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  • American Association for Cancer Research (AACR)  (3)
  • 1
    Online Resource
    Online Resource
    Abstract 180: OPNa variant expression is associated with matrix mineralization in thyroid cancer cell lines
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 180-180
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 180-180
    Abstract: Osteopontin (OPN) and its three spliced variants (OPN-SV: OPNa, OPNb and OPNc) are overexpressed in several tumors and frequently associated with cancer progression. This holds true for papillary thyroid carcinoma (PTC), which is the most common variety of thyroid cancer (TC), being the histologic type which often presents desmoplasia (collagen deposition) and dystrophic calcification, including a fairly typical feature, the psammoma bodies (PB). This study aims to investigate the OPN-SV expression in classical variant of PTC (cPTC) and the role of OPN in calcification and collagen deposition into the extracellular matrix of thyroid cancer cell lines. Total OPN and OPN-SV expression was analyzed by immunohistochemistry and real time PCR in a series of 48 cPTC cases and three diffuse sclerosing PTCs. The association of OPN expression and the presence of PB as well as between PB in cPTC and the clinicopathological features of the tumors were evaluated. TPC-1 and c643 TC cell lines overexpressing OPN-SV were tested for the ability to promote calcification and to synthesize collagen in vitro. We also evaluated the expression of calcification markers, including osteocalcin and collagen I. Overexpression of OPNa transcripts was significantly associated with the presence of PB in cPTC samples. The presence of PB in cPTC was associated with younger patients and lymph node metastasis. Moreover, OPNa overexpression displayed a strong capacity to promote calcification and substantial collagen deposition in thyroid cancer cell lines. Upon OPN knockdown, the mRNA expression levels of calcification markers (osteocalcin and collagen I) were downregulated, further evidencing the involvement of OPN on activating these processes. Our data suggest that OPNa plays a role in the extracellular matrix calcification associated with cPTC. Basic research on the interactions between OPNa overexpression by tumor cells and the surrounding microenvironment can give clues for a better understanding of cPTC biology and phenotype. Citation Format: Luciana B. Ferreira, Raquel T. Lima, Ana Clara Santos da Fonseca Bastos, Andreia Machado Silva, Catarina Tavares, Ana Pestana, Elisabete Rios, Catarina Eloy, Manuel Sobrinho-Simões, Etel Rodrigues Pereira Gimba, Paula Soares. OPNa variant expression is associated with matrix mineralization in thyroid cancer cell lines [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 180.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-180
    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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  • 2
    Online Resource
    Online Resource
    Abstract C118: TERT promoter mutations in human gliomas.
    American Association for Cancer Research (AACR) ; 2013
    In:  Molecular Cancer Therapeutics Vol. 12, No. 11_Supplement ( 2013-11-01), p. C118-C118
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 12, No. 11_Supplement ( 2013-11-01), p. C118-C118
    Abstract: Reactivation of telomerase has been implicated in human tumorigenesis, but the underlying mechanisms remain poorly understood. Recently, two mutations (-124G & gt;A and -146G & gt;A) in the promoter region of the telomerase catalytic subunit (TERT) were found in a significant proportion of human tumors, including gliomas, thyroid carcinomas, bladder carcinomas and melanomas. These mutations resulted in increased expression of telomerase, both in vitro and in vivo. In order to further characterize the prevalence of TERT mutations in human tumors, we screened a cohort of 273 human gliomas and found an overall TERT mutation frequency of 50%. TERT mutations were most commonly found in high grade tumors such as glioblastoma multiforme (GBM) and gliosarcoma (65% and 89%, respectively), whereas low grade tumors such as pilocytic astrocytoma and diffuse astrocytoma showed a low frequency of TERT mutations (6% and 16%, respectively). Oligodendrogliomas (grade II) and anaplastic oligodendrogliomas (grade III) also harbored a high frequency of TERT mutations (44% and 52%, respectively). In GBM patients, the presence of TERT mutations was significantly associated with a higher mean age at diagnosis (p & lt;0.0001) and worse survival (p=0.006). Our results show that TERT promoter mutations are frequent in human GBM and oligodendrogliomas and are associated with worse survival in GBM patients. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):C118. Citation Format: Jorge Lima, Rui M. Reis, Telmo Catarino, Joana Peixoto, Joao Vinagre, Rui Batista, Ligia Castro, Fernando Pardal, Manuel Sobrinho-Simoes, Valdemar Maximo, Paula Soares. TERT promoter mutations in human gliomas. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr C118.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-13-C118
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2062135-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Abstract 1075: STAT3 signaling in thyroid cancer
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1075-1075
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1075-1075
    Abstract: Here, we examined the contribution of STAT3 activation in papillary thyroid carcinoma (PTC), which constitutes 80% of all thyroid malignancies. We initially examined STAT3 activation (i.e. Y705 phosphorylation) by IHC in 80 primary PTCs. Approximately 50% of the tumors expressed nuclear pSTAT3. In general, positive cancer cells were found on the edge of the tumor and in association with the stroma (also strongly pSTAT3 positive). The inner part of the tumor was generally negative, as well as all solid PTCs. Additionally, we examined human thyroid cancer derived cell lines and determined that STAT3 was phosphorylated in ∼50% and was regulated by the IL-6/gp130/JAK pathway, similarly to what has been described in breast and lung cancers. To assess STAT3's role in thyroid cancer, we evaluated the effects of STAT3 under-expression in two models: thyroid cancer derived cell lines where STAT3 levels were reduced using a short hairpin and a transgenic model of PTC lacking STAT3. We observed no significant effects on in vitro growth, migration and invasion as a consequence of reduced STAT3 levels in cancer cell lines. However, in vivo (xenografts in nude mice) the tumors with low STAT3 were significantly larger compared to control (STAT3 expressing) tumors. Similarly, in a transgenic model of PTC lacking STAT3, tumors were larger, more cellular with evidence of increased proliferation compared to the STAT3 expressing cancers. RNA expression analysis of the human xenografts suggested that tumors deficient in STAT3 have downregulated death-promoting genes. In conclusion, our data suggests that in thyroid cancer STAT3 can function as a tumor suppressor, contrary to the current dogma where STAT3 is considered to be oncogenic. We are currently determining whether STAT3's effect on tumorigenesis is dependent on “activated” or total STAT3 and hope to identify the specific molecular pathways involved. 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 1075. doi:10.1158/1538-7445.AM2011-1075
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-1075
    RVK:
    XA 36000
    RVK:
    XA 10000
    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
    Location Call Number Limitation Availability
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