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  • Huang, Cheng-long  (3)
  • 1
    In: The Annals of Thoracic Surgery, Elsevier BV, Vol. 95, No. 4 ( 2013-4), p. 1181-1188
    Type of Medium: Online Resource
    ISSN: 0003-4975
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2013
    detail.hit.zdb_id: 1499869-5
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  • 2
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 345-345
    Abstract: Introduction: Malignant pleural mesotheliomas are aggressive tumors with a poor prognosis. It is considered to be important to identify the molecular targets for the treatment against malignant pleural mesotheliomas. We have recently found the Wnt1 expression to affect tumor progression in non-small cell lung cancers, through the induction of various Wnt-targets (Huang et al, Eur J Cancer 2008). Therefore, we performed a clinical study on the intratumoral expressions of the canonical Wnts, such as Wnt1 and Wnt2B, in relation to their targets, including c-Myc and survivin. Methods: Sixty-five cases with malignant pleural mesotheliomas were investigated. Immunohistochemical assays were performed to evaluate the intratumoral expressions of Wnt1, Wnt2B, c-Myc and survivin. In addition, the Ki-67 proliferation index was evaluated by immunohistochemistry, and the apoptotic index was evaluated by the TUNEL method. Results: The Ki-67 proliferation index was significantly higher in c-Myc-high tumors than in c-Myc-low tumors (P=0.008). In addition, the Ki-67 proliferation index was also significantly higher nuclear-survivin-high tumors than in nuclear-survivin-low tumors (P=0.004). Regarding the intratumoral expressions of canonical Wnts, 18 tumors (27.7%) were Wnt1-high tumors, and 36 tumors (55.4%) were Wnt2B-high tumors. The rate of Wnt2B-high tumors was significantly higher than the rate of Wnt1-high tumors (P=0.024). Regarding tumor histology, the Wnt2B expression was the significantly highest in epithelial type (P & lt;0.001). On the other hand, there was no significant difference in the Wnt1 expression according to the tumor histology (P=0.163). Furthermore, the Wnt 2B expression significantly correlated with expressions of c-Myc and survivin (P & lt;0.001 and P & lt;0.001, respectively). The c-Myc expression was significantly higher in Wnt2B-high tumors than in Wnt2B-low tumors (P & lt;0.001), and the survivin expression was also significantly higher in Wnt2B-high tumors than in Wnt2B-low tumors (P=0.007). In contrast, there was no significant difference in c-Myc or survivin expressions according to the Wnt1 expression (P=0.218 and P=0.688, respectively). Conclusions: The intratumoral Wnt2B expression affects tumor progression of malignant pleural mesothelioma through the induction of c-Myc and survivin. The Wnt2B could be a candidate of targets of the molecular therapy against malignant pleural mesotheliomas. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 345. doi:10.1158/1538-7445.AM2011-345
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5539-5539
    Abstract: Introduction: Malignant pleural mesotheliomas (MPMs) are aggressive tumors with a poor prognosis. Regarding tumor histology, however, the survival has been reported to be lower in patients with non-epitheloid tumors than in those with epitheloid tumors. Therefore, in order to identify molecular targets for the treatment against MPM patients, we investigated several molecules associated with epithelial to mesenchymal transition, such as Snail, Twist, E-cadherin and N-cadherin. Methods: We studied one hundred and nine patients with MPMs, including 61 epitheloid tumors (55.9%), 21 sarcomatoid tumors (19.2%), 20 biphasic tumors (18.3%) and 7 desmoplastic tumors (6.4%). Immunohistochemical assays were performed to evaluate the intratumoral expressions of Snail, Twist, E-cadherin and N-cadherin. Results: Among 109 MPMs, 41 tumors (37.6%) were Snail-high tumors, 30 tumors (27.5%) were Twist-high tumors, 18 tumors (16.5%) were E-cadherin-positive tumors, and 35 tumors (32.1%) were N-cadherin-positive tumors. Regarding tumor histology, the nuclear expression of Snail expression was significantly higher in non-epithelioid tumors than in epitheloid tumors (P & lt;0.001). Furthermore, the E-cadherin expression was significantly lower in Snail-high tumors than in Snail-low tumors (P=0.046). As a result, the E-cadherin expression was significantly lower in non-epithelioid tumors than in epitheloid tumors (P=0.013). In addition, the Snail expression was significantly higher in Twist-high tumors than in Twist-low tumors (P=0.007). The frequency of N-cadherin-positive tumors was also significantly higher in Twist-high tumors than in Twist-low tumors (P=0.005). Regarding patient survival, the overall survival was significantly lower in patients with Snail-high MPMs than in those with Snail-low MPMs (P=0.002), especially among patients with non-epitheloid tumors (P=0.009). A multivariated analysis also demonstrated that the nuclear expression of Snail was a significantly factor of a poor prognosis in MPM patients (P=0.014). Conclusions: Snail expression is associated with epithelial to mesenchymal transition and a poor prognosis in MPMs. The Snail could be a potential molecular target for the treatment of MPM patients. 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 5539. doi:1538-7445.AM2012-5539
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    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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