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1. Zhu XG, Zhao L, Willingham MC, Cheng SY: Thyroid hormone receptors are tumor suppressors in a mouse model of metastatic follicular thyroid carcinoma. Oncogene; 2010 Apr 1;29(13):1909-19
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thyroid hormone receptors are tumor suppressors in a mouse model of metastatic follicular thyroid carcinoma.
  • Aberrant expression and mutations of thyroid hormone receptor genes (TRs) are closely associated with several types of human cancers.
  • As these mice aged, they spontaneously developed follicular thyroid carcinoma with pathological progression from hyperplasia to capsular invasion, vascular invasion, anaplasia and metastasis to the lung, similar to human thyroid cancer.
  • In addition, consistent with the human cancer, AKT-mTOR-p70(S6K) signaling and vascular growth factor and its receptor were activated to facilitate tumor progression.
  • Thus, TRs could function as tumor suppressors in a mouse model of metastatic follicular thyroid cancer.
  • [MeSH-major] Adenocarcinoma, Follicular / genetics. Gene Expression Regulation, Neoplastic. Mice, Transgenic. Receptors, Thyroid Hormone / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Disease Models, Animal. Humans. Mice. Mutation. Signal Transduction / genetics


2. Chiacchio S, Lorenzoni A, Boni G, Rubello D, Elisei R, Mariani G: Anaplastic thyroid cancer: prevalence, diagnosis and treatment. Minerva Endocrinol; 2008 Dec;33(4):341-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic thyroid cancer: prevalence, diagnosis and treatment.
  • Anaplastic thyroid cancer (ATC) is a rare aggressive tumor arising from the follicular cells of the thyroid gland (as does well differentiated thyroid cancer, WDTC), but ATC cells do not retain any of the biological features of the original follicular cells, such as uptake of iodine and synthesis of thyroglobulin.
  • ATC represents 2-5% of all thyroid tumors, with a decreasing trend with respect to the incidence of WDTC.
  • ATC may arise de novo, but in most cases it develops from a pre-existing WDTC, especially the follicular subtype.
  • Because of its aggressive behavior, the latest American Joint Committee on Cancer Staging Manual classifies all ATCs as T4 and Stage IV tumors, regardless of their actual overall tumor burden.
  • Some favourable results have recently been reported with newly developed chemotherapy agents and hyper-fractioned radiation therapy.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma / therapy. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / therapy


3. Dackiw AP, Ezzat S, Huang P, Liu W, Asa SL: Vitamin D3 administration induces nuclear p27 accumulation, restores differentiation, and reduces tumor burden in a mouse model of metastatic follicular thyroid cancer. Endocrinology; 2004 Dec;145(12):5840-6
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  • [Title] Vitamin D3 administration induces nuclear p27 accumulation, restores differentiation, and reduces tumor burden in a mouse model of metastatic follicular thyroid cancer.
  • We have previously demonstrated in vitro that 1alpha,25-dihydroxyvitamin D3 (calcitriol) treatment increases p27 expression and decreases cell proliferation in cultured thyroid carcinoma cell lines.
  • We hypothesized that in vivo treatment with calcitriol would have a beneficial effect on thyroid carcinoma growth and progression.
  • Five x 10(6) WRO (human thyroid follicular carcinoma derived) cells were implanted in the neck in 4- to 5-wk-old female SCID mice in an orthotopic xenograft model.
  • Animals (n = 15) were treated i.p. three times a week for 21 d with 0.75 microg/kg calcitriol or vehicle.
  • Average tumor volume in control mice after 21 d of vehicle treatment was 2002 +/- 207 mm3 compared with a mean tumor volume of 1241 +/- 115 mm3 in animals receiving calcitriol, reflecting a 38% reduction in tumor volume size (P < 0.003).
  • Tumors from vehicle-treated animals demonstrated morphological features of epithelial malignancies with characteristics of insular carcinoma and multiple metastases to the lungs.
  • Tumors excised from calcitriol-treated animals demonstrated signs of differentiation with restoration of thyroglobulin staining.
  • These studies demonstrate that in vivo calcitriol administration can effectively restore p27 accumulation in thyroid carcinoma cells, an effect associated with appreciably enhanced cellular differentiation, reduction in tumor burden, and prevention of metastatic growth.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Cholecalciferol / pharmacology. Proliferating Cell Nuclear Antigen / metabolism. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Line, Tumor. Disease Models, Animal. Humans. Immunohistochemistry. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Mice. Thyroglobulin / metabolism. Xenograft Model Antitumor Assays


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4. Matuszczyk A, Petersenn S, Bockisch A, Gorges R, Sheu SY, Veit P, Mann K: Chemotherapy with doxorubicin in progressive medullary and thyroid carcinoma of the follicular epithelium. Horm Metab Res; 2008 Mar;40(3):210-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy with doxorubicin in progressive medullary and thyroid carcinoma of the follicular epithelium.
  • Twenty-two patients (mean age 61) with metastasizing, progressive, nonradioiodine-accumulating thyroid carcinoma of the follicular epithelium were treated with doxorubicin between 2000 and 2005.
  • Tumors were histologically classified as follicular in 15 patients (68%) and papillary in 7 patients (32%).
  • In addition, nine patients (mean age 51 years) with medullary thyroid carcinoma were treated with doxorubicin between 1997 and 2005.
  • In patients with papillary or follicular thyroid carcinoma, 5% had a partial regression over 6 months, 42% had stable disease for a median of 7 months (range: 1-22), and 53% had continuous progression established over 5 months (range: 1-11).
  • In patients with medullary thyroid carcinoma, 11% had a partial regression over 6 months followed by stable disease for 3 months, 11% had stable disease over 7 months, and 79% demonstrated progressive disease established over 5 months (range: 2-12).
  • Doxorubicin can be a valid chemotherapy option, especially for advanced or metastatic thyroid carcinoma of the follicular epithelium.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Antibiotics, Antineoplastic / therapeutic use. Doxorubicin / therapeutic use. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Carcinoma, Medullary / drug therapy. Carcinoma, Medullary / radiography. Carcinoma, Papillary / drug therapy. Carcinoma, Papillary / radiography. Female. Humans. Male. Middle Aged. Neoplasm Staging. Treatment Outcome

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  • (PMID = 18348081.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
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5. Lopez JP, Wang-Rodriguez J, Chang CY, Sneh G, Yu MA, Pardo FS, Aguilera J, Ongkeko WM: Gefitinib (Iressa) potentiates the effect of ionizing radiation in thyroid cancer cell lines. Laryngoscope; 2008 Aug;118(8):1372-6
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  • [Title] Gefitinib (Iressa) potentiates the effect of ionizing radiation in thyroid cancer cell lines.
  • OBJECTIVES/HYPOTHESIS: To determine whether inactivation of epidermal growth factor receptor (EGFR) kinase activity will sensitize thyroid cancer cell lines to ionizing radiation-induced death.
  • STUDY DESIGN: Established human thyroid cancer cells lines were studied.
  • METHODS: Colony formation assay was used to determine the effect of Gefitinib, a small molecule inhibitor of EGFR, on anaplastic (ARO) and follicular (WRO) thyroid cancer cell lines.
  • Immunohistochemistry was performed on archived thyroid cancer tissue to demonstrate expression of EGFR.
  • RESULTS: Incubation with Gefitinib caused decreased phosphorylation of EGFR protein in established thyroid cancer cell lines as measured by Western blot.
  • Inhibition of EGFR kinase activity by Gefitinib resulted in a dose-dependent decrease in colony formation in both ARO and WRO thyroid cancer cell lines.
  • CONCLUSIONS: Inactivation of the EGFR kinase by Gefitinib potentiates the ionizing radiation-induced inhibition of cell proliferation in thyroid cancer cell lines.
  • Use of this combination treatment of Gefitinib and ionizing radiation may be a promising therapy for anaplastic thyroid and metastatic follicular thyroid cancer and should be extended into animal models.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Adenocarcinoma, Follicular / radiotherapy. Carcinoma / drug therapy. Carcinoma / radiotherapy. Quinazolines / pharmacology. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / radiotherapy
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Down-Regulation. Drug Synergism. Humans. Phosphorylation / drug effects. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 18475209.001).
  • [ISSN] 1531-4995
  • [Journal-full-title] The Laryngoscope
  • [ISO-abbreviation] Laryngoscope
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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6. Lopez JP, Wang-Rodriguez J, Chang C, Chen JS, Pardo FS, Aguilera J, Ongkeko WM: Gefitinib inhibition of drug resistance to doxorubicin by inactivating ABCG2 in thyroid cancer cell lines. Arch Otolaryngol Head Neck Surg; 2007 Oct;133(10):1022-7
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  • [Title] Gefitinib inhibition of drug resistance to doxorubicin by inactivating ABCG2 in thyroid cancer cell lines.
  • OBJECTIVE: To investigate the regulation of the breast cancer resistance protein ABCG2/BRCP1 drug transporter by epidermal growth factor receptor (EGFR) kinase activity, and to determine whether gefitinib, an EGFR small molecule inhibitor, will modulate the effects of doxorubicin hydrochloride by inhibiting its extrusion from thyroid cancer cells.
  • DESIGN: Extrusion assays using flow cytometry analysis were used to determine the ability of thyroid cancer cells to extrude the chemotherapy drug, doxorubicin, via the ABCG2 drug transporter in the presence or absence of gefitinib.
  • Colony formation assays were performed to determine the effect of gefitinib on thyroid cancer cell survival in response to gefitinib, doxorubicin, or the combination of both drugs.
  • RESULTS: Inhibition of EGFR kinase activity by gefitinib causes the translocation of the ABCG2 drug transporter away from the plasma membrane, resulting in a concomitant decrease in doxorubicin extrusion in thyroid cancer cell lines.
  • The addition of gefitinib increases doxorubicin-induced cell death in thyroid cancer cells as measured by colony formation assay.
  • CONCLUSIONS: Epidermal growth factor receptor regulates the function of the drug transporter ABCG2/BCRP1 and correlates with ABCG2 protein expression levels.
  • Inactivation of the EGFR kinase by gefitinib potentiates the cytotoxic effect of doxorubicin in thyroid cancer, most likely by decreasing the ability of the cell to extrude doxorubicin.
  • The expression of ABCG2 may explain in part the ineffectiveness of doxorubicin as a single modality treatment for anaplastic thyroid cancer or for treatment of metastatic follicular thyroid cancer.
  • Use of this combination treatment of gefitinib and doxorubicin may be a promising therapy for anaplastic thyroid and metastatic follicular thyroid cancer and needs to be investigated further.
  • [MeSH-major] ATP-Binding Cassette Transporters / genetics. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm / drug effects. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / genetics. RNA, Neoplasm / genetics. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Blotting, Western. Carcinoma / drug therapy. Carcinoma / metabolism. Carcinoma / pathology. Cell Line, Tumor. Cell Proliferation / drug effects. Culture Media. Doxorubicin / administration & dosage. Drug Resistance, Multiple. Flow Cytometry. Fluorescent Antibody Technique. Humans. In Situ Nick-End Labeling. Quinazolines / administration & dosage. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 17938326.001).
  • [ISSN] 0886-4470
  • [Journal-full-title] Archives of otolaryngology--head & neck surgery
  • [ISO-abbreviation] Arch. Otolaryngol. Head Neck Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Culture Media; 0 / Neoplasm Proteins; 0 / Quinazolines; 0 / RNA, Neoplasm; 80168379AG / Doxorubicin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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7. Zarnegar R, Brunaud L, Kanauchi H, Wong M, Fung M, Ginzinger D, Duh QY, Clark OH: Increasing the effectiveness of radioactive iodine therapy in the treatment of thyroid cancer using Trichostatin A, a histone deacetylase inhibitor. Surgery; 2002 Dec;132(6):984-90; discussion 990
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  • [Title] Increasing the effectiveness of radioactive iodine therapy in the treatment of thyroid cancer using Trichostatin A, a histone deacetylase inhibitor.
  • BACKGROUND: Radioactive iodine is used to identify and treat recurrent and metastatic thyroid cancer of follicular cell origin.
  • Between 30% and 40% of thyroid cancers are either resistant or become resistant to radioactive iodine.
  • In this investigation the effects of Trichostatin A (TSA), a histone deacetylating inhibitor, on human thyroid NIS and PDS gene expression was investigated.
  • METHOD: Cell lines from papillary, Hürthle, and follicular cell carcinomas were treated with TSA for 72 hours at concentrations up to 100 ng/mL.
  • NIS messenger RNA expression in cell carcinomas was increased 107- (1.8-307) and 217- (5.7-408) fold in papillary, 39- (20-63) and 58- (37-80) fold in Hürthle, and 459- (178-810) and 781- (412-1229) fold in follicular after treatment with 50 and 100 ng/mL of TSA, respectively.
  • PDS messenger RNA expression in cell carcinomas was decreased 0.22- (0.05-0.45) and 0.27- (0.09-0.47) fold in papillary, 0.53- (0.46-0.60) and 0.54- (0.44-0.64) fold in Hürthle, and 0.32- (0.26-0.39) and 0.56- (0.47-0.64) fold in follicular, after the same treatment.
  • CONCLUSIONS: In thyroid cancer cell lines, TSA dramatically increased NIS gene expression and reduced PDS expression.
  • The increased NIS expression and reduced PDS expression may make radioiodine therapy more effective in patients with thyroid cancer, especially when the tumors have no or low uptake of radioiodine.
  • [MeSH-major] Carcinoma, Papillary. Enzyme Inhibitors / pharmacology. Hydroxamic Acids / pharmacology. Iodine Radioisotopes / pharmacokinetics. Membrane Transport Proteins. Radiopharmaceuticals / pharmacokinetics. Thyroid Neoplasms
  • [MeSH-minor] Carrier Proteins / genetics. Cell Survival / drug effects. Colonic Neoplasms. Gene Expression / drug effects. Histone Deacetylase Inhibitors. Humans. In Vitro Techniques. Symporters / genetics. Tumor Cells, Cultured / cytology. Tumor Cells, Cultured / enzymology

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  • (PMID = 12490845.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Iodine Radioisotopes; 0 / Membrane Transport Proteins; 0 / Radiopharmaceuticals; 0 / SLC26A4 protein, human; 0 / Symporters; 0 / sodium-iodide symporter; 3X2S926L3Z / trichostatin A
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