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  • American Association for Cancer Research (AACR)  (6)
  • 1
    Online Resource
    Online Resource
    Abstract B4: MicroRNAs differentially expressed in preoperative human serum of ovarian cancer
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 2_Supplement ( 2012-01-08), p. B4-B4
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 2_Supplement ( 2012-01-08), p. B4-B4
    Abstract: MicroRNAs (miRNAs) have been reported to play important regulatory roles in many biological processes and tumorigenesis. To investigate the roles of serum miRNAs in patients before tumor bulk was surgically removed from ovarian cancer patients, we utilized miRNA real-time QPCR profiling technology to characterize the miRNAs in pre-operative and postoperative sera. Six pairs of sera were analyzed using 270 miRNA SyberGreen probes. Upregulation of miR187, miR499-3p, miR548c-5p, miR1, miR107, miR125a-5p, miR18b were identified in the preoperative sera. Targetscan was utilized to identify Dab2 as the target gene of miR187. In vitro studies of SKOV3 cells showed that ectopic expression of miR187 suppressed Dab2 and resulted in increased cell proliferation. We concluded that miR187 may be a potential biomarker in sera of ovarian cancer patients. Further studies with larger sample sizes are warranted to validate our results. Citation Format: Angel Chao, Tzu Hao Wang, Hua-Chien Chen, Shu-Jen Chen, Chyong-Huey Lai. MicroRNAs differentially expressed in preoperative human serum of ovarian cancer [abstract]. In: Proceedings of the AACR Special Conference on Noncoding RNAs and Cancer; 2012 Jan 8-11; Miami Beach, FL. Philadelphia (PA): AACR; Cancer Res 2012;72(2 Suppl):Abstract nr B4.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.NONRNA12-B4
    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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  • 2
    Online Resource
    Online Resource
    Conditioning Regimens are Associated with Distinct Patterns of Microbiota Injury in Allogeneic Hematopoietic Cell Transplantation
    American Association for Cancer Research (AACR) ; 2023
    In:  Clinical Cancer Research Vol. 29, No. 1 ( 2023-01-04), p. 165-173
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 29, No. 1 ( 2023-01-04), p. 165-173
    Abstract: The gut microbiota is subject to multiple insults in allogeneic hematopoietic cell transplantation (allo-HCT) recipients. We hypothesized that preparative conditioning regimens contribute to microbiota perturbation in allo-HCT. Experimental Design: This was a retrospective study that evaluated the relationship between conditioning regimens exposure in 1,188 allo-HCT recipients and the gut microbiome. Stool samples collected from 20 days before transplantation up to 30 days after were profiled using 16S rRNA sequencing. Microbiota injury was quantified by changes in α-diversity. Results: We identified distinct patterns of microbiota injury that varied by conditioning regimen. Diversity loss was graded into three levels of conditioning-associated microbiota injury (CMBI) in a multivariable model that included antibiotic exposures. High-intensity regimens, such as total body irradiation (TBI)–thiotepa-cyclophosphamide, were associated with the greatest injury (CMBI III). In contrast, the nonmyeloablative regimen fludarabine–cyclophosphamide with low-dose TBI (Flu/Cy/TBI200) had a low-grade injury (CMBI I). The risk of acute GVHD correlated with CMBI degree. Pretransplant microbial compositions were best preserved with Flu/Cy/TBI200, whereas other regimens were associated with loss of commensal bacteria and expansion of Enterococcus. Conclusions: Our findings support an interaction between conditioning at the regimen level and the extent of microbiota injury.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-22-1254
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 3
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    Abstract 47: Nucleophosmin/B23 (NPM/B23) and estrogen receptor alpha (ER alpha) in endometrial cancer
    American Association for Cancer Research (AACR) ; 2016
    In:  Clinical Cancer Research Vol. 22, No. 1_Supplement ( 2016-01-01), p. 47-47
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 22, No. 1_Supplement ( 2016-01-01), p. 47-47
    Abstract: Purpose: Unopposed estrogen exposure is an important factor in the tumorigenesis of endometrial cancer. We aim to investigate the regulatory role of NPM/B23 in estrogen signaling in endometrial cancer. Methods: To elucidate the underlying mechanism, we performed RT-qPCR, western blotting, promoter assay, immunoprecipitation, proliferation assay, protein stability assay, and ubiquitination assay in endometrial cancer cell lines. Results: NPM/B23 was required for estrogen-induced endometrial proliferation, and the increase in NPM/B23 was estrogen receptor alpha (ER alpha)-dependent. Furthermore, estrogen increased NPM/B23 protein levels by repressing its ubiquitination and subsequently stabilizing the protein. The overexpression of alternate reading frame (ARF) suppressed the estrogen-induced increase in the NPM/B23 protein levels, indicating that ARF inhibited the observed estrogen-mediated NPM/B23 stabilization. Suppression of the NPM/B23-ARF interfered with the interaction and the subsequent increase in NPM/B23 protein levels. Conclusions: Characterization of NPM/B23 in estrogen-mediated cell proliferation may extend our understanding of the tumorigenesis of endometrial cancers. Targeting B23 with hormonal therapy can be further explored for the treatment of endometrial cancer. Citation Format: Chiao Yun Lin, Angel Chao, Tzu-Hao Wang, Chyong-Huey Lai. Nucleophosmin/B23 (NPM/B23) and estrogen receptor alpha (ER alpha) in endometrial cancer. [abstract]. In: Proceedings of the AACR Precision Medicine Series: Integrating Clinical Genomics and Cancer Therapy; Jun 13-16, 2015; Salt Lake City, UT. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(1_Suppl):Abstract nr 47.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1557-3265.PMSCLINGEN15-47
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 4
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    Abstract 626: Application of patient-derived xenograft model in nasopharyngeal carcinoma research
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 626-626
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 626-626
    Abstract: Nasopharyngeal carcinoma (NPC) was an Epstein Barr virus (EBV)-related malignancy and tumor microenvironment had a pivotal role in tumor progression. Paucity of good NPC animal models hindered the research in this field. Recently, patient-derived xenograft (PDX) had been shown to be a good preclinical model for drug screening and cancer related research. We had developed two PDX mice lines from engrafting NPC metastatic tumors. Positive EBV-encoded small RNAs staining confirmed these tumors harboring EBV. Further gene expression profile analysis showed higher similarity of PDX to primary parent tumor than NPC cell line xenograft. In vivo drug screening in the PDX system demonstrated gemcitabine had the best antitumor effect among the tested drugs. In this PDX corresponding patient also showed excellent response to gemcitabine treatment. Combination of gemcitabine and valproic acid had synergistic antitumor effect. Further adding ganciclovir in this two combined regimen enhancing cytolytic viral activation had the best antitumor response among the tested regimens. This three combined regimen treated group had lower plasma EBV-DNA load and tumor viral concentration and less viable tumor cells than gemcitabine + valproic acid group. These promising results would open a new era for EBV-targeting therapy in NPC treatment. Citation Format: Cheng-Lung Hsu, Yung-Chia Kuo, Yenlin Huang, Yin-Cheng Huang, Kar-Wai Lui, Kai-Ping Chang, Tung-Liang Lin, Hsien-Chi Fan, An-Chi Lin, Chia-Hsun Hsieh, Li-Yu Lee, Hung-Ming Wang, Hsin-Pai Li, Angel Chao, Yu-Sun Chang. Application of patient-derived xenograft model in nasopharyngeal carcinoma research. [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 626.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-626
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
    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 1445: Thyroid hormone receptor represses microRNA-130b to enhance cell metastasis
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 1445-1445
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 1445-1445
    Abstract: Thyroid hormone (T3) and its receptor (TR) are involved in cell growth and cancer progression. Although deregulation of miRNA expression has been detected in many tumor types, the mechanisms underlying functional impairment and specific involvement of miRNA in tumor metastasis remain unclear. We proposed that deregulation of specific miRNAs and target gene expressions mediated by T3/TR constitute critical steps of cancer progression. In the current study, we demonstrated that T3/TR negatively regulates microRNA-130b (miR-130b) expression, both in vitro and in vivo. Overexpression of miR-130b markedly inhibited cell migration and invasion in vitro and in vivo, which was mediated via suppression of interferon regulatory factor 1 (IRF1). Cell migration ability was promoted by T3, but partially suppressed upon miR-130b overexpression. Furthermore, miR-130b suppressed the expression of epithelial-mesenchymal transition (EMT)-related genes, matrix metalloproteinase (MMP)-9, p-AKT and p-signal transducer and activator of transcription (STAT)-3. Notably, miR-130b was downregulated in hepatoma samples and inversely correlated with TR and IRF1. Our data collectively highlight a novel pathway interlinking T3/TR, miR-130b, EMT-related genes, MMP9, p-AKT and p-STAT3 cascade that regulates the motility and invasion of hepatoma cells. Thus, miR-130b activation may be a useful strategy for cancer treatment in metastatic HCC. Citation Format: Yang Hsiang Lin, Meng-Han Wu, Yung-Hsin Yeh, Angel Chao, Kwang-Huei Lin. Thyroid hormone receptor represses microRNA-130b to enhance cell metastasis. [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 1445. doi:10.1158/1538-7445.AM2014-1445
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-1445
    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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  • 6
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    Abstract 3018: Gonadotropin-releasing hormone type II (GnRH-II) agonist regulates the invasiveness of endometrial cancer cells through GnRH-I receptor and mitogen-activated protein kinases (MAPKs)-dependent activation of matrix metalloproteinase (MMP)-2
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 3018-3018
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 3018-3018
    Abstract: Introduction: More than 25% of patients diagnosed with endometrial carcinoma have an invasive primary cancer accompanied by metastases. The GnRH has an important role in reproduction. In mammals, GnRH-II is more widely identified than GnRH-I in peripheral tissues. GnRH-II may regulate tumor progression of endometrial cancer. MAPKs have been considered important components of GnRH-induced signaling pathways. MMPs are largely implicated in promoting angiogenesis and tumor metastasis. In the present study, we examined the action of GnRH-II agonist-promoted motility of endometrial cancer cells and the mechanisms of the action in endometrial cancer. Materials and methods: Endometrial cancer cell line Ishikawa and ECC-1 were derived from an endometrial adenocarcinoma. D-Arg6, AzaGly10-GnRH II was a synthetic decapeptide. Cell motility was estimated by invasion and migration assay. The activities of MMP-2 was assessed by gelatin zymography. Immunoblot analysis was done to study the expression of GnRH-I receptor and the effects of GnRH-II agonist in the activation of ERK1/2, JNK and MMP-2. ERK1/2 inhibitor (U0126), and JNK inhibitor (SP600125) were pretreated for 30 min to evaluate the effects of MAPKs. MMP-2 inhibitor (OA-Hy) was pretreated for 30 min to evaluate the effects of MMP-2 in cell motility. Human GnRH-I receptor siRNA was used to knock down the expression of GnRH-I receptor. Results: The GnRH-I receptor was expressed in endometrial cancer cells. The GnRH-II agonist promoted cell motility in a dose-dependent manner. GnRH-II agonist activated the phosphorylation of ERK1/2 and JNK signaling and the phosphorylation was abolished by 1μM U0126 and 1μM SP600125. GnRH-II agonist-promoted cell motility was suppressed in cells pretreated with U0126 and SP600125. Moreover, U0126 and SP600125 abolished GnRH-II agonist-induced activation of MMP-2. Inhibition of MMP-2 with 10μM OA-Hy suppressed cell motility in response to GnRH-II agonist. GnRH-II agonist-mediated cell motility was suppressed by knockdown of endogenous GnRH-I receptor with siRNA. Conclusion: Our results confirmed that GnRH-I receptor may be a common receptor that mediates the effects of both GnRH-I and GnRH-II in endometrial cancer cells. Our study shows that the GnRH-II agonist promoted the cell motility of endometrial cancer cells through the GnRH-I receptor, and the phosphorylation of ERK1/2 and JNK-dependent activation of MMP-2. Our findings represent a new concept regarding the mechanisms of GnRH-II-promoted cell motility in endometrial cancer cells, suggesting the possibility of GnRH-II as a potential therapeutic intervention for the treatment of human endometrial cancer. 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 3018. doi:1538-7445.AM2012-3018
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-3018
    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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