scholarly journals Differentiated thyroid cancer: Growth factors, oncogenes and environmental influences

2003 ◽  
Vol 11 (3) ◽  
pp. 171-172
Author(s):  
Ivan Paunovic
Keyword(s):  
Thyroid Cancer ◽  
Growth Factors ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Sodium Iodide ◽  
Thyroid Tissue ◽  
Suppressor Gene ◽  
Differentiated Thyroid Carcinoma ◽  
Sodium Iodide Symporter ◽  
Normal Thyroid Tissue

The present data of growth factors, oncogenes, tumor-suppressor-genes and environmental factors can be summarized in thus: thyrotropin, growth factors and other hormones do increase thyrocyte growth and specific mutations of growth factor receptors (thyrotropin receptor [TSH-R], alpha subunit of hetero-trimeric transducer protein [GSP]) cause autonomously functioning thyroid tissue and differentiated thyroid carcinoma. In the thyroid, as in other organs, genes that are found to be differentially expressed between normal thyroid tissue and thyroid carcinomas can be used as targets for molecular-based diagnosis and therapy. Deregulation of tumor suppressor gene p53, however, parallels dedifferentiation of papillary and follicular thyroid cancer but has been found in few cases only. Iodide inhibiting thyrocyte growth will have to be investigated more intensively after sodium-iodide-symporter (NIS) has been cloned, and studies may now be available that could lead to form of conservative treatment in especially dedifferentiated thyroid cancer.

scholarly journals Sodium/iodide symporter (NIS) and pendrin are expressed differently in hot and cold nodules of thyroid toxic multinodular goiter

2001 ◽  
pp. 591-597 ◽  
Author(s):  
D Russo ◽  
S Bulotta ◽  
R Bruno ◽  
F Arturi ◽  
P Giannasio ◽  
...  
Keyword(s):  
Multinodular Goiter ◽  
Normal Tissue ◽  
Sodium Iodide ◽  
Thyroid Tissue ◽  
Sodium Iodide Symporter ◽  
Normal Thyroid Tissue ◽  
Tissue Samples ◽  
Normal Thyroid ◽  
Toxic Multinodular Goiter

OBJECTIVE: The expression of two iodide transporters, the sodium/iodide symporter (NIS) and pendrin, was analyzed in thyroid tissues of patients with toxic multinodular goiter (TMNG) and non-toxic multinodular goiter (MNG). METHODS: The levels of NIS and pendrin proteins were analyzed in total protein extracts from nodular and non-nodular tissues by Western blot. RESULTS: In tissue samples from TMNG, we found an increased expression of NIS (2.5-fold) in the hot nodules, and similar levels between cold nodules and non-nodular tissues. In contrast, the levels of pendrin were slightly increased in both hot and cold nodules from TMNG, and decreased (about twofold) in cold nodules from MNG. We also noticed that there was no relationship between NIS and pendrin expression. CONCLUSIONS: Our data demonstrate that hot nodules from TMNG express a higher number of iodide transporters (mainly NIS), whereas cold nodules from TMNG, but not from MNG, show levels of the two proteins comparable with normal tissue, suggesting a role in vivo of TSH in maintaining the expression of NIS and pendrin protein in normal thyroid tissue. Finally, different mechanisms are involved in the regulation of NIS and pendrin expression.

scholarly journals DKK3 is a potential tumor suppressor gene in papillary thyroid carcinoma

2013 ◽  
Vol 20 (4) ◽  
pp. 507-514 ◽  
Author(s):  
De-tao Yin ◽  
Wenxun Wu ◽  
Mingchuang Li ◽  
Qi-en Wang ◽  
Hongqiang Li ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Promoter Methylation ◽  
Thyroid Tissue ◽  
Inverse Correlation ◽  
Suppressor Gene ◽  
Papillary Thyroid ◽  
Normal Thyroid Tissue ◽  
Tissue Samples ◽  
Normal Thyroid ◽  
Potential Tumor Suppressor

The expression of the Dickkopf homolog 3 (DKK3) gene is downregulated in some human cancers, suggesting a possible tumor suppressor role of this gene. The role and regulation ofDKK3in thyroid cancer have not been examined. In this study, we explored the relationship of promoter methylation with the inactivation ofDKK3and tumor behaviors in papillary thyroid carcinoma (PTC). We used methylation-specific PCR and RT-PCR to examine the promoter methylation and expression ofDKK3and tumor characteristics. We found mRNA expression ofDKK3in 44.9% of the PTC tissue samples vs 100% of the matched normal thyroid tissue samples (P<0.01). In contrast, an opposite distribution pattern ofDKK3gene methylation was observed; specifically, 38.8% of the PTC tissue samples vs 0% of the matched normal thyroid tissue samples harboredDKK3methylation. An inverse correlation between the promoter methylation and mRNA expression ofDKK3in PTC tissue samples was also observed. Moreover, we also found an inverse correlation betweenDKK3expression and some aggressive pathological characteristics of PTC, including high TNM stages and lymph node metastasis, but a positive correlation betweenDKK3promoter hypermethylation and pathological aggressiveness of the tumor. Treatment of the PTC cell line TPC-1 with the demethylating agent 5-azaC reducedDKK3promoter methylation and enhanced its expression, establishing functionally the impact ofDKK3methylation on its expression. Our data thus for the first time demonstrate that theDKK3gene is a potential tumor suppressor gene in thyroid cancer and that aberrant promoter methylation is an important mechanism for its downregulation, which may play a role in the tumorigenesis and aggressiveness of PTC.

An investigation into sodium-iodide symporter (NIS) dimerization and its impact on radioiodide uptake in thyroid cancer

2017 ◽  
Author(s):  
Rebecca J. Thompson ◽  
Alice Fletcher ◽  
Hannah Nieto ◽  
Mohammed Alshahrani ◽  
Katie Baker ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Sodium Iodide ◽  
Sodium Iodide Symporter

Predictive role of nontumoral sodium iodide symporter activity and preoperative thyroid characteristics in remission process of thyroid cancer patients

2014 ◽  
Vol 28 (7) ◽  
pp. 623-631 ◽  
Author(s):  
Nilufer Yildirim-Poyraz ◽  
Aylin Yazgan ◽  
Elif Ozdemir ◽  
Aysegul Gozalan ◽  
Mutlay Keskin ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Patients ◽  
Sodium Iodide ◽  
Sodium Iodide Symporter ◽  
Predictive Role

scholarly journals Autophagy activity is associated with membranous sodium iodide symporter expression and clinical response to radioiodine therapy in non-medullary thyroid cancer

Autophagy ◽  
2016 ◽  
Vol 12 (7) ◽  
pp. 1195-1205 ◽  
Author(s):  
Theo S. Plantinga ◽  
Marika H. Tesselaar ◽  
Hans Morreau ◽  
Eleonora P. M. Corssmit ◽  
Brigith K. Willemsen ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Clinical Response ◽  
Sodium Iodide ◽  
Medullary Thyroid Cancer ◽  
Radioiodine Therapy ◽  
Sodium Iodide Symporter ◽  
Medullary Thyroid ◽  
Autophagy Activity

scholarly journals Novel Chromosomal Abnormalities Identified by Comparative Genomic Hybridization in Parathyroid Adenomas1

1998 ◽  
Vol 83 (5) ◽  
pp. 1766-1770 ◽  
Author(s):  
Nallasivam Palanisamy ◽  
Yasuo Imanishi ◽  
Pulivarthi H. Rao ◽  
Hideki Tahara ◽  
R. S. K. Chaganti ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Comparative Genomic Hybridization ◽  
Tumor Suppressor Genes ◽  
Chromosomal Abnormalities ◽  
Suppressor Gene ◽  
Comparative Genomic ◽  
Parathyroid Tumor ◽  
Genomic Hybridization ◽  
Suppressor Genes ◽  
Parathyroid Adenomas

The molecular basis of parathyroid adenomatosis includes defects in the cyclin D1/PRAD1 and MEN1 genes but is, in large part, unknown. To identify new locations of parathyroid oncogenes or tumor suppressor genes, and to further establish the importance of DNA losses described by molecular allelotyping, we performed comparative genomic hybridization (CGH) on a panel of 53 typical sporadic (nonfamilial) parathyroid adenomas. CGH is a new molecular cytogenetic technique in which the entire tumor genome is screened for chromosomal gains and/or losses. Two abnormalities, not previously described, were found recurrently: gain of chromosome 16p (6 of 53 tumors, or 11%) and gain of chromosome 19p (5 of 53, or 9%). Losses were found frequently on 11p (14 of 53, or 26%), as well as 11q (18 of 53, or 34%). Recurrent losses were also seen on chromosomes 1p, 1q, 6q, 9p, 9q, 13q, and 15q, with frequencies ranging from 8–19%. Twenty-four of the 53 adenomas were also extensively analyzed with polymorphic microsatellite markers for allelic losses, either in this study (11 cases) or previously (13 cases). Molecular allelotyping results were highly concordant with CGH results in these tumors (concordance level of 97.5% for all informative markers/chromosome arms examined). In conclusion, CGH has identified the first two known chromosomal gain defects in parathyroid adenomas, suggesting the existence of direct-acting parathyroid oncogenes on chromosomes 16 and 19. CGH has confirmed the locations of putative parathyroid tumor suppressor genes, also defined by molecular allelotyping, on chromosomes 1p, 6q, 9p, 11q, 13q, and 15q. Finally, CGH has provided new evidence favoring the possibility that distinct parathyroid tumor suppressors exist on 1p and 1q, and has raised the possibility of a parathyroid tumor suppressor gene on 11p, distinct from the MEN1 gene on 11q. CGH can identify recurrent genetic abnormalities in hyperparathyroidism, especially chromosomal gains, that other methods do not detect.

scholarly journals Steroid receptor coactivator-1 interacts with NF-κB to increase VEGFC levels in human thyroid cancer

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Bo Gao ◽  
Lingji Guo ◽  
Donglin Luo ◽  
Yan Jiang ◽  
Jianjie Zhao ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Thyroid Tissue ◽  
Lymphatic Vessels ◽  
Steroid Receptor ◽  
Human Thyroid ◽  
Normal Thyroid Tissue ◽  
Normal Thyroid ◽  
Steroid Receptor Coactivator ◽  
Lymphatic Metastases ◽  
Factor C

Thyroid cancer is the most common endocrine cancer, and has a high incidence of lymphatic metastasis. Vascular endothelial growth factor C (VEGFC) is essential for development of lymphatic vessels and lymphatic metastases during carcinogenesis. Steroid receptor coactivator-1 (SRC-1) interacts with nuclear receptors and transcription factors to promote tumor proliferation and metastasis. However, the correlation between SRC-1 and VEGFC levels in the lymphatic metastases of thyroid cancer remains unclear. We analyzed 20-paired specimens of thyroid cancer tissue and normal thyroid tissue and found increased levels of SRC-1 and VEGFC proteins in 13/20 and 15/20 thyroid cancer specimens, respectively, when compared with those levels in specimens of normal thyroid tissue. A high level of SRC-1 expression was positively correlated with VEGFC and lymphatic endothelial cell marker LYVE-1 expression. Papillary thyroid carcinoma cell line TPC-1 displayed high levels of SRC-1 and VEGFC expression and was selected for stable knockdown of SRC-1 in vitro. Inhibition of SRC-1 significantly reduced the VEGFC levels in TPC-1 cells. We found that SRC-1 binds to transcription factor NF-kB (p50/p65), and that this coactivation complex directly promoted VEGFC transcription, which could be abrogated by SRC-1 knockdown. Up-regulated NF-kB signaling was also confirmed in thyroid cancer tissues. In vivo studies showed that SRC-1 knockdown restricted tumor growth, reduced the numbers of LYVE-1-positive lymphatic vessels, and decreased the levels of VEGFC in tumor tissues. These results suggest a tumorigenic role for SRC-1 in thyroid cancer via its ability to regulate VEGFC expression.

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