신효식 교수

Abstract Purpose: Thyroid-stimulating hormone (TSH) suppression is widely used to treat well-differentiated thyroid cancer, whereas its role in poorly differentiated thyroid cancer (PDTC) is undetermined. Besides thyrocytes, TSH also binds to stromal cells, comprising tumor microenvironments. This study aimed to investigate the effects of TSH on tumor microenvironments in PDTC. Experimental Design: An ectopic tumor model using PDTC cells (BHP10-3SCp and FRO), which exhibit TSH/cAMP-independent c

Background: Metformin has antitumoral actions in human cancers, including the thyroid, while its effects on metastatic lesions are unclear. Patients with bone metastasis (BM) from thyroid cancers have poor survival. Because metformin inhibits the activation of osteoclasts, which has essential roles in BM, the aim of this study was to investigate the therapeutic effects of metformin on thyroid cancer BM and osteoclast activation in the bone microenvironment. Methods: The anaplastic thyroid cancer

Abstract Thyroid cancer is associated with genetic alterations, e.g. BRAF V600E , which may cause carcinomatous changes in hormone‐secreting epithelial cells. Epidemiological studies have shown that overnutrition is related to the development and progression of cancer. In this study, we attempted to identify the cell nonautonomous factor responsible for the progression of BRAF V600E thyroid cancer under overnutrition conditions. We developed a mouse model for inducible thyrocyte‐specific activat

Introduction Securing a well-established mouse model is important in identifying and validating new therapeutic targets for immuno-oncology. The C57BL/6 mouse is one of the most fully characterised immune system of any animal and provides powerful platform for immuno-oncology discovery. An orthotopic tumor model has been established using TBP3743 (murine anaplastic thyroid cancer [ATC]) cells in B6129SF1 hybrid mice, this model has limited data on tumor immunology than C57BL/6 inbred mice. This

Abstract Endotrophin (ETP), a cleaved fragment of the C5 domain of the Type VI collagen α3 (Col6α3), has been shown to play pro-tumorigenic roles in breast and liver cancers. However, the ETP actions in tumor microenvironment (TME) is still undetermined. This study aimed to investigate the role and the mechanism of ETP in macrophage-enriched thyroid cancer TMEs. First, the expression of ETP on various human thyroid tissues was studied. Immunohistochemical staining showed that the ETP was express

<div>AbstractPurpose:<p>Thyroid-stimulating hormone (TSH) suppression is widely used to treat well-differentiated thyroid cancer, whereas its role in poorly differentiated thyroid cancer (PDTC) is undetermined. Besides thyrocytes, TSH also binds to stromal cells, comprising tumor microenvironments. This study aimed to investigate the effects of TSH on tumor microenvironments in PDTC.</p>Experimental Design:<p>An ectopic tumor model using PDTC cells (BHP10-3SCp and FRO), w

<p>Supplementary Fig. S1. TSH-independent growth of poorly-differentiated thyroid cancer cells. Supplementary Fig. S2. Expression of thyroid differentiation-related genes in thyroid cancer cell lines and effects of TSH on PAX-8 expression in BHP10-3SCp cells. Supplementary Fig. S3. Western blot analysis of the effect of TSH on VEGFR2 expression in PDTC tumors. *P< 0.05 versus controls. All data are expressed as mean {plus minus}SD. Supplementary Fig. S4. Effects of TSH on tumor growth a

Abstract Endotrophin (ETP), a cleaved fragment of the C5 domain of the Type VI collagen α3 (Col6α3), has been shown to play pro-tumorigenic roles in breast and liver cancers. However, the ETP actions in tumor microenvironment (TME) is still undetermined. This study aimed to investigate the role and the mechanism of ETP in macrophage-enriched thyroid cancer TMEs. First, the expression of ETP on various human thyroid tissues was studied. Immunohistochemical staining showed that the ETP was express

<p>Supplementary Fig. S1. TSH-independent growth of poorly-differentiated thyroid cancer cells. Supplementary Fig. S2. Expression of thyroid differentiation-related genes in thyroid cancer cell lines and effects of TSH on PAX-8 expression in BHP10-3SCp cells. Supplementary Fig. S3. Western blot analysis of the effect of TSH on VEGFR2 expression in PDTC tumors. *P< 0.05 versus controls. All data are expressed as mean {plus minus}SD. Supplementary Fig. S4. Effects of TSH on tumor growth a

<p>Supplementary Materials and Methods</p>

<div>AbstractPurpose:<p>Thyroid-stimulating hormone (TSH) suppression is widely used to treat well-differentiated thyroid cancer, whereas its role in poorly differentiated thyroid cancer (PDTC) is undetermined. Besides thyrocytes, TSH also binds to stromal cells, comprising tumor microenvironments. This study aimed to investigate the effects of TSH on tumor microenvironments in PDTC.</p>Experimental Design:<p>An ectopic tumor model using PDTC cells (BHP10-3SCp and FRO), w

<p>Supplementary Table S1. Nucleotide sequences of primers used for quantitative RT-PCR Supplementary Table S2. Associations of VEGF-A with tumor angiogenesis, macrophage infiltration, and CXCL8 expression and associations among serum TSH levels, VEGF-A, and tumor size in 35 human papillary thyroid cancer tumors larger than 2cm in size</p>

BACKGROUND: The combination of epirubicin, cisplatin, and 5-fluorouracil (ECF) is widely used for gastric cancer treatment. However, cancer cells can acquire chemoresistance over multiple treatment cycles, leading to recurrence. This study aimed to investigate a novel biomarker for predicting ECF resistance and its biological roles in gastric cancer. METHODS: ECF-resistant (ECF-R) gastric cancer cell lines were established through stepwise ECF treatment. Transcriptome analysis was performed to i

<p>Supplementary Table S1. Nucleotide sequences of primers used for quantitative RT-PCR Supplementary Table S2. Associations of VEGF-A with tumor angiogenesis, macrophage infiltration, and CXCL8 expression and associations among serum TSH levels, VEGF-A, and tumor size in 35 human papillary thyroid cancer tumors larger than 2cm in size</p>

<p>Supplementary Materials and Methods</p>