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Indicator report of the rate of thyroid cancer in Utah per 100,000 population.

Indicator report of the rate of thyroid cancer in Utah per 100,000 population.

Indicator report of the rate of thyroid cancer in Utah per 100,000 population.

Ho Wing Man., On t.p. "gamma" appears as the Greek letter., Thesis submitted in: December 2007., Thesis (M.Phil.)--Chinese University of Hong Kong, 2008., Includes bibliographical references (leaves 95-106)., s in English and Chinese., p.I, 摘要 --- p.III, ACKNOWLEDGMENTS --- p.V, ABBREVIATIONS --- p.VI, LIST OF FIGURES --- p.IX, LIST OF TABLES --- p.X, CONTENTS --- p.XII, Chapter CHAPTER ONÉؤ --- GENERAL INTRODUCTION --- p.1, Chapter 1.1 --- Background --- p.2, Chapter 1.1.1 --- Thyroid cancer --- p.2, Chapter 1.1.2 --- Apoptosis and thyroid cancer --- p.4, Chapter 1.2 --- Estrogen receptors and apoptosis --- p.5, Chapter 1.2.1 --- Estrogen receptor-α (ERα) and estrogen receptor-β (ERβ) --- p.5, Chapter 1.2.2 --- Differential roles of estrogen receptor-α(ERα) and estrogen receptor-β (ERβ) in apoptosis --- p.6, Chapter 1.2.3 --- Bcl-2 family --- p.8, Chapter 1.3 --- Peroxisome proliferator-activated receptor-γ (PPARγ) --- p.9, Chapter 1.3.1 --- Molecular aspects of PPAR --- p.9, Chapter 1.3.2 --- PPAR/RXR complex --- p.13, Chapter 1.3.3 --- PPARγ ligands --- p.16, Chapter 1.3.4 --- PPARγ and apoptosis in thyroid cancer --- p.19, Chapter 1.3.5 --- PPARγ ligands-mediated apoptosis pathway --- p.21, Chapter 1.4 --- Previous results from our laboratory --- p.25, Chapter 1.5 --- Summary of previous studies --- p.27, Chapter 1.6 --- Perspectives --- p.28, Chapter 1.7 --- Objectives of this project --- p.29, Chapter CHAPTER TWÓؤ --- GENERAL MATERIALS AND METHODS --- p.30, Chapter 2.1 --- Materials --- p.31, Chapter 2.1.1 --- Cell lines --- p.31, Chapter 2.1.2 --- Plasmid vectors used in this study --- p.31, Chapter 2.1.3 --- Antibodies --- p.32, Chapter 2.1.4 --- Culture media and transfection reagents --- p.32, Chapter 2.1.5 --- Materials for protein manipulation --- p.33, Chapter 2.1.6 --- Drugs for treatment --- p.34, Chapter 2.1.7 --- Kits --- p.35, Chapter 2.1.8 --- Instruments --- p.35, Chapter 2.2 --- Methods --- p.36, Chapter 2.2.1 --- Cell culture --- p.36, Chapter 2.2.2 --- Cell viability analysis --- p.36, Chapter 2.2.3 --- Preparation of protein extract --- p.37, Chapter 2.2.4 --- Determination of the concentration of target protein --- p.37, Chapter 2.2.5 --- Gel electrophoresis and protein transfer --- p.38, Chapter 2.2.6 --- Immunoblotting --- p.39, Chapter 2.2.7 --- Apoptosis detected by Cell Death ELISAplus --- p.41, Chapter 2.2.8 --- PPARγ-ligand Enzyme Immunoassay --- p.45, Chapter 2.2.8.1 --- 15d-PGJ3 Enzyme Immunoassay --- p.45, Chapter 2.2.8.2 --- 15(S)-HETE Enzyme Immunoassay --- p.46, Chapter 2.2.8.3 --- 13(S)-HODE Enzyme Immunoassay --- p.46, Chapter 2.2.9 --- Transient tranfection and luciferase activity assay --- p.47, Chapter 2.2.10 --- Statistical Analysis --- p.52, Chapter CHAPTER THREÉؤ --- ESTROGEN RECEPTORa (ERa) AND ESTROGEN RECEPTORP(ERP) MEDIATE THE PROLIFERATION AND APOPTOSIS OF HUMAN THYROID PAPILLARY CARCINOMA CELLS --- p.53, Chapter 3.1 --- Introduction --- p.54, Chapter 3.2 --- Materials and Methods --- p.56, Chapter 3.2.1 --- Cell culture and treatment --- p.56, Chapter 3.2.2 --- Western Blot --- p.56, Chapter 3.2.3 --- Cell proliferation determined by MTT assay --- p.57, Chapter 3.2.4 --- Apoptosis detected by Cell Death ELISAplus assay --- p.58, Chapter 3.3 --- Results --- p.59, Chapter 3.3.1 --- "The expression of ERα, ERβ and PPARγ in NPA, FRO, ARO and WRO thyroid cancer cell lines" --- p.59, Chapter 3.2.2 --- Effects of PPT and DPN on cell viability --- p.61, Chapter 3.3.3 --- Apoptotic cells quantification by Cell Death ELISAplus assay --- p.64, Chapter 3.4 --- Discussion --- p.67, Chapter CHAPTER FOUŔؤ --- THE RELATIONSHIP BETWEEN PPARγ AND ESTROGEN RECEPTOR AND THE REGULATION OF THE APOPTOSIS IN THYROID CANCER CELL LINES --- p.70, Chapter 4.1 --- Introduction --- p.71, Chapter 4.2 --- Material and Methods --- p.74, Chapter 4.2.1 --- Transient transfection --- p.74, Chapter 4.2.2 --- Luciferase assay --- p.74, Chapter 4.2.3 --- 15d-PGJ2 ELISA assay --- p.75, Chapter 4.2.4 --- 15S-HETE ELISA assay --- p.76, Chapter 4.2.5 --- 13S-HODE ELISA assay --- p.77, Chapter 4.3 --- Results --- p.78, Chapter 4.3.1 --- "PPT, ERα-agonist, increased thyroid cancer cell proliferation and caused the decrease the level of PPARγ ligands" --- p.78, Chapter 4.3.2 --- "DPN, ERβ-agonist, inhibited thyroid cancer cell proliferation, induced apoptosis and caused the increase the level of PPARγ ligands" --- p.83, Chapter 4.3.3 --- PPT did not alter the transcriptional activity of PPARγ --- p.88, Chapter 4.4 --- Discussion --- p.90, Chapter CHAPTER FIVÉؤ --- CONCLUSIONS AND FUTURE PROSPECT --- p.92, Chapter 5.1 --- Summary of results --- p.93, Chapter 5.2 --- Conclusion --- p.94, Chapter 5.3 --- Future prospects --- p.94, REFERENCE LIST --- p.95, http://library.cuhk.edu.hk/record=b5896774, Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Although there is strong evidence that thyroid tumors occur more frequently in females than in males, few studies have investigated the role sex hormones play in thyroid carcinogenesis, especially the role of estrogen (E2). This laboratory has previously shown that estrogen receptors (ERs) exist in thyroid papillary carcinoma cells. Continuing along this line of research, we studied the role of E2 and its receptors on the regulation of human thyroid cancer., In conclusion, we have demonstrated (1) a novel mechanism by which E2 contributes to the proliferation and growth of thyroid cancer cells, (2) that E2 influences the expression of ERalpha and ERbeta differently, causing an imbalance between them, which may change the biological behavior of thyroid cancer cells, giving them the ability to proliferate and resist apoptosis by influencing the level of ERK1/2 activity and subsequently the ratio of anti-apoptotic Bcl-2 to pro-apoptotic Bax, and (3) that the subcellular localization of ERalpha and ERbeta may be a factor that contributes to the differing pathogeneses of papillary and anaplastic thyroid cancers., To further clarify the mechanism by which E2 promotes cellular proliferation in thyroid cancer cells, we studied the localization of ERalpha and ERbeta in both KAT5 and anaplastic carcinoma cells (FRO) by immunofluorescence staining and by immunoblotting of the proteins in subcellular fractions. Cell proliferation and apoptosis were examined together with the expression of selected apoptotic proteins such as Bax, AIF and cytochrome c. We showed that the subcellular localization of ERalpha and ERbeta differed in papillary and anaplastic thyroid cancer. E2 administration led to an increase in the level of ERalpha in the nuclei of papillary cancer cells while the levels of ERbeta remained unchanged. However, the level of mitochondrial ERbeta surpassed that of ERalpha in anaplastic cancer cells. We also showed that E2 affected caspase-dependent and/or independent apoptosis via ERs in thyroid cancers., We first studied the molecular pathways by which E2 promotes cellular proliferation in thyroid cancer cells using a human thyroid cancer cell line (KAT5) treated with E2, a selective E2 alpha receptor (ERalpha) agonist (PPT), a selective E2 beta receptor (ERbeta) agonist (DPN), an ERalpha antagonist (MPP), an E2 antagonist (ICI182780) and siRNA, which blocks ERalpha and ERbeta, by MTT assay, DNA fragmentation ELISA, BrdU cell proliferation assay and Western blot. We found that E2 and PPT gradually promoted cell proliferation by increasing the expression of ERalpha and by up-regulating the expression of Bcl-2 and pERK1/2. In contrast, we found that DPN had a negative effect on cell growth by enhancing the expression of ERbeta and Bax and by down-regulating pERK1/2 expression. At the same time, blocking ERalpha significantly reduced the E2-mediated Bcl-2 and pERK1/2 expression. On the other hand, blocking ERbeta markedly enhanced their expression. These results suggest that E2 regulates cellular growth of KAT5 cells by an ER-ERK1/2-MAPK pathway and also that E2 affects mitochondrial homeostasis., Zeng, Qiang., "September 2007.", Adviser: George Gong Chen., Source: Dissertation Abstracts International, Volume: 69-08, Section: B, page: 4616., Thesis (Ph.D.)--Chinese University of Hong Kong, 2007., Includes bibliographical references (p. 136-154)., Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web., Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web., in English and Chinese., School code: 1307., isbn: 9780549774259, Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/)