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  • 1
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 4515-4515
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 4515-4515
    Abstract: Background and Aims: X-linked inhibitor of apoptosis (XIAP)-associated factor 1(XAF1) is a novel identified XIAP antagonist and a potential tumor suppressor. Our previous study has shown that stable overexpression of XAF1 could induce apoptosis and inhibit tumorigenesis in hepatocellular carcinoma (HCC). However, the therapeutic effect and mechanism of XAF1 on HCC remains unknown. Materials and Methods: Recombinant adenovirus Ad5/F35-XAF1 and control virus Ad5/F35-Null were generated. Cellular proliferation was detected by methyl thiazolyl tetrazolium (MTT). Cell apoptosis was determined by Flow cytometry using Annexin V-FITC/PI double staining and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL). The expression of genes was detected by RT-PCR, Western Blot and immunohistochemistry (IHC). Tumor growth in vivo was determined in a nude mice xenograft model. Microvessel density (MVD) was measured by CD31 IHC staining. Results: The expression of XAF1 was extremely low or undectable in four HCC cell lines (SMMC7721, Hep3B, HepG2, Bel7404) and 30 human HCC tissues compared with the paired non-cancer liver tissues, while the high expression of XIAP was detected in HCC tissues than in normal live tissues. Infection of Ad5/F35-XAF1 virus increased the expression of XAF1 in all 4 HCC cell lines, significantly inhibited cell proliferation and induced cell apoptosis in a dose- and -time dependent manner, resulting in the cleavage of caspase-3, −8, −9 and PARP, release of cytochrome c, upregulation of pro-apoptotic protein Bax and BNIP3L, and downregulation of XIAP. Furthermore, intra-tumoral injection of Ad5/F35-XAF1 virus significantly induced apoptosis in vivo and inhibited HCC xenograft growth. Notably, Ad5/F35-XAF1 virus treatment significantly upregulated the expression of angiopoietin-2 protein and decreased MVD in tumor xenograft tissues. Furthermore, adeno-XAF1 treatment significantly prolonged the survival time of animals bearing tumor xenografts. No obvious pathological changes in main organs were observed in XAF1 virus-treated mice. Conclusion: Our results show that restoration of XAF1 expression obviously induces cell apoptosis and inhibits the HCC both in vitro and in vivo. Expression of XAF1 could significantly suppressed tumor angiogenesis probably through upregulating angiopoietin-2 expression to remold the newly-born vessels. Our results suggest that XAF1 may have a potential candidate for HCC gene therapy. The project was supported by National Nature Science foundation of China No. 30500221 (Tu SP) and NIH grant R01CA120915 (Yang CS). *Corresponding author: Shui-Ping Tu, E-mail: Tushuiping@yahoo.com. 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 4515.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 2
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1412-1412
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1412-1412
    Abstract: Background: The tumor microenvironment plays a pivotal role in carcinogenesis. Myofibroblasts, a major component of tumor stroma, have been demonstrated to be derived in a large part from bone marrow. However, the specific contributions of bone marrow-derived myofibroblasts to cancer growth and progression are not completely understood. In this study, we established bone marrow-derived (BMD) inflammation-related gastric myofibroblasts (MF) and investigated the role of BMD-MF in tumor growth. Methods: Gastric myofibroblast were isolated from EGFP bone marrow-transplanted IL-1β transgenic mice and wild type mice. Gene expression was assessed by real-time RT-PCR, immunocytochemistry staining and Western blot. The levels of cytokines and chemokines were measured by ELISA. Cell migration and invasion were determined by transwell migration assay and 3-D organic co-culture system, respectively. Tumor growth in vivo was determined in a SCID xenograft model. Results: We isolated and cultured successfully gastric myofibroblasts from BMT-IL-1β mice and WT mice. The pure BMD-MF (EGFP+) expressed myofibroblast markers (a-SMA and vimentin), but did not expressed markers of epithelial cells (E-cadherin). The mRNA expression of IL-1β, TNF-α, IL-6, SDF-1, MMP-1, TGF-β and COX-2 was significantly higher in the BMD-IL-1β-MF than WT-MF. Furthermore, BMD-IL-1β-MF secreted much higher levels IL-6 and SDF1 peptides in the culture medium than did WF-MF. The BMD-IL-1β MF significantly increased gastric cancer cell migration and invasion compared to WT-MF, and CXCR4 inhibitor (AMD3100) reduced cell migration induced by both myofibroblasts, indicating that the SDF1/CXCR4 axis is responsible for cell migration and invasion. Furthermore, in xenograft studies SCID mice co-injected gastric cancer cells (105 MKN45) and BMD-IL-1β MF formed larger size tumor compared those co-injected with WT-MF and those injected alone with gastric cancer cells. Mice injected with MKN45 alone on the left side and BMD-IL-1β-MF alone on the right side, surprisingly formed larger size tumors on the left side compared to those non-injected with BMD-IL-1β-MF on the right side. Furthermore, the EGFP+ MF could be detected in the xenograft tumor on the left side, suggesting that MF can migrate to the contralateral tumor and promote tumor growth. Moreover, treatment of CXCR4 inhibition (AMD3100) reduced tumor growth and the migration of MF to the contralateral tumor, indicating that SDF1/CXCR4 axis plays an important in the migration of myofibroblast and tumor growth. Conclusion: Our results for the first time show that tumor-associated myofibroblasts in the IL-1β gastric cancer model are bone marrow derived and have a stronger capacity to promote growth and invasion. The project was support by NIH grant 5U54CA126513, R01CA093405 and R01CA120979 (Wang TC) and NIH grant R01A120915 (Yang CS). 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 1412.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 3
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Prevention Research Vol. 3, No. 12_Supplement ( 2010-12-01), p. CN12-04-CN12-04
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 3, No. 12_Supplement ( 2010-12-01), p. CN12-04-CN12-04
    Abstract: Most gastrointestinal cancers arise in the setting of chronic inflammation, but which leads to the recruitment of additional stromal cells, but the nature of these cells have not been well-defined. Carcinoma-associated fibroblasts (CAFs) that express alpha-smooth-muscle-actin (αSMA+) are thought to contribute to cancer progression but their precise origin has not been established. We have employed IL-1β transgenic mice and Helicobacter felis-infected mice that develop gastric dysplasia and cancer to investigate the origins and contributions of CAFs. These studies suggest that chronic inflammation of the GI tract, along with other carcinogenic stimuli, results in remodeling of the bone marrow and recruitment of bone marrow-derived cells to the incipient cancer site. At least 20% of CAFs originate from BM cells, and BM-derived CAFs promote tumor growth in organotypic and xenograft models. Thus, BM-derived fibroblastic cells create a new cancer niche that contributes to the progression of cancer, and as such represent a potential target for cancer prevention therapy. Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN12-04.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 4
    In: Journal of Membrane Science, Elsevier BV, Vol. 676 ( 2023-06), p. 121606-
    Type of Medium: Online Resource
    ISSN: 0376-7388
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 1491419-0
    SSG: 12
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  • 5
    In: Journal of Molecular Catalysis A: Chemical, Elsevier BV, Vol. 410 ( 2015-12), p. 193-201
    Type of Medium: Online Resource
    ISSN: 1381-1169
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2015
    detail.hit.zdb_id: 2020478-4
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  • 6
    In: Cancer Cell, Elsevier BV, Vol. 19, No. 1 ( 2011-01), p. 154-
    Type of Medium: Online Resource
    ISSN: 1535-6108
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2011
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    detail.hit.zdb_id: 2078448-X
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    American Society of Clinical Oncology (ASCO) ; 2023
    In:  Journal of Clinical Oncology Vol. 41, No. 16_suppl ( 2023-06-01), p. e15592-e15592
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 41, No. 16_suppl ( 2023-06-01), p. e15592-e15592
    Abstract: e15592 Background: The treatment in patients with metastatic colorectal cancer (mCRC) have limited effectiveness and options. And research findings have revealed that combining anti-angiogenesis inhibitors with programmed death-1(PD-1) inhibitors can reverse the immunosuppressive tumor microenvironment and synergistically enhance the antitumor immune response. The goal of the study was to add more real-world data to prove the clinical efficacy and safety of this regimen. Methods: We conducted a Real-World observation study by comparison of the efficacy and safety of fruquintinib versus fruquintinib combined with PD-1 inhibitor in patients with mCRC who received treatment between June 2019 and October 2022 in our center. Results: A total of 106 patients with mCRC were observed to receive fruquintinib(F group) (n = 26, mean age = 63 years, female = 46.2%) or fruquintinib combined with PD-1 inhibitor (FP group)(n = 80, mean age = 62 years, female = 46.3%). 3.8% of patients achieved partial response (PR) in FP group and 47.5% had stable disease (SD). Of the F group, no patient had PR and SD was 50%. No difference was found for median progression-free survival(PFS) (F group 6.7 months vs. FP group 4.5 months, p = 0.271). Median overall survival(OS) was significantly prolonged with F group compared with FP group (18.7 months vs. 13.6 months, p = 0.008), which was mainly attributed to the disease course before the treatment of fruquintinib or fruquintinib combined with PD-1 inhibitor in the two groups (42.9 months vs. 31.8 months, p = 0.031). And univariate Cox regression analysis showed that clinical factors (Stage at first diagnosis, PD-L1 gene, number of organs with metastases, and operative treatment) were associated with OS in the FP group (p 〈 0.05), while only PD-L1 gene positive had significant difference in multivariate analysis (p = 0.024). In the F group, no factors had a significant impact on OS in Cox analysis. Further analysis on immune indices in the FP group indicated that total-MDSCs and PMN-MDSCs significantly decreased after treatment (p = 0.039), mainly resulting from the PR/SD subgroup (p = 0.019) rather than the PD subgroup (p = 1.000). Most adverse events occurred between these two groups were very similar, while any grade of myelosuppression, hepatic injury, abdominal pain, palmar-plantar erythrodysesthesia and hypothyroidism were more frequently observed in the FP group and≥grade 3 myelosuppression was more common. Conclusions: Among patients with metastatic CRC, fruquintinib combined with PD-1 inhibitor couldn't significantly prolong PFS and OS compared with only fruquintinib therapy, but could made a few patients partial response. Total/PMN-MDSCs may be an important indicator of the efficacy of the combined therapy. The combined treatment increased more side effects, yet showed an acceptable safety profile.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2023
    detail.hit.zdb_id: 2005181-5
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  • 8
    In: Gastroenterology, Elsevier BV, Vol. 134, No. 4 ( 2008-4), p. A-84-
    Type of Medium: Online Resource
    ISSN: 0016-5085
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    Language: English
    Publisher: Elsevier BV
    Publication Date: 2008
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  • 9
    In: Gastroenterology, Elsevier BV, Vol. 134, No. 4 ( 2008-4), p. A-249-
    Type of Medium: Online Resource
    ISSN: 0016-5085
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    Language: English
    Publisher: Elsevier BV
    Publication Date: 2008
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  • 10
    In: Gastroenterology, Elsevier BV, Vol. 144, No. 5 ( 2013-05), p. S-168-
    Type of Medium: Online Resource
    ISSN: 0016-5085
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    Language: English
    Publisher: Elsevier BV
    Publication Date: 2013
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