Status and expression of thep16INK4 gene in human thyroid tumors and thyroid-tumor cell lines

1996 ◽  
Vol 67 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Viola Calabr� ◽  
Maria Strazzullo ◽  
Girolama La Mantia ◽  
Monica Fedele ◽  
Christian Paulin ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Thyroid Tumor ◽  
Human Thyroid ◽  
Thyroid Tumors ◽  
Tumor Cell Lines

Expression of Matrix Metalloproteinases and Their Specific Inhibitors in Normal and Different Human Thyroid Tumor Cell Lines

Thyroid ◽  
2004 ◽  
Vol 14 (11) ◽  
pp. 881-888 ◽  
Author(s):  
E. Baldini ◽  
M. Toller ◽  
F.M. Graziano ◽  
F.P. Russo ◽  
M. Pepe ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Tumor Cell ◽  
Cell Lines ◽  
Thyroid Tumor ◽  
Human Thyroid ◽  
Tumor Cell Lines ◽  
Specific Inhibitors

scholarly journals Human Thyroid Tumor Cell Lines Derived from Different Tumor Types Present a Common Dedifferentiated Phenotype

2007 ◽  
Vol 67 (17) ◽  
pp. 8113-8120 ◽  
Author(s):  
Wilma C.G. van Staveren ◽  
David Weiss Solís ◽  
Laurent Delys ◽  
Laurence Duprez ◽  
Guy Andry ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Thyroid Tumor ◽  
Human Thyroid ◽  
Tumor Cell Lines ◽  
Tumor Types

Normal human thyroid cells, BCPAP, and TPC-1 thyroid tumor cell lines display different profile in both basal and TNF-α-induced CXCL8 secretion

Endocrine ◽  
2015 ◽  
Vol 54 (1) ◽  
pp. 123-128 ◽  
Author(s):  
Francesca Coperchini ◽  
Patrizia Pignatti ◽  
Paola Leporati ◽  
Andrea Carbone ◽  
Laura Croce ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Thyroid Tumor ◽  
Human Thyroid ◽  
Tumor Cell Lines ◽  
Thyroid Cells ◽  
Cxcl8 Secretion ◽  
Tnf Α ◽  
Normal Human

scholarly journals Lack of Mutations in the Thyroid Hormone Receptor (TR) α and β Genes but Frequent Hypermethylation of the TRβ Gene in Differentiated Thyroid Tumors

2007 ◽  
Vol 92 (12) ◽  
pp. 4766-4770 ◽  
Author(s):  
Biju Joseph ◽  
Meiju Ji ◽  
Dingxie Liu ◽  
Peng Hou ◽  
Mingzhao Xing
Keyword(s):  
Thyroid Cancer ◽  
Thyroid Hormone ◽  
Tumor Cell ◽  
Gene Mutation ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Thyroid Tumor ◽  
Thyroid Tumors ◽  
Tumor Cell Lines ◽  
Thyroid Adenomas

Abstract Context: It remains inconclusive whether mutations in thyroid hormone receptor (TR) genes naturally occur in thyroid cancer and whether these genes could be suppressors of this cancer. Objectives: Our objectives were to examine further mutations of TRα and TRβ genes in thyroid cancer and also to examine their methylation as an epigenetic silencing mechanism in thyroid cancer. Experimental Design: Instead of using a cDNA sequencing approach used in previous studies, we used genomic DNA to sequence directly the coding regions of the TRα and TRβ genes to search mutations in various differentiated thyroid tumors and used methylation-specific PCR to analyze promoter methylation of these genes. Allelic zygosity status at TRβ was also analyzed. Results: We found no TRα gene mutation in 17 papillary thyroid cancers (PTCs) and 11 follicular thyroid cancers (FTCs), and no TRβ gene mutation in 16 PTCs and 12 FTCs. We also found no methylation of the TRα gene in 33 PTCs, 31 FTCs, 20 follicular thyroid adenomas (FTAs), and 10 thyroid tumor cell lines. In contrast, we found hypermethylation of the TRβ gene in 10 of 29 (34%) PTCs, 22 of 27 (81%) FTCs, five of 20 (25%) follicular thyroid adenomas, and three of 10 (30%) thyroid tumor cell lines, with the highest prevalence in FTC. We additionally examined loss of heterozygosity at TRβ and found it in three of nine (33%) PTCs and three of nine (33%) FTCs. Conclusions: Mutation is not common in TR genes, whereas hypermethylation of the TRβ gene as an alternative gene silencing mechanism is highly prevalent in thyroid cancer, particularly FTC, consistent with a possible tumor suppressor role of this gene for FTC.

scholarly journals High periostin expression correlates with aggressiveness in papillary thyroid carcinomas

2008 ◽  
Vol 197 (2) ◽  
pp. 401-408 ◽  
Author(s):  
Cinzia Puppin ◽  
Dora Fabbro ◽  
Mariavittoria Dima ◽  
Carla Di Loreto ◽  
Efisio Puxeddu ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Thyroid Tumor ◽  
Specific Gene ◽  
Mrna Levels ◽  
Tumor Cell Lines ◽  
Papillary Thyroid ◽  
Osteoblastic Cell Line ◽  
Thyroid Carcinomas ◽  
Normal Tissues

Periostin is a mesenchyme-specific gene product, which acts as an adhesion molecule during bone formation and supports osteoblastic cell line attachment and spreading. However, periostin expression is activated in a large variety of epithelial human tumors and correlates with their aggressiveness. Knowledge of expression of periostin in thyroid tumors is still scanty. The aim of the present work was to investigate periostin expression in differentiated neoplasms of the thyroid and to correlate it with several clinical and molecular features of these tumors. Periostin expression was evaluated by quantitative PCR and immunohistochemistry in normal thyroid tissues, papillary thyroid carcinomas (PTCs), follicular thyroid carcinomas (FTCs), and follicular adenomas (FAs). Periostin mRNA levels were also evaluated in several thyroid tumor cell lines. PTCs show mean periostin mRNA levels significantly higher than corresponding normal tissues. In five PTCs, periostin mRNA values were at least 30-fold higher than corresponding normal tissues. Conversely, mean periostin mRNA levels of FTCs and FAs were similar to those of normal tissues. Consistent with mRNA studies, periostin was detectable by immunohistochemistry in cancerous epithelial cells only in several cases of PTCs but not in normal tissue, FTCs, and FAs. In PTCs, periostin mRNA levels positively correlate with extrathyroidal invasion, distant metastasis, and higher grade staging. A negative correlation between periostin and expression of some markers of the thyroid-differentiated phenotype (thyroglobulin, thyrotropin receptor) was also present in the PTCs. These results indicate that an increase in periostin gene expression is present in several PTCs, in which it appears as a marker of aggressiveness. Experiments in thyroid tumor cell lines indicate that high levels of periostin mRNA are due, at least in part, to the increase in periostin promoter activity.

Interaction of Human Tumor Cells with Human Platelets and the Coagulation System

1983 ◽  
Vol 50 (03) ◽  
pp. 726-730 ◽  
Author(s):  
Hamid Al-Mondhiry ◽  
Virginia McGarvey ◽  
Kim Leitzel
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Lines ◽  
Human Tumor ◽  
Human Platelets ◽  
Factor Vii ◽  
Coagulation System ◽  
Breast Adenocarcinoma ◽  
Activate Factor ◽  
Tumor Cell Lines

SummaryThis paper reports studies on the interaction between human platelets, the plasma coagulation system, and two human tumor cell lines grown in tissue culture: Melanoma and breast adenocarcinoma. The interaction was monitored through the use of 125I- labelled fibrinogen, which measures both thrombin activity generated by cell-plasma interaction and fibrin/fibrinogen binding to platelets and tumor cells. Each tumor cell line activates both the platelets and the coagulation system simultaneously resulting in the generation of thrombin or thrombin-like activity. The melanoma cells activate the coagulation system through “the extrinsic pathway” with a tissue factor-like effect on factor VII, but the breast tumor seems to activate factor X directly. Both tumor cell lines activate platelets to “make available” a platelet- derived procoagulant material necessary for the conversion of prothrombin to thrombin. The tumor-derived procoagulant activity and the platelet aggregating potential of cells do not seem to be inter-related, and they are not specific to malignant cells.

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