 PsA derivatives inhibited in vitro cell survival with 50% inhibitory concentrations ranging 16-150 μM (A549) and 15-50 μM (U373MG). MA7, MA9 and MA5M significantly enhanced radiation lethality in A549 cells, while compounds MA2, MA3 and MA7 showed a significant radiosensitization in U373MG cells (p & lt;0.05). MA3 and MA6 marginally radiosensitized A549 and U373MG cells, respectively (p & lt;0.10). For further investigation, we selected MA3 and MA7, because only these two compounds showed radiosensitization in both A549 and U373MG cell lines. A DNMT activity assay showed that MA3 inhibited DNMT1 activity, but that MA7 showed no inhibitory effect on DNMT1. Pharmacokinetic parameters were determined in mice by a validated LC-MS/MS assay method using a non-compartmental analysis. The average degradation half-life of MA3 and MA7 was under 10 minutes in mouse serum. In the present study, we synthesized two novel PsA-derived compounds that enhanced radiation lethality in two human cancer cell lines. However, they lacked chemical stability to allow for in vivo experiments. Based on the present study, a further study is necessary to improve bioavailability of PsA-derived radiosensitizers. [Supported by 2013M2A2A7043683] Citation Format: Jin Ho Kim, Chan Woo Wee, Hak Jae Kim, Soo Youn Suh, Eun Sook Ma, Boom Soo Shin, Il Han Kim. Synthetic novel Psammaplin A derivatives enhance radiation lethality in human cancer cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3057.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-3057
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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    detail.hit.zdb_id: 410466-3
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  • 3
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    Abstract B28: Clinicopathological features associated with late recurrence of gastric cancer
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 26, No. 5_Supplement ( 2017-05-01), p. B28-B28
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 26, No. 5_Supplement ( 2017-05-01), p. B28-B28
    Abstract: Background: Because most cases of cancer recurrence occur within 5 years, routine surveillance is also recommended for first five years. However, few patients experience late recurrence of disease, and the mechanism of late recurrence is not clearly revealed. The purpose of this study is to evaluate the clinicopathological features predicting the risk of late recurrence in gastric cancer patients. Methods: From January 2006 to December 2013, we retrospectively reviewed 813 patients who were diagnosed and treated with gastric cancer in Yonsei cancer center. Result: Among 226 patients who experienced recurrence of gastric cancer, 212 patients were diagnosed with recurrence within first five years from the curative resection of primary cancer, and 14 patients were diagnosed with recurrence of disease beyond 5 years. In comparison with early recurrence (≤ 5 years), the patients with late recurrence ( & gt; 5 years) had primary disease of stage I/II (vs. stage III; HR, 4.5; 95% CI, 1.5-14.1; P=0.009), well or moderately differentiated histology (vs. poorly differentiated or signet ring cell; HR, 4.2; 95% CI, 1.4-13.1; P=0.013), and did not receive adjuvant chemotherapy (HR, 0.3; 95% CI, 0.1-0.9; P=0.028). All the 21 patients with HER2 positive gastric cancer experienced early recurrence. Conclusion: Late recurrence of gastric cancer is possibly not influenced by advanced stage of primary disease. More attempts to find high risk groups for late recurrence of gastric cancer are needed. Citation Format: Ji Soo Park, Chu Ree Won, Taeil Son, Hyoung-Il Kim, Woo Jin Hyung, Sung Hoon Noh, Tae Il Kim. Clinicopathological features associated with late recurrence of gastric cancer. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr B28.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1538-7755.CARISK16-B28
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 4
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    Abstract 2669: Identification of a novel small-molecule inhibitor for treatment of human colon cancer patients
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 2669-2669
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 2669-2669
    Abstract: As the representative targeted anticancer drug for colon cancer patients, Erbitux is the EGFR targeted therapeutic antibody and used for treatment of KRAS wild-type colon cancer patients. Even some patients with KRas wt gene did not respond to Erbitux. However, there is no treatment available for Erbitux-resistant patient group with KRAS WT gene, which is almost 50% of KRAS WT gene holders. Recently, our team identified Erbitux primary resistant related proteins named as CRG (Cetuximab-Resistant Gene) by array analysis based Erbitux responder or nonresponder colon cancer patients derived tissues and confirmed by in vitro and in vivo assay system. Based on these results, we synthesized a novel series of CRG targeted inhibitor. CRG inhibitor (CRG i;WM compound) is a lead compound for treating colon cancer patients who do not respond to Erbitux and have KRAS wild-type gene. CRG i has potent in vitro enzyme activity and high anticancer activity against various colon cancer cell lines with good selectivity in in vitro and in vivo system. Furthermore, the compound has good potent ADME/Tox. profiles for optimized lead. CRG i also displays strong anticancer effect in in vivo xenograft models and patient-derived xenograft (PDX) models. In addition, CRG i shows promising signs of overcoming Erbitux resistance in CRG knockout cells-derived xenograft model. We continue to discover improved preclinical candidates with better selectivity and ADME/Tox. profiles and validate predictive biomarker in colon cancer patients. In these efforts, we found some compounds with better profiles than CRG i. We are also trying to develop small molecules having highly potent activity against mutant CRG. In conclusion, active CRG is a promising biomarker and target for Erbitux-resistant KRAS wt colon cancer patients. Our compounds can be promising therapeutic agents for Erbitux-resistant KRAS wt colon cancer patients. Citation Format: Chun-Ho Park, Sun-Chul Hur, Joseph Kim, Dae Hee Lee, Yoon Sun Park, Jae-Sik Shin, Seung-Woo Hong, Jai-Hee Moon, Hyojin Kim, So Hee Lee, Hyebin Park, Joonyee Jung, Mi Jin Kim, Sang Soo Park, Jun Ki Hong, Ji Hee Gong, Jieun Kim, Il-Whea Ku, Hyun Ho Lee, Dong-Hoon Jin. Identification of a novel small-molecule inhibitor for treatment of human colon cancer patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2669.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-2669
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    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 2909: Development of new mechanism based therapeutic antibodies in non-small cell lung cancer
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 2909-2909
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 2909-2909
    Abstract: Lung cancer is second most common cancer in the world. Non Small Cell Lung Cancer (NSCLC) accounts approximately 80-85% of all lung cancer diagnosis. Traditional therapies of this disease were surgical resection, chemotherapy, and radiotherapy, alone or in combination. In addition, targeted therapeutic approach was based on the concept of discovering genetic alterations and the signaling pathways in cancer. Recently, to overcome the critical points for standard therapies, many groups were studied immunotherapeutic approaches, such as programed cell-death protein 1 (PD-1) antibody. However, rational use of these agents has been limited by the lack of a definitive predictive biomarker. Therefore, we identified new target, cancer immunotherapy related gene, CMG by shRNA libraries screening analysis on chemo-agents & target therapy resistant non-small cell lung cancer cells. First of all, we investigated CMG expression by immunohistochemistry in various tissue microarray (TMA). These results show that CMG highly expressed in Lung cancer, Liver cancer, and gastric cancer. We investigated target potentials on lung cancer, liver cancer, and gastric cancer cell lines using in vitro and in vivo assay system. Knockdown of CMG by CMG shRNA was induced cell death in various cancer cell lines. In addition, suppression of CMG was induced tumor size regression in CMG shRNA stable cell lines-derived xenograft model. Based on these results, we synthesized a novel series of CMG therapeutic antibody. CMG therapeutic antibody is a lead antibody for treating Lung cancer patients who express CMG gene. These antibodies have anti-cancer effects and immunotherapeutic effects in lung cancer (NSCLC), liver cancer, and gastric cancer. In addition, the in vivo efficacy of CMG antibody was assessed in mouse lung cancer derived syngeneic mouse model. The CMG antibody was tri-daily i.p. injected and the tumor volume was measured and compared between groups. Dramatic tumor regression was observed in CMG antibody treated group. These results were shown that these antibodies have immunotherapeutic potentials. In conclusion, CMG is a promising target for Lung cancer patients (chemo-agents resistant or PD-1 resistant Lung cancer patienrts). Our antibodies can be promising therapeutic agents for lung cancer, Liver cancer, and gastric cancer. Citation Format: Jai-hee Moon, Dae Hee Lee, Jae-Sik Shin, Joseph Kim, Yoon Sun Park, Seung-Woo Hong, So Hee Lee, Mi Jin Kim, Joonyee Jung, Chun-Ho Park, Sun-Chul Hur, Hyojin Kim, Hyebin Park, Sang Soo Park, Jun Ki Hong, Ji Hee Gong, Jieun Kim, Hyun Ho Lee, Il-Whea Ku, Dong-Hoon Jin. Development of new mechanism based therapeutic antibodies in non-small cell lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2909.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-2909
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 6
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    Abstract 4872: Disulfiam, a re-positioned aldehyde dehydrogenase inhibitor, enhances radiosensitivity of human glioblastoma cells in vitro
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 4872-4872
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 4872-4872
    Abstract: Purpose : Glioblastoma, the most common brain tumor in adults, has poor prognosis. The purpose of this study was to determine the effect of disulfiram (DSF), an aldehyde dehydrogenase inhibitor, on in vitro radiosensitivity of glioblastoma cells with different methylation status of O6-methylguanine-DNA methyltransferase (MGMT) promoter and the underlying mechanism of such effect. Materials and Methods : Five human glioblastoma cells (U138MG, T98G, U251MG, U87MG, and U373MG) and one normal human astrocyte (NHA) cell were cultured and treated with DSF or 6MV x-rays (0, 2, 4, 6, 8 Gy). For combined treatment, cells were treated with DSF before irradiation. Surviving fractions fit from cell survival based on colony forming ability. Apoptosis, DNA damage repair, and cell cycle distribution were assayed by Western blot for cleaved caspase-3, γH2AX staining, and flow cytometry, respectively. Results : DSF induced radiosensitization in most of the glioblastoma cells, especially, in the cells with radioresistance as wildtype unmethylated promoter (MGMT-wt), but did not in normal NHA cell. DSF augmented or induced cleavage of caspase-3 in all cells after irradiation. DSF inhibited repair of radiation-induced DNA damage in MGMT-wt cells, but not in cells with methylated MGMT promoter (MGMT-meth). DSF abrogated radiation-induced G2/M arrest in T98G and U251MG cells. Conclusion : Radiosensitivity of glioblastoma cells were preferentially enhanced by pre-irradiation DSF treatment compared to normal cell, especially radioresistant cells such as MGMT-wt cells. Induction of apoptosis or inhibition of DNA damage repair may underlie DSF-induced radiosensitization. Clinical benefit of combining DSF with radiotherapy should be investigated in the future. Citation Format: Hyeon Kang Koh, Soo Yeon Seo, Jin Ho Kim, Hak Jae Kim, Eui Kyu Chie, Seung-Ki Kim, Il Han Kim. Disulfiam, a re-positioned aldehyde dehydrogenase inhibitor, enhances radiosensitivity of human glioblastoma cells in vitro [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4872.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-4872
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 7
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    Abstract 5589: Detection of epidermal growth factor receptor mutations from circulating tumor DNA versus archival tissue of lung cancer
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 5589-5589
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 5589-5589
    Abstract: Background: Epidermal growth factor receptor (EGFR) mutations are well known predictive marker of targeted therapy. We compared the sensitivity of EGFR mutation detection techniques between matched achival lung cancer tissue and peripheral blood sample. Methods: We collected the paired samples from plasma and paraffin-embedded tumor tissue obtained before EGFR-tyrosine kinase inhibitor (EGFR-TKI). DNA extraction was performed using the QIAamp MinElute virus spin kit and EGFR mutation analysis was done by two detection methods. The current standard test is the PNAClampTM (Clamp) which is the PNA-based PCR clamping that selectively amplifies only the mutated target DNA sequence. The new technique is the PANAMutyperTM EGFR test (Mutyper), which use PNA clamping-assisted fluorescence melting curve analysis. Results: A total of 295 (188 male and 107 female) patients were analyzed in this study. The histologic types were composed of 258 adenocarcinoma, 22 squamous cell carcinoma and 15 others. Most were clinical stage IV (137, 46.4%) and the EGFR mutation rate of tissue sample by standard Clamp test was 25.7%. Plasma sensitivity was significantly higher in Mutyper than Clamp (71.2% vs. 30.0%, p & lt;0.001) with tissue as reference. The overall concordance and degree of agreement between two samples were better in Mutyper (91.9%, k=0.762, p & lt;0.001) than Clamp (81.7%, k=0.344, p & lt;0.001). In tissue sample, the median progression-free survival (PFS) of EGFR sensitive group was significantly longer than negative group regardless of the two methods. In plasma sample, the median PFS was significantly longer only by Mutyper (9.9 vs. 2.2 months, p=0.001), not by Clamp (9.8 vs. 7.6 months, p=0.968). Conclusions: Mutyper was useful liquid biopsy technique with better sensitivity than standard Clamp test. Citation Format: In-Jae Oh, Hyeong-Won Seo, Hyun-Ju Cho, Ha-Young Park, Bo-Gun Kho, Jin-Sun Chang, Tae-Ok Kim, Hong-Jun Shin, Cheol Kyu Park, Jung-Hwan Lim, Yong-Soo Kwon, Yu-Il Kim, Sung-Chul Lim, Young-Chul Kim, Yoo-Duk Choi. Detection of epidermal growth factor receptor mutations from circulating tumor DNA versus archival tissue of lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5589.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-5589
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    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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    AHNAK Loss in Mice Promotes Type II Pneumocyte Hyperplasia and Lung Tumor Development
    American Association for Cancer Research (AACR) ; 2018
    In:  Molecular Cancer Research Vol. 16, No. 8 ( 2018-08-01), p. 1287-1298
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 16, No. 8 ( 2018-08-01), p. 1287-1298
    Abstract: AHNAK is known to be a tumor suppressor in breast cancer due to its ability to activate the TGFβ signaling pathway. However, the role of AHNAK in lung tumor development and progression remains unknown. Here, the Ahnak gene was disrupted to determine its effect on lung tumorigenesis and the mechanism by which it triggers lung tumor development was investigated. First, AHNAK protein expression was determined to be decreased in human lung adenocarcinomas compared with matched nonneoplastic lung tissues. Then, Ahnak−/− mice were used to investigate the role of AHNAK in pulmonary tumorigenesis. Ahnak−/− mice showed increased lung volume and thicker alveolar walls with type II pneumocyte hyperplasia. Most importantly, approximately 20% of aged Ahnak−/− mice developed lung tumors, and Ahnak−/− mice were more susceptible to urethane-induced pulmonary carcinogenesis than wild-type mice. Mechanistically, Ahnak deficiency promotes the cell growth of lung epithelial cells by suppressing the TGFβ signaling pathway. In addition, increased numbers of M2-like alveolar macrophages (AM) were observed in Ahnak−/− lungs, and the depletion of AMs in Ahnak−/− lungs alleviated lung hyperplastic lesions, suggesting that M2-like AMs promoted the progression of lung hyperplastic lesions in Ahnak-null mice. Collectively, AHNAK suppresses type II pneumocyte proliferation and inhibits tumor-promoting M2 alternative activation of macrophages in mouse lung tissue. These results suggest that AHNAK functions as a novel tumor suppressor in lung cancer. Implications: The tumor suppressor function of AHNAK, in murine lungs, occurs by suppressing alveolar epithelial cell proliferation and modulating lung microenvironment. Mol Cancer Res; 16(8); 1287–98. ©2018 AACR.
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-17-0726
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    detail.hit.zdb_id: 2097884-4
    SSG: 12
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  • 9
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    Abstract 1938: Comprehesive RNA-sequencing pipeline of cancer xenograft models
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1938-1938
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1938-1938
    Abstract: Since a solid pipeline for massively parallel sequencing in cancer xenograft model has not been built yet, it is necessary to establish a precise analysis pipeline. Massively parallel sequencing on xenograft samples result in mixed sequencing reads from the engrafted human tumor cells and murine tissue. It is necessary to accurately distinguish between these reads for subsequent data analysis. In the present study, we constructed an integrated RNA-Seq pipeline including genomic variation, expression profiling, and fusion gene analysis. To distinguish these reads into individual species, we used the merged reference that incorporates the two genome reference from human (hg19) and mouse (mm10). We tested our pipeline using 6 Primary and 4 metastatic gastric tumor of 6 patients and their derivative xenografts sequencing data. There were almost same amount of ambiguous reads when we aligned sequencing reads to merged reference or separate reference genome. Using merged reference, we efficiently distinguished compound sequencing reads between human and mouse without repetitive alignment processes. The proportion of sequencing reads from mouse in xenograft samples widely ranged from 2.64% to 49.25% per each sample. For expression profiling, we used HTSeq-count for measuring expression level of each sample. As expected, human-specific reads of ECM-receptor and focal adhesion related genes were specifically down-regulated in the xenograft tumors compared to primary tumor and normal tissues suggesting the depletion of human cells from the microenvironment of engrafted tumor tissues. Mouse-specific reads of those genes were highly expressed in the engrafted tissue. Differentially expressed genes between engraft tumor and paired normal tissue were shown to be enriched in the cell cycle and p53 signaling pathway and these showed that engrafted tumor tissues well represent characteristics of cancer cells. Note: This abstract was not presented at the meeting. Citation Format: Jinha Hwang, Jong-Il Kim, Jee-Soo Choi, Min Jung Kim, Charles Lee. Comprehesive RNA-sequencing pipeline of cancer xenograft models. [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 1938. doi:10.1158/1538-7445.AM2015-1938
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-1938
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
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    Abstract LB-092: Programmed death-ligand 1 is overexpressed in bronchial preneoplastic lesions: can it be a risk indicator
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. LB-092-LB-092
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. LB-092-LB-092
    Abstract: Compared to the vigorous development of targeted drugs and some of them are already become one of the best treatment of choices in lung adenocarcinoma, squamous lung carcinoma has no definite targets and treatment outcome is not yet superior to lung adenocarcinoma. Demonstration of initial carcinogenesis is benefitial in two aspects: cancer prevention and development of its targets. Studying preneoplastic lesions of bronchus can answer those questions. Preneoplastic lesion, which is considered to have malignant potential, may develop into invasive cancer by escaping from host immune response. CD274 (programmed death-ligand 1, PD-L1) interacts with PD-1, is known to inhibit CD8+ cytotoxic T lymphocyte and induce apoptosis and, also to promote the differentiation of CD4+ T cells into regulatory T cells, so finally evade immune surveillance. We hypothesized that PD-L1 may work as an immune evader in preneoplastic lesion during its carcinogenesis. We performed white light and/or autofluorescence bronchoscopy in patients who have risk factor(s) of lung cancer or are suspected to have a lung cancer. Interestingly, PD-L1 was also overexpressed in preneoplastic lesions especially in severe dysplasia of the bronchus. This finding implies overexpression of PD-L1 can involve at early step of carcinogenesis. Further studies are needed to demonstrate the role of PD-L1 in preneoplastic bronchial lesion potential to develop invasive cancer. Citation Format: Hee Sun Park, Bo Mi Park, Dong Il Park, Chung Jae Uk, Jae Young Moon, Jung Sung Soo, Choong Sik Lee, Ju Ock Kim, Sun Young Kim, Jaseok Peter Koo. Programmed death-ligand 1 is overexpressed in bronchial preneoplastic lesions: can it be a risk indicator. [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 LB-092. doi:10.1158/1538-7445.AM2015-LB-092
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-LB-092
    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: 1432-1
    detail.hit.zdb_id: 410466-3
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