Biomarkers For Thyroid Cancer Research Articles

Can VAP-1 Protein be used as a Biomarker in Thyroid Cancer?

Can VAP-1 Protein be used as a Biomarker in Thyroid Cancer?

The precursor for nerve growth factor (proNGF) is not a serum or biopsy-rinse biomarker for thyroid cancer diagnosis

BackgroundNerves and neurotrophic growth factors are emerging promoters of cancer growth. The precursor for Nerve Growth Factor (proNGF) is overexpressed in thyroid cancer, but its potential role as a clinical biomarker has not been reported. Here we have examined the value of proNGF as a serum and biopsy-rinse biomarker for thyroid cancer diagnosis.MethodsPatients presenting for thyroid surgery or biopsy were enrolled in separate cohorts examining serum (n = 204, including 46 cases of thyroid cancer) and biopsy-rinse specimens (n = 188, including 26 cases of thyroid cancer). ProNGF levels in clinical samples were analysed by ELISA. Univariate and multivariate statistical analyses were used to compare proNGF levels with malignancy status and clinicopathological parameters.ResultsProNGF was not detected in the majority of serum samples (176/204, 86%) and the detection of proNGF was not associated with thyroid cancer diagnosis. In the few cases where proNGF was detected in the serum, thyroidectomy did not affect proNGF concentration, demonstrating that the thyroid was not the source of serum proNGF. Intriguingly, an association between hyperthyroidism and serum proNGF was observed (OR 3.3, 95% CI 1.6–8.7 p = 0.02). In biopsy-rinse, proNGF was detected in 73/188 (39%) cases, with no association between proNGF and thyroid cancer. However, a significant positive association between follicular lesions and biopsy-rinse proNGF was found (OR 3.3, 95% CI 1.2–8.7, p = 0.02).ConclusionsProNGF levels in serum and biopsy-rinse are not increased in thyroid cancer and therefore proNGF is not a clinical biomarker for this condition.

Identification of Molecular Biomarkers for Thyroid Cancer

Identification of Molecular Biomarkers for Thyroid Cancer

Uridine phosphorylase 1 associates to biological and clinical significance in thyroid carcinoma cell lines.

Thyroid cancer incidence has been continuity increasing worldwide. Uridine phosphorylase 1 (UPP1) is a protein‐coding gene and has been detected that UPP1 was the higher expression in many solid malignancies, just as head and neck cancers, breast cancer, compared with paired normal tissue. But the act of UPP1 in thyroid cancer is not explicit. In this article, we investigate the function of UPP1 expression in thyroid cancer. The Cancer Genome Atlas (TCGA) unpaired thyroid cancer and normal RNA‐seq data were downloaded, and our paired thyroid cancer and normal samples were analysed by a polymerase chain reaction. The expression of UPP1 was regulated by transfected small interfering RNA, and the function of UPP1 was determined via migration, invasion and cell proliferation assays. Western blot assay was achieved to determine the UPP1 expression correlates with the function of 5‐FU regulate epithelial‐mesenchymal transition. The significant upregulation of UPP1 in thyroid cancer tissues compared with normal thyroid tissues was revealed by our data and TCGA data. UPP1 overexpression was significantly correlated with lymph node metastasis, tumour stage and tumour size. In the cell, experiments showed that UPP1 low expression significantly suppressed the migration, invasion and proliferation. Western blot assay proves the effect of UPP1 expression on 5‐FU regulates epithelial‐mesenchymal transition pathway. UPP1 plays a crucial oncogene in thyroid cancer. Our findings indicate that UPP1 might be a biomarker of thyroid cancer and may act by regulating epithelial‐mesenchymal transition (EMT).

Sulfasalazine suppresses thyroid cancer cell proliferation and metastasis through T-cell originated protein kinase.

Thyroid cancer patients with radioactive iodine-refractory or rapidly progressing presentation require effective treatment. T-cell originated protein kinase (TOPK) is highly expressed in a number of different tumor types, where it promotes proliferation and metastasis. However, the expression of TOPK in thyroid cancer is poorly documented. Therefore, immunohistochemistry was used to detect the expression of TOPK in thyroid cancer tissues, and its clinical significance in this disease was investigated. Sulfasalazine, a targeted inhibitor of TOPK that directly binds the protein with a dissociation constant (Kd) of 228 µM, was also investigated using microscale thermophoresis. Sulfasalazine inhibited TOPK activity, as determined by an in vitro pull-down assay. Furthermore, sulfasalazine inhibited the proliferation and metastasis of thyroid cancer cells. The results indicated that TOPK may be a potential therapeutic target and diagnostic biomarker for thyroid cancer and may be used as an index to evaluate malignant thyroid nodules. Therefore, sulfasalazine is a potential novel compound for the targeted treatment of thyroid cancer.

Identification of key genes and pathways of thyroid cancer by integrated bioinformatics analysis.

Thyroid cancer is a common endocrine malignancy with a rapidly increasing incidence worldwide. Although its mortality is steady or declining because of earlier diagnoses, its survival rate varies because of different tumour types. Thus, the aim of this study was to identify key biomarkers and novel therapeutic targets in thyroid cancer. The expression profiles of GSE3467, GSE5364, GSE29265 and GSE53157 were downloaded from the Gene Expression Omnibus database, which included a total of 97 thyroid cancer and 48 normal samples. After screening significant differentially expressed genes (DEGs) in each data set, we used the robust rank aggregation method to identify 358 robust DEGs, including 135 upregulated and 224 downregulated genes, in four datasets. Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes pathway enrichment analyses of DEGs were performed by DAVID and the KOBAS online database, respectively. The results showed that these DEGs were significantly enriched in various cancer-related functions and pathways. Then, the STRING database was used to construct the protein-protein interaction network, and modules analysis was performed. Finally, we filtered out five hub genes, including LPAR5, NMU, FN1, NPY1R, and CXCL12, from the whole network. Expression validation and survival analysis of these hub genes based on the The Cancer Genome Atlas database suggested the robustness of the above results. In conclusion, these results provided novel and reliable biomarkers for thyroid cancer, which will be useful for further clinical applications in thyroid cancer diagnosis, prognosis and targeted therapy.

Long Non-Coding RNA ZFAS1 as a Novel Potential Biomarker for Predicting the Prognosis of Thyroid Cancer.

BackgroundThyroid cancer is a type of endocrine cancers with rapidly increased incidence. Recent studies have indicated long non-coding RNAs (lncRNAs) played crucial roles in thyroid cancer tumorigenesis and progression. However, the roles of most lncRNAs in thyroid cancer were still unclear.Material/MethodsWe used TCGA (The Cancer Genome Atlas), GSE50901, GSE29265, and GSE33630 datasets to analyze the expression pattern of ZFAS1 (ZNFX1 antisense RNA 1). The correlation between ZFAS1 and clinicopathological features in thyroid cancer was analyzed. Cell proliferation and cell cycle assays were used to validate the roles of ZFAS1 in thyroid cancer cell lines. DAVID (the database for annotation, visualization and integrated discover) system was used to perform GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analysis. The starBase datasets and Cytoscape was used to perform ceRNA (competitive endogenous RNA) network.ResultsWe demonstrated ZFAS1 was highly expressed in thyroid cancer compared to normal samples. Moreover, upregulation of ZFAS1 was positively correlated with clinicopathological features and poor prognosis in thyroid cancer. Functional validation showed knockdown of ZFAS1 suppressed cell proliferation and cell cycle in thyroid cancer cells. Bioinformatics analysis showed ZFAS1 was associated with translation, rRNA processing, intra-Golgi vesicle-mediated transport, ribosome, and ubiquitin-mediated proteolysis.ConclusionsOur study suggested ZFAS1 could serve as a biomarker for thyroid cancer.

Identification of β-hydroxybutyrate as a potential biomarker for female papillary thyroid cancer.

Aim: β-Hydroxybutyrate (BHB) was proved to be a differential metabolite of papillary thyroid cancer (PTC) by semiquantitative analysis, while whether BHB could be used as a potential biomarker for female PTC still needed to be validated. Materials & methods: An LC-MS/MS method with surrogate matrix was established to validate serum BHB in specified PTC patients. Conclusion: Serum BHB levels in PTCs were significantly higher than those in HCs. For both serum BHB with a cut-off value of 312.5 ng/ml and serum BHB/creatinine of 33.5 μmol/mmol, a promising prediction rate to distinguish low-grade PTCs from HCs with satisfactory sensitivity and specificity was achieved,indicating that serum BHB might be proved as a useful biomarker for low-grade female PTC.

Oncometabolites as biomarkers in thyroid cancer: a systematic review.

IntroductionThyroid cancer (TC) is an important common endocrine malignancy, and its incidence has increased in the past decades. The current TC diagnosis and classification tools are fine-needle aspiration (FNA) and histological examination following thyroidectomy. The metabolite profile alterations of thyroid cells (oncometabolites) can be considered for current TC diagnosis and management protocols.MethodsThis systematic review focuses on metabolite alterations within the plasma, FNA specimens, and tissue of malignant TC contrary to benign, goiter, or healthy TC samples. A systematic search of MEDLINE (PubMed), Scopus, Embase, and Web of Science databases was conducted, and the final 31 studies investigating metabolite biomarkers of TC were included.ResultsA total of 15 targeted studies and 16 untargeted studies revealed several potential metabolite signatures of TC such as glucose, fructose, galactose, mannose, 2-keto-d-gluconic acid and rhamnose, malonic acid and inosine, cholesterol and arachidonic acid, glycosylation (immunoglobulin G [IgG] Fc-glycosylation), outer mitochondrial membrane 20 (TOMM20), monocarboxylate transporter 4 (MCT4), choline, choline derivatives, myo-/scyllo-inositol, lactate, fatty acids, several amino acids, cell membrane phospholipids, estrogen metabolites such as 16 alpha-OH E1/2-OH E1 and catechol estrogens (2-OH E1), and purine and pyrimidine metabolites, which were suggested as the TC oncometabolite.ConclusionCitrate was suggested as the first most significant biomarker and lactate as the second one. Further research is needed to confirm these biomarkers as the TC diagnostic oncometabolite.

Liquid Biopsy as a Minimally Invasive Source of Thyroid Cancer Genetic and Epigenetic Alterations.

In the blood of cancer patients, some nucleic acid fragments and tumor cells can be found that make it possible to trace tumor changes through a simple blood test called “liquid biopsy”. The main components of liquid biopsy are fragments of DNA and RNA shed by tumors into the bloodstream and circulate freely (ctDNAs and ctRNAs). Tumor cells which are shed into the blood (circulating tumor cells or CTCs), and exosomes that have been investigated for non-invasive detection and monitoring several tumors including thyroid cancer. Genetic and epigenetic alterations of a thyroid tumor can be a driver for tumor genesis or essential for tumor progression and invasion. Liquid biopsy can be real-time representative of such genetic and epigenetic alterations to trace tumors. In thyroid tumors, the circulating BRAF mutation is now taken into account for both thyroid cancer diagnosis and determination of the most effective treatment strategy. Several recent studies have indicated the ctDNA methylation pattern of some iodine transporters and DNA methyltransferase as a diagnostic and prognostic biomarker in thyroid cancer as well. There has been a big hope that the recent advances of genome sequencing together with liquid biopsy can be a game changer in oncology.

Network-based approach to identify key candidate genes and pathways shared by thyroid cancer and chronic kidney disease

Abstract Thyroid cancer (TC) is one of the fastest-growing cancers in the world. Thyroid dysfunction has an influence on chronic kidney disease (CKD), but the possible relations between TC and CDK have not been explored yet. The present study aimed to identify shared candidate genes and pathways between TC and CKD from the transcriptomics datasets to identify important clues to the pathological mechanisms in these diseases. The gene expression datasets of TC and CKD were obtained from Gene Expression Omnibus and analyzed to identify common genes between TC and CKD. We have detected 84 common differentially expressed genes (DEGs) between TC and CKD. We have integrated the DEGs with protein-protein interaction (PPI) network and identified ten significant hub proteins (TLE1, CTNNA1, TEK, TPM2, FGFR2, MMP2, SDC2, NRP1, TCF7L1, GSN) based on topological analysis. The integration of DEGs with biomolecular networks revealed transcription factors (FOXC1, GATA2, FOXL1, HINFP, LIMK2, E2F1, POU2F2, TFAP2A, YY1, RERE) and microRNAs (mir-335–5p, mir-26b-5p, mir-124–3p, mir-181a-5p, mir-98–5p, mir-16–5p, mir-7-5p, mir-129–5p, mir-8485, mir-1827). The present study identified biomolecules shared by TC and CKD at protein levels (hub proteins, transcription factors), and RNA levels (mRNAs, microRNAs). Basic biological experiments will be needed to establish them as biomarkers in TC and CKD.

The roles and role-players in thyroid cancer angiogenesis.

Thyroid cancer is the most prevalent endocrine cancer worldwide. Angiogenesis, the formation of new blood vessels, plays a pivotal role in the development and progression of tumors. Over the past years, cancer research has focused on the ability of tumors to induce newly formed blood vessel, because tumor growth and the process of cancer metastasis mainly depends on angiogenesis. Tumor neovascularization occurs following the imbalance between pro-angiogenic and anti-angiogenic factors until the tumor switches to an angiogenic phenotype. A number of signaling factors and receptors that are implicated in the regulation of angiogenesis have been identified and characterized; most notably, the vascular endothelial growth factors (VEGFs) family and their receptors, which are the main pro-angiogenic molecules during early development and in pathological conditions such as cancer. Although thyroid is a highly vascularized organ, angiogenic switch in tumors of this organ leads to the formation of a vast network of blood vessels that favors the dissemination of tumor cells to distant organs and results in deterioration of patient conditions. Accordingly, the identification of key angiogenic biomarkers for thyroid cancer can facilitate diagnosis, prognosis and clinical decision-making and also may help to discover targeting factors for effective cancer therapy as well as monitoring response to therapy. Hence, the main purposes of this review are to summarize the types and mechanisms of angiogenesis emphasizing the prominent factors implicated in thyroid cancer angiogenesis.

Identification of Long Noncoding RNA MIR22HG as a Novel Biomarker in Thyroid Cancer.

Thyroid cancer (TC) is the one of the most common endocrine malignancy. However, currently there are no specific and sensitive biomarkers for predicting the prognosis for TC. In this study, we for the first time showed MIR22HG was down-regulated in thyroid cancer by analyzing public datasets, including TCGA, GSE29265, GSE33630, and GSE55091. Furthermore, we observed the lower expression levels of MIR22HG were significantly related to higher age, lymph node metastasis status, residual tumor status, N stage, Grade, and T stage in TC. We also observed higher MIR22HG expression was associated with longer overall and disease-free survival time in TC. In order to explore the potential mechanisms of MIR22HG regulating TC progression, 4 hub gene networks regulated by MIR22HG were constructed in the present study. Bioinformatics analysis showed MIR22HG was associated with apoptotic process, regulation of transcription, mRNA splicing, regulation of cell cycle, and Hippo signaling pathway in TC. These results suggested MIR22HG could serve as a novel biomarker for thyroid cancer.

The role of matrix metalloproteinase-9 as a prognostic biomarker in papillary thyroid cancer

BackgroundThe aim of the present study was to investigate the association between matrix metalloproteinase-9 (MMP-9) expression with BRAF V600E mutation and clinicopathological features, in Iranian papillary thyroid cancer (PTC) patients.MethodsIn total, 90 participants including 60 PTC patients (15 males and 45 females) and 30 individuals with benign multinodular goiter (MNG) (5 males and 25 females) which were confirmed by surgical pathology, were investigated. MMP-9 was evaluated at both mRNA and protein levels, using SYBR-Green Real-Time PCR and enzyme-linked immune sorbent assay (ELISA), respectively. BRAF V600E mutation was detected by sequencing.ResultsMean age of PTC and MNG patients was 37.6 ± 12.6 and 48.1 ± 13.3 years, respectively (P = 0.001). BRAF V600E mutation was found in 24 of the 60 (40%) PTC cases, with mean tumor size of 1.59 ± 1.20 cm. MMP-9 mRNA levels were elevated in tumoral compared to the adjacent non-tumoral tissues (P = 0.039); moreover, this rise was also observed in PTC patients compared to MNG patients (P = 0.001). The mRNA levels of MMP-9 increased in patients aged≥45 years (P = 0.015), those with lymphovascular invasion (P = 0.003), and higher tumor stages (III and IV) (P = 0.011). The protein level of MMP-9 increased in tumoral compared to adjacent non-tumoral tissues (P < 0.001); this increase was also found in PTC patients compared to MNG participants (P = 0.004). MMP-9 protein level was higher in patients aged≥45 years (P = 0.001), those with lymphovascular invasion (P = 0.036) and higher TNM stages (III and IV) (P = 0.001). Area under the ROC curve (AUC) was 0.70 (95%CI: 0.57–0.83, P = 0.003), with 91.4% sensitivity and 51.9% specificity at the cutoff value of 0.50.ConclusionThe mRNA and protein levels of MMP-9 had no association with BRAF V600E mutation in Iranian PTC patients. These levels were associated with age, TNM stages, and lymphovascular invasion, being defined as malignant factors. Thus, elevated levels of MMP-9 in PTC patients compared to MNG participants illustrated that it can be used as a potential biomarker to differentiate PTC patients from those with MNG.

CCND1 Splice Variant as A Novel Diagnostic and Predictive Biomarker for Thyroid Cancer.

Cyclin D1 protein is aberrantly overexpressed in thyroid cancers, but mutations of the CCND1 gene are rare in these tumors. We investigated the CCND1 rs9344 (G870A) polymorphism and the expression profiles of wild-type CCND1a and shortened oncogenic isoform CCND1b at the mRNA and protein levels in 286 thyroid tumors. Genotype AA of rs9344 was associated with high expression of CCND1b mRNA and was more frequently found in thyroid cancer than in benign tumors. The mRNA expression levels of CCND1b were higher in papillary thyroid carcinoma (PTC) than in benign or other malignant tumors. However, the expression of CCND1a mRNA showed no association with the parameters. Noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP) was distinguished from PTC by low expression of CCND1b at mRNA and protein levels. We further observed that cyclin D1b immunostaining helped to avoid the misdiagnosis of classic PTC with predominant follicular pattern as NIFTP in a separate cohort. Nuclear cyclin D1b expression was associated with aggressive clinicopathologic features in PTC. These findings suggest that cyclin D1b overexpression can be used as a diagnostic and predictive biomarker in thyroid tumors and may be functionally involved in the development and progression of the disease.

The construction and analysis of gene co-expression network of differentially expressed genes identifies potential biomarkers in thyroid cancer

Background: The incidence and mortality of thyroid cancer has been increasing steadily in the United States. However, the molecular pathogenesis of thyroid cancer is not fully characterized. Methods: The R package of DESeq2 was applied to detect differentially expressed genes (DEGs) between 57 paired thyroid cancer and noncancerous tissues using RNA sequencing data from The Cancer Genome Atlas database. Weighted gene co-expression network analysis was used to construct co-expression modules and study the relationship between co-expression modules and clinical traits. Gene ontology (GO) enrichment analysis was performed on these genes from interested co-expression modules. Results: A cohort of 750 up-regulated and 296 down-regulated genes were identified in thyroid cancer. The weighted gene co-expression network analysis identified 5 gene co-expression modules. Two modules were significantly associated with patients’ age, cancer stage and multifocality. SERPINA1 and MRO were their hub genes respectively. Conclusions: The bioinformatics study for those co-expression modules and hub genes paves the way for the development of molecular biomarkers in thyroid cancer.

The construction and analysis of gene co-expression network of differentially expressed genes identifies potential biomarkers in thyroid cancer

Background: The incidence and mortality of thyroid cancer has been increasing steadily in the United States. However, the molecular pathogenesis of thyroid cancer is not fully characterized.

Circulating tumour DNA is a potential biomarker for disease progression and response to targeted therapy in advanced thyroid cancer

BackgroundConventional biomarkers in thyroid cancer are not disease specific and fluctuate in advanced disease, making interpretation difficult. Circulating tumour DNA (ctDNA) has been shown to be a useful biomarker in other solid tumours. This is a multimutational study of ctDNA over multiple timepoints, designed to test the hypothesis that ctDNA is a potential biomarker in patients with advanced thyroid cancer. MethodsMutational analysis of archival tumour tissue was performed using NGS with a targeted gene panel. Custom TaqMan assays were designed for plasma ctDNA testing using digital droplet polymerase chain reaction. Concentrations of detected ctDNA were correlated with the conventional biomarker concentration and axial imaging status defined by the Response Evaluation Criteria in Solid Tumours criteria. ResultsTumour tissue from 51 patients was obtained, with the following histologies: 32 differentiated (differentiated thyroid cancer [DTC]), 15 medullary (medullary thyroid cancer [MTC]), three poorly differentiated and one anaplastic. NGS analysis detected variants in 42 (82%) of cases. Plasma was assayed for these patients in 190 samples, and ctDNA was detected in 67% of patients. Earlier detection of disease progression was noted in three patients with MTC. In two cases (PTC and ATC), where conventional biomarkers were not detectable, ctDNA was detected before disease progression. Changes in ctDNA concentration occurred earlier than conventional markers in response to disease progression in multiple patients with DTC receiving targeted therapies. ConclusionThe majority of patients with advanced thyroid cancer had detectable ctDNA. ctDNA measurement may offer superiority over conventional markers in several scenarios: earlier detection of progression in MTC; as an alternative biomarker when conventional markers are not available; more rapid assessment of the disease status in response to targeted therapies, thereby potentially allowing prompter discontinuation of futile therapies. These early results support the hypothesis that ctDNA may be a clinically useful biomarker in thyroid cancer.

Up-regulated lipocalin-2 in pediatric thyroid cancer correlated with poor clinical characteristics.

The incidence of thyroid cancer is fast increasing in both adults and children. The pediatric thyroid cancer had often already progressed to a more advanced stage of the disease at diagnosis. Early detection of pediatric thyroid cancer has been a problem for many years. Lipocalin-2 (Lcn2) has been reported to be over-expressed in cancers of diverse histological origin and it facilitates tumorigenesis by promoting survival, growth, and metastasis. The plasma Lcn2 concentration of 28 Chinese papillary thyroid cancer (PTC) children and 24 healthy controls was measured. Immunostaining for Ki-67 of tumor tissue from PTC children was performed. The expression levels of Lcn2 and NFκB in PTC tissue and peri-carcinoma tissue of PTC children were measured through Western blot. The plasma concentration of Lcn2 was significantly elevated in pediatric PTC patients compared with healthy controls. Besides, the plasma Lcn2 concentration significantly correlated with clinical characteristics, NFκB level, and Ki-67 positive rate of nucleus in tissue of PTC. This is the first study to evaluate the plasma Lcn2 in pediatric PTC patients. It is possible that the plasma Lcn2 may be a new biomarker of pediatric thyroid cancer. Further studies are needed to explore the definite role and mechanism of Lcn2 in thyroid cancer, which will help to explore novel diagnostic or therapeutic strategies.

Abstract 5171: Tfap2b overexpression contributes to tumor growth &amp; progression of thyroid cancer through AKT&amp;VEGF/PEDF signaling pathway

Abstract TFAP2 is a family of transcription factors implicated in many aspects of development.TFAP2B is a member of the AP2 transcription factor family, which orchestrates a variety of cell processes. However, the roles of TFAP2B in regulating thyroid carcinogenesis remain largely unknown. Here, we investigated the regulatory effects of TFAP2B on thyroid cancer growth &amp; identified the underlying mechanisms of actions in thyroid cancer cells.We examined the expression of TFAP2B in thyroid cancer cell lines &amp; tumor tissues. We also analyzed the TNM staging of TFAP2B in thyroid cancer. Then we investigated the molecular mechanisms by which TFAP2B knockdown or overexpression regulated thyroid cancer cell growth, angiogenesis &amp; apoptosis, &amp; further confirmed the role of TFAP2B in tumor growth in a thyroid cancerxenograft mouse model.TFAP2B was expressed in thyroid cancer lines &amp;tumortissues,especially in anaplastic thyroid cancer. Strong TFAP2B expression showed a positive correlation with the poor differentiation of patients with thyroid cancer . TFAP2B knockdown by siRNA significantly inhibited cell growth &amp; induced apoptosis in thyroid cancer cells in vitro &amp; in a thyroid cancersubcutaneous xenograft model, whereas TFAP2B overexpression promoted cell growth. The observed regulation of cell growth was accompanied by the TFAP2B-mediated modulation of the VEGF/PEDF-dependent signaling pathways in thyroid cancer cells.These results indicate that TFAP2B plays a critical role in regulating thyroid cancer growth &amp; could serve as a promising therapeutic target or diagonistic biomarker for thyroid cancer . Citation Format: Xiaoyan Fu, Zhongyuan Yang, Shuwei Chen. Tfap2b overexpression contributes to tumor growth &amp; progression of thyroid cancer through AKT&amp;VEGF/PEDF signaling pathway [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 5171.