PURPOSE: Whole body Positron Emission Tomography (PET) was used to evaluate the existence of cancer cells. However, PET had limitations in identifying thyroid cancer cells because of their slow progression, and evidence regarding its accuracy in finding thyroid cancer cells is insufficient. Therefore, we investigated the usefulness of PET for evaluation of patients with thyroid nodules by studying the relationships between PET and thyroid ultrasonography. METHODS: We evaluated 4,627 patients who had undergone PET from January 2007 to October 2011 and selected 370 patients who had undergone thyroid ultrasonography. We compared and analyzed the amount of thyroid SUVmax of PET, the pattern of glucose uptake, and findings of thyroid ultrasonography based on their size, shape, location, and FNAC. RESULTS: Of 370 patients, 197 (53.2%) subjects were found to have thyroid nodules, and 211 (57.0%) subjects had higher sugar metabolism, regardless of having thyroid nodules. No statistical correlations were observed among nodule size, nodule location,and higher sugar metabolism, however, noticeable relationships were observed between the shape of the cells on thyroid ultrasonography and FDG uptake of PET. In cases of papillary thyroid cancer, there was higher FDG uptake, compared to benign lesions in particular, SUVmax of the papillary thyroid cancer showed a significantly elevated level of FDG uptake. CONCLUSION: Despite its limited usefulness in identifying the characteristics of thyroid nodules being benign or malignant, PET is appropriate for evaluation of the malignancy of thyroid cells
Diagnosis* ; Electrons* ; Glucose ; Humans ; Metabolism ; Positron-Emission Tomography* ; Thyroid Gland* ; Thyroid Neoplasms ; Thyroid Nodule* ; Ultrasonography

OBJECTIVE: To investigate the expression and clinical significance of EphA2 and E cadherin proteins in papillary thyroid carcinoma tissues, and to explore the relationship between them. METHOD: Using immunohistochemical SP/PV method, we detected the expression of EphA2 and E cadherin in tumors of 43 papillary thyroid carcinomas, 11 thyroid adenoma and 10 normal thyroid tissues, then studied their relationships with clinic pathological factors. RESULT: The total positive rates of EphA2 and E cadherin expression were 58. 14% and 32. 56% in papillary thyroid carcinoma tissues, 18. 18% and 81. 81% in thyroid adenoma.tissues and they were 10. 00% and 100. 00% in normal thyroid tissues respectively. The positive expression of EphA2 in carcinoma tissues was higher than in the thyroid adenoma tissues and normal thyroid tissues (P<0. 05) and the positive expression of E cadherin in carcinoma tissues was lower than that in the thyroid adenoma tissues and normal thyroid tissues (P<0. 05). The positive expression of EphA2 and E cadherin was associated with lymph node metastasis and histological grade (P<0. 05), but it was not associated with all the clinic-pathological factors including age, sex and the tumor size (P>0. 05). In papillary thyroid carcinoma tissues, the expression of EphA2 was negatively correlated with the expression of E cadherin protein (r= -0. 416, P<0. 01). CONCLUSION EphA2 and E cadherin may be involved in carcinogenesis and development of papillary thyroid carcinoma.
Adenoma ; metabolism ; pathology ; Antigens, CD ; Cadherins ; metabolism ; Carcinoma ; metabolism ; pathology ; Carcinoma, Papillary ; Humans ; Lymphatic Metastasis ; Receptor, EphA2 ; metabolism ; Thyroid Cancer, Papillary ; Thyroid Gland ; metabolism ; Thyroid Neoplasms ; metabolism ; pathology

Carrier Proteins ; metabolism ; Humans ; Microfilament Proteins ; metabolism ; Neoplasm Proteins ; metabolism ; Thyroid Neoplasms ; metabolism ; pathology

Primary thyroid cancers including papillary, follicular, poorly differentiated, and anaplastic carcinomas show substantial differences in biological and clinical behaviors. Even in the same pathological type, there is wide variability in the clinical course of disease progression. The molecular carcinogenesis of thyroid cancer has advanced tremendously in the last decade. However, specific inhibition of oncogenic pathways did not provide a significant survival benefit in advanced progressive thyroid cancer that is resistant to radioactive iodine therapy. Accumulating evidence clearly shows that cellular energy metabolism, which is controlled by oncogenes and other tumor-related factors, is a critical factor determining the clinical phenotypes of cancer. However, the role and nature of energy metabolism in thyroid cancer remain unclear. In this article, we discuss the role of cellular energy metabolism, particularly mitochondrial energy metabolism, in thyroid cancer. Determining the molecular nature of metabolic remodeling in thyroid cancer may provide new biomarkers and therapeutic targets that may be useful in the management of refractory thyroid cancers.
Carcinogenesis ; Carcinoma ; Disease Progression ; Energy Metabolism* ; Iodine ; Mitochondria ; Oncogenes ; Phenotype ; Thyroid Gland* ; Thyroid Neoplasms ; Biomarkers

Metabolic reprogramming of cancer cell is one of essential hallmarks of cancer. Otto Warburg first demonstrated that cancer cells utilized more glucose and enhanced glycolytic pathway in the presence of oxygen in 1926. Scientific observations of basic and clinical research in several decades supported that cancer-specific metabolism can be an emerging target for treatment of cancer. Metabolic reprogramming is regulated by both oncogenic signaling and tumor suppressor genes associated with critical signaling pathways in metabolism. These changes provided energy, substrates for cell growth and proliferation, favoring microenvironment, and important for redox balancing for cancer cells. Recent advance of several tools for evaluation comprehensive metabolic profiles of cancer cells provided us to identification of metabolic Achilles' heel of cancers including thyroid cancer. This approach can be a useful strategy for advance in treatment of cancer patients.
Genes, Tumor Suppressor ; Glucose ; Heel ; Humans ; Metabolism* ; Metabolome ; Oxidation-Reduction ; Oxygen ; Thyroid Gland* ; Thyroid Neoplasms*

Adenocarcinoma ; Carcinoma, Papillary ; Estrogens ; metabolism ; Humans ; Receptors, Estrogen ; metabolism ; Thyroid Neoplasms ; metabolism

Increasing evidences have demonstrated the roles of epithelial-mesenchymal transition in tumor invasion and metastasis. In the invasive front of papillary thyroid carcinoma, the expressions of adhesion molecules are often lost. In anaplastic thyroid carcinoma, tumor cells showing cancer stem cell characteristics have been identified. Epithelial-mesenchymal transition may thus play a key role in the progression of thyroid cancer. Therefore, it provide new insight for the development of targeted drugs for anaplastic thyroid carcinoma.
Cadherins ; metabolism ; Epithelial-Mesenchymal Transition ; Humans ; Thyroid Neoplasms ; pathology ; Transcription Factors ; metabolism

OBJECTIVE: To raise clinical awareness of carcinoembryonic antigen(CEA) increased as initial manifestation of medullary thyroid cancer(MTC) and explore the diagnosis and treatment. METHOD: Clinical data of 2 cases CEA increased as the initial presentation of MTC were retrospectively analyzed and clinical manifestations of the disease, diagnosis, treatment were also discussed by literature reviewing. RESULT: Two patients received thyroid ipsilateral lobe total resection, MTC was confirmed by intraoperative frozen pathology, re-total resection of the contralateral lobe and bilateral VI lymph node dissection were performed. Lymph nodes had no metastasis confirmed by pathological frozen examination. CEA returned to normal within 2 months after surgery. No tumor recurrence and metastasis were found after follow-up for 3 to 24 months. CONCLUSION CEA increased as the initial presentation MTC was rare and clinical identification of CEA increased disease should be taken into account the MTC as possible. Total thyroidectomy and bilateral VI lymph node dissection was the main surgical treatment for it.
Adult ; Carcinoembryonic Antigen ; metabolism ; Carcinoma, Neuroendocrine ; Female ; Humans ; Middle Aged ; Retrospective Studies ; Thyroid Neoplasms ; metabolism ; pathology

The purpose of this review is to investigate the value of the calcification in differentiating malignant thyroid neoplasm and the molecular mechanisms for the formation of the calcification. Many published reports have proved the presence of calcifications in thyroid neoplasm and calcified nodules in these studies are more frequently malignant than noncalcified nodules. Through viewing the related references, we found that psammoma bodies (PBs), Runx2, osteocalcin, osteopontin, CD44v6 play an important role in the molecular mechanisms in the formation of the calcification in PTC. But further study is required for elucidating the mode of action.
Calcinosis ; diagnosis ; pathology ; Core Binding Factor Alpha 1 Subunit ; metabolism ; Humans ; Hyaluronan Receptors ; metabolism ; Osteocalcin ; metabolism ; Osteopontin ; metabolism ; Thyroid Neoplasms ; diagnosis ; pathology ; Thyroid Nodule ; pathology

Targeted gene therapy has become a promising approach for lung cancer treatment. In our previous work, we reported that the targeted expression of microRNA-7 (miR-7) operated by thyroid transcription factor-1 (TTF-1) promoter inhibited the growth of human lung cancer cells in vitro and in vivo; however, the intervention efficiency needed to be further improved. In this study, we identified the core promoter of TTF-1 (from -1299 bp to -871 bp) by 5' deletion assay and screened out the putative transcription factors nuclear factor-1 (NF-1) and activator protein-1 (AP-1). Further analysis revealed that the expression level of NF-1, but not AP-1, was positively connected with the activation of TTF-1 core promoter in human non-small-cell lung cancer (NSCLC) cells. Moreover, the silencing of NF-1 could reduce the expression level of miR-7 operated by TTF-1 core promoter. Of note, we optimized four distinct sequences to form additional NF-1-binding sites (TGGCA) in the sequence of TTF-1 core promoter (termed as ^optTTF-1 promoter), and verified the binding efficiency of NF-1 on the ^optTTF-1 promoter by electrophoretic mobility shift assay (EMSA). As expected, the ^optTTF-1 promoter could more effectively drive miR-7 expression and inhibit the growth of human NSCLC cells in vitro, accompanied by a reduced transduction of NADH dehydrogenase (ubiquinone) 1α subcomplex 4 (NDUFA4)/protein kinase B (Akt) pathway. Consistently, ^optTTF-1 promoter-driven miR-7 expression could also effectively abrogate the growth and metastasis of tumor cells in a murine xenograft model of human NSCLC. Finally, no significant changes were detected in the biological indicators or the histology of some important tissues and organs, including heart, liver, and spleen. On the whole, our study revealed that the optimized TTF-1 promoter could more effectively operate miR-7 to influence the growth of human NSCLC cells, providing a new basis for the development of microRNA-based targeting gene therapy against clinical lung cancer.
Animals ; Humans ; Mice ; Carcinoma, Non-Small-Cell Lung/therapy* ; Lung Neoplasms/metabolism* ; MicroRNAs/metabolism* ; Nuclear Proteins/metabolism* ; Thyroid Gland/pathology* ; Thyroid Nuclear Factor 1/genetics* ; Transcription Factors/metabolism*