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4. Guida T, Salvatore G, Faviana P, Giannini R, Garcia-Rostan G, Provitera L, Basolo F, Fusco A, Carlomagno F, Santoro M: Mitogenic effects of the up-regulation of minichromosome maintenance proteins in anaplastic thyroid carcinoma. J Clin Endocrinol Metab; 2005 Aug;90(8):4703-9
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  • [Title] Mitogenic effects of the up-regulation of minichromosome maintenance proteins in anaplastic thyroid carcinoma.
  • CONTEXT: Anaplastic thyroid carcinomas (ATC) are among the most aggressive human malignancies and are characterized by high mitotic activity.
  • OBJECTIVE: In an attempt to cast light on the mechanisms governing ATC, we evaluated MCM5 and MCM7 expression in human normal, papillary (PTC), and anaplastic thyroid samples, as well as in primary culture cells and transgenic mouse models.
  • RESULTS: MCM5 and MCM7 expression was high in 65% of ATC and negligible in normal thyroid tissue and papillary thyroid carcinomas.
  • An analysis of human ATC primary cell cultures and of a transgenic mouse model of ATC confirmed these findings.
  • An increased transcription rate accounted for MCM7 up-regulation, because the activity of the MCM7 promoter was more than 10-fold higher in ATC cells compared with normal thyroid cells.
  • Treatment with small inhibitory duplex RNAs, which decrease MCM7 protein levels, reduced the rate of DNA synthesis in ATC cells.
  • [MeSH-major] Carcinoma, Papillary / physiopathology. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Thyroid Neoplasms / physiopathology
  • [MeSH-minor] Animals. Cell Division / physiology. Cells, Cultured. DNA / biosynthesis. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Neoplastic. Humans. Mice. Mice, Transgenic. Minichromosome Maintenance Complex Component 2. Minichromosome Maintenance Complex Component 6. Minichromosome Maintenance Complex Component 7. Mitogens / metabolism. RNA, Messenger / analysis. Up-Regulation

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  • (PMID = 15899946.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / MCM5 protein, human; 0 / Mitogens; 0 / Nuclear Proteins; 0 / RNA, Messenger; 9007-49-2 / DNA; EC 3.6.4.12 / MCM2 protein, human; EC 3.6.4.12 / MCM6 protein, human; EC 3.6.4.12 / MCM7 protein, human; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 6; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 7
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5. Wiseman SM, Masoudi H, Niblock P, Turbin D, Rajput A, Hay J, Bugis S, Filipenko D, Huntsman D, Gilks B: Anaplastic thyroid carcinoma: expression profile of targets for therapy offers new insights for disease treatment. Ann Surg Oncol; 2007 Feb;14(2):719-29
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  • [Title] Anaplastic thyroid carcinoma: expression profile of targets for therapy offers new insights for disease treatment.
  • BACKGROUND: Anaplastic thyroid cancer is an endocrine malignancy.
  • Little is known regarding the expression by anaplastic tumors of molecular targets for new human anticancer agents that have been studied in the preclinical or clinical setting.
  • The objective of this work was to evaluate the expression profile of anaplastic thyroid tumors for molecular targets for treatment.
  • METHODS: Of the 94 cases of anaplastic thyroid cancers diagnosed and treated in British Columbia, Canada over a 20-year period (1984-2004), 32 cases (34%) had adequate archival tissue available for evaluation.
  • A tissue microarray was constructed from these anaplastic thyroid tumors and immunohistochemistry was utilized to evaluate expression of 31 molecular markers.
  • RESULTS: A single tumor with strong calcitonin expression was identified as a poorly differentiated medullary carcinoma and excluded from the study cohort.
  • The mean age of the anaplastic cohort was 66 years; 16 patients (51%) were females, and the median patient survival was 23 weeks.
  • A wide range in molecular marker expression was observed by the anaplastic thyroid cancer tumors (0-100%).
  • The therapeutic targets most frequently and most strongly overexpressed by the anaplastic tumors were: beta-catenin (41%), aurora A (41%), cyclin E (67%), cyclin D1 (77%), and EGFR (84%).
  • CONCLUSIONS: Anaplastic thyroid tumors exhibit considerable derangement of their cell cycle and multiple signal transduction pathways that leads to uncontrolled cellular proliferation and the development of genomic instability.
  • This report is the first to comprehensively evaluate a panel of molecular targets for therapy of anaplastic thyroid cancer and supports the development of clinical trials with agents such as cetuximab, small-molecule tyrosine kinase inhibitors, and aurora kinase inhibitors, which may offer new hope for individuals diagnosed with this fatal thyroid malignancy.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma / genetics. Carcinoma / metabolism. Thyroid Neoplasms / genetics. Thyroid Neoplasms / metabolism


6. Noh TW, Soung YH, Kim HI, Gil HJ, Kim JM, Lee EJ, Chung J: Effect of {beta}4 integrin knockdown by RNA interference in anaplastic thyroid carcinoma. Anticancer Res; 2010 Nov;30(11):4485-92
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  • [Title] Effect of {beta}4 integrin knockdown by RNA interference in anaplastic thyroid carcinoma.
  • BACKGROUND: Integrin α6β4 is a known tumor antigen; however, its function in different subtypes of thyroid cancer is not known.
  • This study reports that α6β4 expression is selectively up-regulated in anaplastic thyroid cancer (ATC) cells, the most malignant subtype of human thyroid cancer.
  • MATERIALS AND METHODS: To assess the contribution of α6β4 in ATC progression, cell proliferation, motility and soft agar assay were performed in vitro and a xenograft tumor growth assay was performed in vivo.
  • CONCLUSION: These data suggest that integrin α6β4 contributes to the development of aggressive forms of thyroid cancer with poor prognostic potential, such as ATC, and thus may be a novel therapeutic target for the treatment for this subtype of thyroid cancer.
  • [MeSH-major] Carcinoma / genetics. Cell Movement. Cell Proliferation. Integrin alpha6beta4 / genetics. RNA Interference. RNA, Small Interfering / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Animals. Apoptosis. Blotting, Western. Breast Neoplasms / genetics. Breast Neoplasms / pathology. Breast Neoplasms / prevention & control. Cell Adhesion. Cell Line, Tumor. Female. Flow Cytometry. Humans. Mice. Mice, Nude. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Survival Rate. Xenograft Model Antitumor Assays

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  • (PMID = 21115897.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Integrin alpha6beta4; 0 / RNA, Messenger; 0 / RNA, Small Interfering
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10. Shi Y, Zou M, Collison K, Baitei EY, Al-Makhalafi Z, Farid NR, Al-Mohanna FA: Ribonucleic acid interference targeting S100A4 (Mts1) suppresses tumor growth and metastasis of anaplastic thyroid carcinoma in a mouse model. J Clin Endocrinol Metab; 2006 Jun;91(6):2373-9
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  • [Title] Ribonucleic acid interference targeting S100A4 (Mts1) suppresses tumor growth and metastasis of anaplastic thyroid carcinoma in a mouse model.
  • Despite advances in the management of thyroid carcinoma and other solid tumors, metastasis continues to be the most significant cause in cancer mortality.
  • OBJECTIVE: Our objective was to examine the effects of S100A4 expression knockdown by RNA interference on the growth and metastasis of human anaplastic thyroid carcinoma cells (ARO) and the sensibility of ARO to paclitaxel after S100A4 knockdown.
  • DESIGN: A plasmid construct was made that expressed small hairpin RNA (shRNA) specific for S100A4.
  • The growth rate of ARO/S100A4-shRNA was reduced by 46 +/- 7.6% in a cell proliferation assay.
  • Cell cycle analysis showed increased G(2)/M accumulation in ARO/S100A4-shRNA.
  • [MeSH-major] RNA Interference. S100 Proteins / antagonists & inhibitors. Thyroid Neoplasms / therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Proliferation. Disease Models, Animal. Female. Mice. Mice, Inbred BALB C. Neoplasm Invasiveness. Neoplasm Metastasis. Paclitaxel / pharmacology

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  • (PMID = 16551737.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / S100 Proteins; 0 / S100a4 protein, mouse; P88XT4IS4D / Paclitaxel
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11. Takakura S, Mitsutake N, Nakashima M, Namba H, Saenko VA, Rogounovitch TI, Nakazawa Y, Hayashi T, Ohtsuru A, Yamashita S: Oncogenic role of miR-17-92 cluster in anaplastic thyroid cancer cells. Cancer Sci; 2008 Jun;99(6):1147-54
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  • [Title] Oncogenic role of miR-17-92 cluster in anaplastic thyroid cancer cells.
  • Micro RNAs (miRNAs) are non-coding small RNAs and constitute a novel class of negative gene regulators that are found in both plants and animals.
  • Several miRNAs play crucial roles in cancer cell growth.
  • To identify miRNAs specifically deregulated in anaplastic thyroid cancer (ATC) cells, we performed a comprehensive analysis of miRNA expressions in ARO cells and primary thyrocytes using miRNA microarrays.
  • On the other hand, miR-18a inhibitor only moderately attenuated the cell growth.
  • [MeSH-major] Carcinoma / genetics. Cell Transformation, Neoplastic. Gene Expression Regulation, Neoplastic / genetics. MicroRNAs / genetics. Oncogenes / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Apoptosis / physiology. Blotting, Northern. Blotting, Western. Caspases / metabolism. Cell Aging. Cell Line, Tumor. Cell Proliferation. Down-Regulation. Enzyme Activation. Gene Expression Profiling. Humans. Membrane Proteins / metabolism. Oligonucleotides, Antisense / pharmacology. PTEN Phosphohydrolase / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Retinoblastoma Protein / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18429962.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / MicroRNAs; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / Retinoblastoma Protein; EC 3.1.3.48 / TPTE protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.4.22.- / Caspases
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12. Ishihara T, Tsuda H, Hotta A, Kozaki K, Yoshida A, Noh JY, Ito K, Imoto I, Inazawa J: ITCH is a putative target for a novel 20q11.22 amplification detected in anaplastic thyroid carcinoma cells by array-based comparative genomic hybridization. Cancer Sci; 2008 Oct;99(10):1940-9
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  • [Title] ITCH is a putative target for a novel 20q11.22 amplification detected in anaplastic thyroid carcinoma cells by array-based comparative genomic hybridization.
  • Anaplastic thyroid carcinoma (ATC) is one of the most virulent of all human malignancies, with a mean survival time among patients of less than 1 year after diagnosis.
  • During the course of a program to screen a panel of ATC cell lines for genomic copy-number aberrations using array-based comparative genomic hybridization, we identified a high-level amplification of the ITCH gene, which is mapped to 20q11.22 and belongs to the homologous to the E6-associated protein carboxylterminus ubiquitin ligase family.
  • The expression of ITCH was increased in 4 of 14 ATC cell lines (28.6%), including 8305C in which there was a copy-number amplification of this gene, and six of seven primary cases (85.7%).
  • Among the primary thyroid tumors, a considerable number of ITCH high expressers was found in ATC (40/45, 88.9%), papillary thyroid carcinoma (25/25, 100%), and papillary microcarcinoma (25/25, 100%).
  • Furthermore, knockdown of ITCH by specific small interfering RNA significantly inhibited the growth of ITCH-overexpressing cells, whereas ectopic overexpression of ITCH promoted growth of ATC cell lines with relatively weak expression.
  • These observations indicate ITCH to be the most likely target for 20q11.22 amplification and to play a crucial role in the progression of thyroid carcinoma.
  • [MeSH-major] Chromosomes, Human, Pair 20. Gene Amplification. Repressor Proteins / genetics. Thyroid Neoplasms / genetics. Thyroid Neoplasms / pathology. Ubiquitin-Protein Ligases / genetics
  • [MeSH-minor] Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Cell Line, Tumor. Comparative Genomic Hybridization. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis

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  • (PMID = 19016753.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Repressor Proteins; EC 6.3.2.19 / ITCH protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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13. Zito G, Richiusa P, Bommarito A, Carissimi E, Russo L, Coppola A, Zerilli M, Rodolico V, Criscimanna A, Amato M, Pizzolanti G, Galluzzo A, Giordano C: In vitro identification and characterization of CD133(pos) cancer stem-like cells in anaplastic thyroid carcinoma cell lines. PLoS One; 2008;3(10):e3544
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  • [Title] In vitro identification and characterization of CD133(pos) cancer stem-like cells in anaplastic thyroid carcinoma cell lines.
  • BACKGROUND: Recent publications suggest that neoplastic initiation and growth are dependent on a small subset of cells, termed cancer stem cells (CSCs).
  • Anaplastic Thyroid Carcinoma (ATC) is a very aggressive solid tumor with poor prognosis, characterized by high dedifferentiation.
  • CD133 has been identified as a stem cell marker for normal and cancerous tissues, although its biological function remains unknown.
  • METHODOLOGY/PRINCIPAL FINDINGS: ATC cell lines ARO, KAT-4, KAT-18 and FRO were analyzed for CD133 expression.
  • Furthermore, ARO/CD133(pos) showed levels of thyroid transcription factor TTF-1 similar to the fetal thyroid cell line TAD-2, while the expression in ARO/CD133(neg) was negligible.
  • The expression of the stem cell marker OCT-4 detected by RT-PCR and flow cytometry was markedly higher in ARO/CD133(pos) in comparison to ARO/CD133(neg) cells.
  • The stem cell markers c-KIT and THY-1 were negative.
  • CONCLUSIONS/SIGNIFICANCE: We describe CD133(pos) cells in ATC cell lines.
  • ARO/CD133(pos) cells exhibit stem cell-like features--such as high proliferation, self-renewal ability, expression of OCT-4--and are characterized by higher resistance to chemotherapy.
  • The simultaneous positivity for thyroid specific factor TTF-1 and onfFN suggest they might represent putative thyroid cancer stem-like cells.
  • [MeSH-major] Antigens, CD / metabolism. Carcinoma / pathology. Glycoproteins / metabolism. Neoplastic Stem Cells / pathology. Peptides / metabolism. Thyroid Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Biomarkers, Tumor / analysis. Biomarkers, Tumor / isolation & purification. Biomarkers, Tumor / metabolism. Cell Culture Techniques. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Separation. Fibronectins / metabolism. Fibronectins / physiology. Humans. Nuclear Proteins / metabolism. Nuclear Proteins / physiology. Transcription Factors / metabolism. Transcription Factors / physiology. Tumor Stem Cell Assay

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  • (PMID = 18958156.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Fibronectins; 0 / Glycoproteins; 0 / Nuclear Proteins; 0 / Peptides; 0 / Transcription Factors; 0 / oncofetal fibronectin; 0 / thyroid nuclear factor 1
  • [Other-IDs] NLM/ PMC2568821
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14. Yu W, Imoto I, Inoue J, Onda M, Emi M, Inazawa J: A novel amplification target, DUSP26, promotes anaplastic thyroid cancer cell growth by inhibiting p38 MAPK activity. Oncogene; 2007 Feb 22;26(8):1178-87
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  • [Title] A novel amplification target, DUSP26, promotes anaplastic thyroid cancer cell growth by inhibiting p38 MAPK activity.
  • Anaplastic thyroid cancer (ATC) is one of the most lethal of all human tumors, but cytogenetic information concerning ATC is extremely limited.
  • Using our in-house array-based comparative genomic hybridization and 14 ATC cell lines with further fluorescence in situ hybridization analysis, we demonstrated amplification of the DUSP26 gene, known by another report as MAP kinase phosphatase-8.
  • DUSP26 was overexpressed in ATC cell lines and primary ATC tumor samples.
  • [MeSH-major] Carcinoma / pathology. Gene Amplification. Protein Tyrosine Phosphatases / genetics. Thyroid Neoplasms / pathology. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • [MeSH-minor] Apoptosis / genetics. Caspase 3 / genetics. Cell Line, Tumor. Cell Proliferation. Cloning, Molecular. Dual-Specificity Phosphatases. Humans. In Situ Hybridization, Fluorescence. Mitogen-Activated Protein Kinase Phosphatases. RNA, Small Interfering / pharmacology

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  • (PMID = 16924234.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Small Interfering; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.1.3.- / Mitogen-Activated Protein Kinase Phosphatases; EC 3.1.3.48 / DUSP26 protein, human; EC 3.1.3.48 / Dual-Specificity Phosphatases; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.4.22.- / Caspase 3
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15. Aiello A, Pandini G, Frasca F, Conte E, Murabito A, Sacco A, Genua M, Vigneri R, Belfiore A: Peroxisomal proliferator-activated receptor-gamma agonists induce partial reversion of epithelial-mesenchymal transition in anaplastic thyroid cancer cells. Endocrinology; 2006 Sep;147(9):4463-75
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  • [Title] Peroxisomal proliferator-activated receptor-gamma agonists induce partial reversion of epithelial-mesenchymal transition in anaplastic thyroid cancer cells.
  • Anaplastic thyroid cancer (ATC) is an extremely aggressive tumor characterized by marked epithelial mesenchymal transition, which leads, almost invariably, to death.
  • To establish whether ATC could be a target of PPAR gamma agonists, we first examined PPAR gamma protein expression in a panel of six ATC cell lines and then studied the biologic effects of two PPAR gamma agonists, ciglitazone and rosiglitazone, that belong to the class of thiazolidonediones.
  • PPAR gamma protein was present and functional in all ATC cell lines.
  • Rosiglitazone-induced growth inhibition was associated with cell cycle arrest and changes in cell cycle regulators, such as an increase of cyclin-dependent kinases inhibitors p21(cip1) and p27(kip1), a decrease of cyclin D1, and inactivation of Rb protein.
  • Finally, rosiglitazone increased the expression of thyroid-specific differentiation markers.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma / pathology. Epithelial Cells / pathology. Mesoderm / pathology. PPAR gamma / agonists. Thyroid Neoplasms / pathology
  • [MeSH-minor] Apoptosis / drug effects. Caspase 3. Caspase 7. Caspases / metabolism. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cyclin D1 / analysis. Cyclin-Dependent Kinase Inhibitor p21 / analysis. Cyclin-Dependent Kinase Inhibitor p27. Gene Expression / drug effects. Humans. Insulin-Like Growth Factor I / antagonists & inhibitors. Intracellular Signaling Peptides and Proteins / analysis. Luciferases / genetics. PTEN Phosphohydrolase / genetics. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / pharmacology. Retinoblastoma Protein / analysis. Thiazolidinediones / pharmacology. Transfection. bcl-X Protein / analysis


16. Afrasiabi E, Ahlgren J, Bergelin N, Törnquist K: Phorbol 12-myristate 13-acetate inhibits FRO anaplastic human thyroid cancer cell proliferation by inducing cell cycle arrest in G1/S phase: evidence for an effect mediated by PKCdelta. Mol Cell Endocrinol; 2008 Sep 24;292(1-2):26-35
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  • [Title] Phorbol 12-myristate 13-acetate inhibits FRO anaplastic human thyroid cancer cell proliferation by inducing cell cycle arrest in G1/S phase: evidence for an effect mediated by PKCdelta.
  • Phorbol 12-myristate 13-acetate (PMA) is known to affect a variety of cellular processes, including cell proliferation, differentiation, and migration.
  • Our findings show that PMA induced a strong antiproliferative effect in two anaplastic (FRO and ARO) and one follicular (ML-1) thyroid cancer cell lines, and increased the fraction of FRO cells in G1 phase of the cell cycle.
  • Moreover, PMA evoked a significant increase in the levels of the cell cycle regulators p21Waf1/Cip1 and p27Kip1.
  • PMA stimulated the translocation of protein kinase C (PKC) alpha, betaI and delta isoforms to the cell membrane.
  • PKCdelta small interfering RNA attenuated the PMA-induced antiproliferative effect and prevented the upregulation of p21Waf1/Cip1 and p27Kip1.
  • In addition, PMA inhibited FRO, ARO and ML-1 cell migration toward serum.
  • The results indicate that PMA is an effective inhibitor of thyroid cancer cell proliferation and migration by a mechanism involving PKC-MAP kinase/Akt and FOXO signaling.
  • [MeSH-major] Carcinoma / pathology. G1 Phase / drug effects. Protein Kinase C-delta / metabolism. S Phase / drug effects. Tetradecanoylphorbol Acetate / pharmacology. Thyroid Neoplasms / enzymology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Forkhead Transcription Factors / metabolism. Humans. Isoenzymes / metabolism. Mitogen-Activated Protein Kinases / metabolism. Phorbols / pharmacology. Phosphorylation / drug effects. Protein Transport / drug effects. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / metabolism. Transfection

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  • (PMID = 18541361.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / FOXO1 protein, human; 0 / Forkhead Transcription Factors; 0 / Isoenzymes; 0 / Phorbols; 0 / RNA, Small Interfering; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.13 / Protein Kinase C-delta; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; NI40JAQ945 / Tetradecanoylphorbol Acetate; XUZ76S9127 / phorbol
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17. Mitsiades CS, Negri J, McMullan C, McMillin DW, Sozopoulos E, Fanourakis G, Voutsinas G, Tseleni-Balafouta S, Poulaki V, Batt D, Mitsiades N: Targeting BRAFV600E in thyroid carcinoma: therapeutic implications. Mol Cancer Ther; 2007 Mar;6(3):1070-8
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  • [Title] Targeting BRAFV600E in thyroid carcinoma: therapeutic implications.
  • B-Raf is an important mediator of cell proliferation and survival signals transduced via the Ras-Raf-MEK-ERK cascade.
  • BRAF mutations have been detected in several tumors, including papillary thyroid carcinoma, but the precise role of B-Raf as a therapeutic target for thyroid carcinoma is still under investigation.
  • We analyzed a panel of 93 specimens and 14 thyroid carcinoma cell lines for the presence of BRAF mutations and activation of the mitogen-activated protein/ERK kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway.
  • We also compared the effect of a B-Raf small inhibitory RNA construct and the B-Raf kinase inhibitor AAL881 on both B-Raf wild-type and mutant thyroid carcinoma cell lines.
  • We found a high prevalence of the T1799A (V600E) mutation in papillary and anaplastic carcinoma specimens and cell lines.
  • Immunodetection of phosphorylated and total forms of MEK and ERK revealed no difference in their phosphorylation between wild-type and BRAF(V600E) patient specimens or cell lines.
  • Furthermore, a small inhibitory RNA construct targeting the expression of both wild-type B-Raf and B-Raf(V600E) induced a comparable reduction of viability in both wild-type and BRAF(V600E) mutant cancer cells.
  • We conclude that B-Raf is important for the pathophysiology of thyroid carcinomas irrespective of mutational status.
  • Small molecule inhibitors that selectively target B-Raf(V600E) may provide clinical benefit for patients with thyroid cancer.
  • [MeSH-major] Adenocarcinoma, Follicular / genetics. Carcinoma, Papillary / genetics. Isoquinolines / pharmacology. Mutation / genetics. Proto-Oncogene Proteins B-raf / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Apoptosis / drug effects. Carcinoma / genetics. Carcinoma / pathology. Carcinoma / prevention & control. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / prevention & control. Cell Proliferation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Female. Humans. Male. Middle Aged. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Tumor Cells, Cultured / drug effects

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  • (PMID = 17363500.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AAL 881; 0 / Isoquinolines; 0 / RNA, Messenger; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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18. Nehs MA, Nagarkatti S, Nucera C, Hodin RA, Parangi S: Thyroidectomy with neoadjuvant PLX4720 extends survival and decreases tumor burden in an orthotopic mouse model of anaplastic thyroid cancer. Surgery; 2010 Dec;148(6):1154-62; discussion 1162
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  • [Title] Thyroidectomy with neoadjuvant PLX4720 extends survival and decreases tumor burden in an orthotopic mouse model of anaplastic thyroid cancer.
  • BACKGROUND: B-Raf(V600E) is a frequent mutation in anaplastic thyroid cancers and is a novel therapeutic target.
  • METHODS: Orthotopic anaplastic thyroid tumors were induced in severe combined immunodeficient mice.
  • All 6 mice receiving PLX4720 + sham had small tumors (average 1.3 mm(3)) and maintained their weight.
  • Three out of 6 mice receiving PLX4720+thyroidectomy had no evidence of tumor at 35 days; the other 3 mice had small tumors (average 1.4 mm(3)) and showed no signs of metastatic disease.
  • CONCLUSION: Thyroidectomy with neoadjuvant PLX4720 could be an effective therapeutic strategy for early anaplastic thyroid cancers that harbor the B-Raf(V600E) mutation and are refractory to conventional therapeutic modalities.

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  • [Copyright] Copyright © 2010 Mosby, Inc. All rights reserved.
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  • (PMID = 21134546.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA149738; United States / NIDDK NIH HHS / DK / T32 DK007754; United States / NIDDK NIH HHS / DK / 5T32 DK007754-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indoles; 0 / PLX 4720; 0 / Sulfonamides; EC 2.7.11.1 / Braf protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
  • [Other-IDs] NLM/ NIHMS251897; NLM/ PMC3413092
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19. Mineva I, Gartner W, Hauser P, Kainz A, Löffler M, Wolf G, Oberbauer R, Weissel M, Wagner L: Differential expression of alphaB-crystallin and Hsp27-1 in anaplastic thyroid carcinomas because of tumor-specific alphaB-crystallin gene (CRYAB) silencing. Cell Stress Chaperones; 2005;10(3):171-84
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  • [Title] Differential expression of alphaB-crystallin and Hsp27-1 in anaplastic thyroid carcinomas because of tumor-specific alphaB-crystallin gene (CRYAB) silencing.
  • Expression of the small heat shock protein alphaB-crystallin in differentiated thyroid tumors has been described recently.
  • In this study, we investigated the molecular mechanisms that affect the expression of alphaB-crystallin in benign goiters (n = 7) and highly malignant anaplastic thyroid carcinomas (ATCs) (n = 3).
  • Immunoblot and quantitative real-time (RT) polymerase chain reaction revealed marked downregulation of alphaB-crystallin in all the tested ATCs and the ATC-derived cell line C-643 .
  • In contrast, considerable expression of Hsp27-1 in benign and malignant thyroid tissue was demonstrated.
  • [MeSH-major] Carcinoma / genetics. Gene Expression Regulation, Neoplastic. Intermediate Filament Proteins / genetics. Nerve Tissue Proteins / genetics. Protein Kinases / genetics. Repressor Proteins / genetics. Thyroid Neoplasms / genetics. Transcription Factors / genetics
  • [MeSH-minor] Animals. COS Cells. Cell Line, Tumor. Cloning, Molecular. DNA, Complementary / biosynthesis. Down-Regulation. Gene Silencing. Genes, Reporter. Goiter. HSP27 Heat-Shock Proteins. Heat-Shock Proteins / analysis. Heat-Shock Proteins / metabolism. Humans. Luciferases / genetics. Neoplasm Proteins / analysis. Neoplasm Proteins / metabolism. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. RNA, Messenger / metabolism. Tissue Extracts / chemistry. Tissue Extracts / genetics. Tissue Extracts / metabolism. Transfection. alpha-Crystallin B Chain

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  • (PMID = 16184762.001).
  • [ISSN] 1355-8145
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRYAB protein, human; 0 / DNA, Complementary; 0 / HSP27 Heat-Shock Proteins; 0 / HSPB1 protein, human; 0 / Heat-Shock Proteins; 0 / Intermediate Filament Proteins; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / TFCP2L1 protein, human; 0 / Tissue Extracts; 0 / Transcription Factors; 0 / alpha-Crystallin B Chain; EC 1.13.12.- / Luciferases; EC 2.7.- / Protein Kinases
  • [Other-IDs] NLM/ PMC1226015
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20. Mooney CJ, Nagaiah G, Fu P, Wasman JK, Cooney MM, Savvides PS, Bokar JA, Dowlati A, Wang D, Agarwala SS, Flick SM, Hartman PH, Ortiz JD, Lavertu PN, Remick SC: A phase II trial of fosbretabulin in advanced anaplastic thyroid carcinoma and correlation of baseline serum-soluble intracellular adhesion molecule-1 with outcome. Thyroid; 2009 Mar;19(3):233-40
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  • [Title] A phase II trial of fosbretabulin in advanced anaplastic thyroid carcinoma and correlation of baseline serum-soluble intracellular adhesion molecule-1 with outcome.
  • BACKGROUND: Fosbretabulin is a novel vascular-disrupting agent that has antitumor activity against anaplastic thyroid cancer (ATC) cell lines, xenografts, and demonstrable efficacy in a phase I trial.
  • Despite a small sample size, low baseline sICAM levels were predictive of event-free survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bibenzyls / therapeutic use. Carcinoma / drug therapy. Neural Cell Adhesion Molecules / metabolism. Organophosphorus Compounds / therapeutic use. Thyroid Neoplasms / drug therapy

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  • (PMID = 19265494.001).
  • [ISSN] 1557-9077
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00060242
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR024989; United States / NCRR NIH HHS / RR / M01 RR-00080; United States / NCI NIH HHS / CA / P30 CA43703
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Bibenzyls; 0 / NCAM1 protein, human; 0 / Neural Cell Adhesion Molecules; 0 / Organophosphorus Compounds; 0 / Stilbenes; BG3F62OND5 / Carboplatin; I5590ES2QZ / fosbretabulin; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC2913806
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21. Pan J, Huang H, Sun L, Fang B, Yeung SC: Bcl-2-associated X protein is the main mediator of manumycin a-induced apoptosis in anaplastic thyroid cancer cells. J Clin Endocrinol Metab; 2005 Jun;90(6):3583-91
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  • [Title] Bcl-2-associated X protein is the main mediator of manumycin a-induced apoptosis in anaplastic thyroid cancer cells.
  • We previously demonstrated that the combination of paclitaxel and manumycin A, a farnesyltransferase inhibitor, enhanced apoptosis of anaplastic thyroid cancer (ATC) cells.
  • Silencing Bax with a specific small interfering RNA blocked manumycin-induced mitochondrial condensation and cytochrome c release, arguing the dependence of manumycin-induced apoptosis on Bax.
  • [MeSH-major] Apoptosis / drug effects. Polyenes / toxicity. Proto-Oncogene Proteins c-bcl-2 / physiology. Thyroid Neoplasms / pathology. Thyroid Neoplasms / physiopathology
  • [MeSH-minor] Animals. Carcinoma. Cell Line, Tumor. Enzyme Inhibitors / toxicity. Humans. Mice. Mice, Nude. Mitochondria / drug effects. Mitochondria / pathology. Mitochondria / ultrastructure. Paclitaxel / toxicity. Polyunsaturated Alkamides. Transplantation, Heterologous. bcl-X Protein

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  • (PMID = 15769983.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 16672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / Enzyme Inhibitors; 0 / Polyenes; 0 / Polyunsaturated Alkamides; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; 52665-74-4 / manumycin; P88XT4IS4D / Paclitaxel
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22. Zeng Q, Chen GG, Vlantis AC, van Hasselt CA: Oestrogen mediates the growth of human thyroid carcinoma cells via an oestrogen receptor-ERK pathway. Cell Prolif; 2007 Dec;40(6):921-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oestrogen mediates the growth of human thyroid carcinoma cells via an oestrogen receptor-ERK pathway.
  • OBJECTIVES: Although thyroid cancer occurs much more frequently in females, the role of sex hormones in thyroid carcinogenesis is unknown.
  • In this study, it has been investigated how 17beta-oestradiol (E2) influenced proliferation and growth of thyroid cancer cells.
  • MATERIALS AND METHODS: Cell proliferation and its related molecules were examined in thyroid papillary carcinoma cells (KAT5), follicular thyroid carcinoma cells (FRO) and anaplastic carcinoma cells (ARO).
  • RESULTS: E2 promoted cell proliferation.
  • Such an effect was positively related to ERalpha but negatively to ERbeta; PPT enhanced cell proliferation while DPN inhibited it.
  • PPT elevated the level of phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2), suggesting a positive role of ERK1/2 in E2-induced cell proliferation.
  • CONCLUSIONS: Oestrogen stimulates proliferation of thyroid cancer cells, associated with increase in Bcl-2 and decrease in Bax levels in an ERK1/2-related pathway.
  • Imbalance between ERalpha and ERbeta may contribute to thyroid carcinogenesis.
  • [MeSH-major] Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Estrogens / pharmacology. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Thyroid Neoplasms / enzymology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Estradiol / pharmacology. Humans. Nitriles / pharmacology. Phenols. Phosphorylation / drug effects. Propionates / pharmacology. Pyrazoles / pharmacology. RNA Interference. RNA, Small Interfering. bcl-2-Associated X Protein / metabolism

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  • (PMID = 18021179.001).
  • [ISSN] 1365-2184
  • [Journal-full-title] Cell proliferation
  • [ISO-abbreviation] Cell Prolif.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1,3,5-tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Estrogens; 0 / Nitriles; 0 / Phenols; 0 / Propionates; 0 / Pyrazoles; 0 / RNA, Small Interfering; 0 / bcl-2-Associated X Protein; 0 / diarylpropionitrile; 4TI98Z838E / Estradiol; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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23. Salvatore G, De Falco V, Salerno P, Nappi TC, Pepe S, Troncone G, Carlomagno F, Melillo RM, Wilhelm SM, Santoro M: BRAF is a therapeutic target in aggressive thyroid carcinoma. Clin Cancer Res; 2006 Mar 1;12(5):1623-9
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  • [Title] BRAF is a therapeutic target in aggressive thyroid carcinoma.
  • PURPOSE: Oncogenic conversion of BRAF occurs in approximately 44% of papillary thyroid carcinomas and 24% of anaplastic thyroid carcinomas.
  • In papillary thyroid carcinomas, this mutation is associated with an unfavorable clinicopathologic outcome.
  • Our aim was to exploit BRAF as a potential therapeutic target for thyroid carcinoma.
  • EXPERIMENTAL DESIGN: We used RNA interference to evaluate the effect of BRAF knockdown in the human anaplastic thyroid carcinoma cell lines FRO and ARO carrying the BRAF V600E (V600EBRAF) mutation.
  • We also exploited the effect of BAY 43-9006 [N-(3-trifluoromethyl-4-chlorophenyl)-N'-(4-(2-methylcarbamoyl pyridin-4-yl)oxyphenyl)urea], a multikinase inhibitor able to inhibit RAF family kinases in a panel of six (V600E)BRAF-positive thyroid carcinoma cell lines and in nude mice bearing ARO cell xenografts.
  • RESULTS: Knockdown of BRAF by small inhibitory duplex RNA, but not control small inhibitory duplex RNA, inhibited the mitogen-activated protein kinase signaling cascade and the growth of ARO and FRO cells (P < 0.0001).
  • These effects were mimicked by thyroid carcinoma cell treatment with BAY 43-9006 (IC50 = 0.5-1 micromol/L; P < 0.0001), whereas the compound had negligible effects in normal thyrocytes.
  • ARO cell tumor xenografts were significantly (P < 0.0001) smaller in nude mice treated with BAY 43-9006 than in control mice.
  • CONCLUSIONS: BRAF provides signals crucial for proliferation of thyroid carcinoma cells spontaneously harboring the (V600E)BRAF mutation and, therefore, BRAF suppression might have therapeutic potential in (V600E)BRAF-positive thyroid cancer.
  • [MeSH-major] Benzenesulfonates / therapeutic use. Carcinoma / therapy. Mutation / genetics. Proto-Oncogene Proteins B-raf / metabolism. Pyridines / therapeutic use. Thyroid Neoplasms / therapy
  • [MeSH-minor] Animals. Carcinoma, Papillary / genetics. Carcinoma, Papillary / metabolism. Carcinoma, Papillary / therapy. Cell Proliferation / drug effects. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinases / metabolism. Niacinamide / analogs & derivatives. Phenylurea Compounds. RNA, Small Interfering / pharmacology. Signal Transduction / drug effects. Thyroid Gland / drug effects. Transplantation, Heterologous

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  • (PMID = 16533790.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 0 / RNA, Small Interfering; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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24. Sala E, Mologni L, Truffa S, Gaetano C, Bollag GE, Gambacorti-Passerini C: BRAF silencing by short hairpin RNA or chemical blockade by PLX4032 leads to different responses in melanoma and thyroid carcinoma cells. Mol Cancer Res; 2008 May;6(5):751-9
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  • [Title] BRAF silencing by short hairpin RNA or chemical blockade by PLX4032 leads to different responses in melanoma and thyroid carcinoma cells.
  • BRAF-activating mutations have been reported in several types of cancer, including melanoma ( approximately 70% of cases), thyroid (30-70%), ovarian (15-30%), and colorectal cancer (5-20%).
  • BRAF silencing induces regression of melanoma xenografts, indicating the essential role of BRAF for cell survival.
  • We set up an inducible short hairpin RNA system to compare the role of oncogenic BRAF in thyroid carcinoma versus melanoma cells.
  • Although BRAF knockdown led to apoptosis in the melanoma cell line A375, the anaplastic thyroid carcinoma cell ARO underwent growth arrest upon silencing, with little or no cell death.
  • Reexpression of the thyroid differentiation marker, sodium iodide symporter, was induced after long-term silencing.
  • The different outcome of BRAF down-regulation in the two cell lines was associated with an opposite regulation of p21(CIP1/WAF1) expression levels in response to the block of the BRAF mitogenic signal.
  • These results were confirmed using a specific BRAF small-molecule inhibitor, PLX4032.
  • Altogether, our data indicate that oncogenic BRAF inhibition can have a different effect on cell fate depending on the cellular type.
  • Furthermore, we suggest that a BRAF-independent mechanism of cell survival exists in anaplastic thyroid cancer cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma / drug therapy. Carcinoma / metabolism. Gene Expression Regulation, Neoplastic. Gene Silencing. Melanoma / drug therapy. Melanoma / metabolism. Proto-Oncogene Proteins B-raf / genetics. Proto-Oncogene Proteins B-raf / metabolism. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / metabolism
  • [MeSH-minor] Caspase 3 / metabolism. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Humans. Inhibitory Concentration 50. Models, Biological. RNA / chemistry. Symporters / metabolism

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  • (PMID = 18458053.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Symporters; 0 / sodium-iodide symporter; 63231-63-0 / RNA; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.4.22.- / Caspase 3
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25. Zou M, Al-Baradie RS, Al-Hindi H, Farid NR, Shi Y: S100A4 (Mts1) gene overexpression is associated with invasion and metastasis of papillary thyroid carcinoma. Br J Cancer; 2005 Nov 28;93(11):1277-84
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  • [Title] S100A4 (Mts1) gene overexpression is associated with invasion and metastasis of papillary thyroid carcinoma.
  • Tumour cell invasion and metastasis are the hallmark of malignant neoplasm.
  • S100A4 is a member of small calcium-binding protein family and is involved in the cell proliferation and cancer progression.
  • We previously identified S100A4 as a candidate gene involved in anaplastic thyroid cancer metastasis by microarray analysis.
  • To further determine whether S100A4 overexpression is associated with thyroid tumour invasion and metastasis, in the present study, we examined S100A4 gene expression in six benign multinodular goitres (MNG) and 28 matched samples of adjacent normal thyroid tissue (N), primary (T) and metastatic (M) papillary thyroid carcinomas (PTC) by immunohistochemistry and real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis.
  • No S100A4 staining was observed in normal thyroid tissues and simple MNG.
  • These data suggest that overexpression of S100A4 is associated with thyroid tumour invasion and metastasis and it may be a potential target for therapeutic intervention.
  • [MeSH-major] Carcinoma, Papillary / genetics. Carcinoma, Papillary / pathology. Gene Expression Regulation, Neoplastic. S100 Proteins / biosynthesis

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  • (PMID = 16265347.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / S100 Proteins; 142662-27-9 / S100A4 protein, human
  • [Other-IDs] NLM/ PMC2361511
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26. Nix PA, Nicolaides A, Coatesworth AP: Thyroid cancer review 3: management of medullary and undifferentiated thyroid cancer. Int J Clin Pract; 2006 Jan;60(1):80-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thyroid cancer review 3: management of medullary and undifferentiated thyroid cancer.
  • This is the last of the three review articles dealing with thyroid cancer.
  • Over 90% of thyroid cancer is of the differentiated type associated with a very good 10-year disease-free survival rate.
  • In contrast, the rare forms of thyroid cancer which comprise medullary thyroid cancer arising from parafollicluar C cells, Hurthle cell carcinoma, anaplastic carcinoma, thyroid lymphoma and squamous cell carcinoma are typically associated with a poorer survival rate.
  • Management is based upon small retrospective cohort studies.
  • [MeSH-major] Carcinoma / therapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Carcinoma, Squamous Cell / diagnosis. Humans. Lymphoma / diagnosis. Neoplasm Staging / methods

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  • (PMID = 16409432.001).
  • [ISSN] 1368-5031
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 37
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27. Hemminki K, Eng C, Chen B: Familial risks for nonmedullary thyroid cancer. J Clin Endocrinol Metab; 2005 Oct;90(10):5747-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Familial risks for nonmedullary thyroid cancer.
  • OBJECTIVE: We wanted to define familial risks for histopathology-specific nonmedullary thyroid cancers through parental and sibling probands.
  • PATIENTS: Cancer data were retrieved from the Swedish Cancer Registry from years 1958 to 2002, including 3292 patients with thyroid adenocarcinoma.
  • The Systematized Nomenclature of Medicine histology was available from 1993 onward, with 1449 papillary, 288 follicular, 148 anaplastic, and 68 Hurthle cell tumors.
  • RESULTS: The familial risk for papillary carcinoma was 3.21 and 6.24 when a parent and a sibling, respectively, were diagnosed with thyroid cancers.
  • Thyroid adenocarcinoma was shown to be associated with melanoma and connective tissue tumors, and probably also with neurinomas (schwannomas).
  • Associations found in single comparisons with papillary thyroid cancer and other sites included right-sided colon, breast, ovarian, and kidney cancers.
  • Hurthle cell tumors were associated with Hodgkin's and non-Hodgkin's lymphoma, but the numbers of cases were small.
  • CONCLUSIONS: The present findings were based on a limited number of cases, but they display a complex and heterogeneous pattern of familial nonmedullary thyroid cancer.
  • The high risk for papillary carcinoma among women requires clinical attention, although the absolute risks for this rare cancer are still low.
  • [MeSH-major] Adenocarcinoma / epidemiology. Adenocarcinoma / genetics. Thyroid Neoplasms / epidemiology. Thyroid Neoplasms / genetics

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  • (PMID = 16030170.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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28. Menon MP, Khan A: Micro-RNAs in thyroid neoplasms: molecular, diagnostic and therapeutic implications. J Clin Pathol; 2009 Nov;62(11):978-85
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  • [Title] Micro-RNAs in thyroid neoplasms: molecular, diagnostic and therapeutic implications.
  • Micro-RNAs (miRNAs) belong to a class of small non-coding messenger RNA species that have emerged as potent regulators of a variety of biological processes including oncogenesis.
  • Thyroid carcinomas encompass a wide spectrum ranging from well-differentiated thyroid carcinomas to poorly differentiated and anaplastic carcinoma.
  • Currently, a considerable degree of interobserver variability exists in the morphological diagnosis of certain types of thyroid carcinomas especially the follicular pattern neoplasm.
  • The prediction of progression of these differentiated carcinoma to more aggressive forms like poorly differentiated and anaplastic types is of considerable interest to physicians and pathologists for determining prognosis and making therapeutic decisions.
  • Several investigators have proposed a more cohesive approach to thyroid cancer diagnosis incorporating molecular and proteomics based tools in addition to the conventional morphological diagnosis.
  • In this context, miRNAs serve as an important diagnostic tool, and several studies have demonstrated their utility as class identifiers especially in the context of follicular thyroid carcinoma, papillary thyroid carcinoma and anaplastic thyroid carcinoma.
  • [MeSH-major] MicroRNAs / genetics. RNA, Neoplasm / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma, Follicular / diagnosis. Adenocarcinoma, Follicular / genetics. Adenocarcinoma, Papillary / diagnosis. Adenocarcinoma, Papillary / genetics. Adenoma / diagnosis. Adenoma / genetics. Carcinoma / diagnosis. Carcinoma / genetics. Cell Differentiation / genetics. Diagnosis, Differential. Disease Progression. Gene Expression Regulation, Neoplastic / genetics. Humans. Prognosis

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  • (PMID = 19625289.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Neoplasm
  • [Number-of-references] 93
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29. 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.
  • EGFR protein expression on the cell lines and inactivation of EGFR kinase by Gefitinib was analyzed by Western blot.
  • 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.
  • Addition of Gefitinib in combination with ionizing radiation reduced cell proliferation in ARO (P = .0084) and WRO (P = .0252) as measured by colony formation assay.
  • 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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30. Milano A, Chiofalo MG, Basile M, Salzano de Luna A, Pezzullo L, Caponigro F: New molecular targeted therapies in thyroid cancer. Anticancer Drugs; 2006 Sep;17(8):869-79
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  • [Title] New molecular targeted therapies in thyroid cancer.
  • Carcinoma of the thyroid gland is the most common malignancy of the endocrine system.
  • A small percentage of such patients, however, do not undergo remission and need new therapeutic approaches.
  • Both anaplastic and medullary thyroid carcinomas exhibit aggressive behavior and are usually resistant to current therapeutic modalities.
  • Thyroid carcinoma represents a fascinating model and a particularly promising paradigm for targeted therapy because some of the key oncogenic events are activating mutations of genes coding for tyrosine kinases, and these occur early in cancer development.
  • Mutations in the RET proto-oncogene have been identified as causative for papillary carcinoma and familial medullary thyroid carcinoma, making it an attractive target for selective inhibition in these subtypes.
  • ZD 6474 has shown promising activity in preclinical models against RET kinase, and its contemporary inhibition of vascular endothelial growth factor and epidermal growth factor pathways renders it a very attractive drug for clinical trials in thyroid cancer.
  • Activating point mutation of B-RAF can occur early in the development of papillary carcinoma.
  • Clinical evaluation of B-RAF-targeting drugs is undergoing and trials in thyroid cancer are planned.
  • Agents that restore radioiodine uptake, such as histone deacetylase inhibitors and retinoids, represent another exciting field in new drug development in thyroid cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma / drug therapy. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Cell Membrane / drug effects. Cell Membrane / metabolism. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cytoplasm / drug effects. Cytoplasm / metabolism. Humans. Models, Biological. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-ret / genetics. Proto-Oncogene Proteins c-ret / metabolism. Receptor Protein-Tyrosine Kinases / metabolism


31. Zhang HY, Wang HQ, Liu HM, Guan Y, Du ZX: Regulation of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by DJ-1 in thyroid cancer cells. Endocr Relat Cancer; 2008 Jun;15(2):535-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by DJ-1 in thyroid cancer cells.
  • The expression of DJ-1 and its influence on thyroid cancer cell death has not been investigated so far.
  • We analyzed DJ-1 expression in human thyroid carcinoma cell lines and the effect of DJ-1 on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis.
  • DJ-1 was expressed in human thyroid carcinoma cell lines; small interfering RNA-mediated downregulation of its levels significantly sensitized thyroid carcinoma cells to TRAIL-induced apoptosis, whereas the forced exogenous expression of DJ-1 significantly suppressed cell death induced by TRAIL.
  • We also report here that TRAIL-induced thyroid cancer cell apoptosis is mediated by oxidative stress and that DJ-1, a potent nutritional antioxidant, protects cancer cells from apoptosis at least in part by impeding the elevation of reactive oxygen species levels induced by TRAIL and impairing caspase-8 activation.
  • Subsequently, we investigated DJ-1 expression in 52 normal and 74 primary thyroid carcinomas from patients of China Medical University.
  • The protein was not detectable in the 52 specimens of normal thyroid, while 70 out of 74 analyzed carcinomas (33 out of 33 follicular, 17 out of 19 papillary, 12 out of 13 medullar, and 8 out of 9 anaplastic) were clearly positive for DJ-1 expression.
  • Our data demonstrated that DJ-1 is specifically expressed in thyroid carcinomas and not in the normal thyroid tissue.
  • In addition, the protein modulates the response to TRAIL-mediated apoptosis in human neoplastic thyroid cells, at least partially through its antioxidant property.
  • [MeSH-major] Apoptosis / physiology. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / metabolism. Oncogene Proteins / genetics. Oncogene Proteins / metabolism. TNF-Related Apoptosis-Inducing Ligand / metabolism. Thyroid Neoplasms / metabolism. Thyroid Neoplasms / pathology
  • [MeSH-minor] Antioxidants / metabolism. Caspase 8 / metabolism. Cell Line, Tumor. Down-Regulation / physiology. Gene Expression Regulation, Neoplastic. Humans. RNA, Small Interfering. Reactive Oxygen Species / metabolism. Up-Regulation / physiology

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  • (PMID = 18430896.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Intracellular Signaling Peptides and Proteins; 0 / Oncogene Proteins; 0 / PARK7 protein, human; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8
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32. Chiappetta G, Ammirante M, Basile A, Rosati A, Festa M, Monaco M, Vuttariello E, Pasquinelli R, Arra C, Zerilli M, Todaro M, Stassi G, Pezzullo L, Gentilella A, Tosco A, Pascale M, Marzullo L, Belisario MA, Turco MC, Leone A: The antiapoptotic protein BAG3 is expressed in thyroid carcinomas and modulates apoptosis mediated by tumor necrosis factor-related apoptosis-inducing ligand. J Clin Endocrinol Metab; 2007 Mar;92(3):1159-63
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  • [Title] The antiapoptotic protein BAG3 is expressed in thyroid carcinomas and modulates apoptosis mediated by tumor necrosis factor-related apoptosis-inducing ligand.
  • OBJECTIVE: The objective of this study was to analyze BAG3 expression in thyroid neoplastic cells and investigate its influence in cell apoptotic response to TNF-related apoptosis-inducing ligand (TRAIL).
  • DESIGN, SETTING, AND PATIENTS: We investigated BAG3 expression in human thyroid carcinoma cell lines, including NPA, and the effect of BAG3-specific small interfering RNA on TRAIL-induced apoptosis in NPA cells.
  • MAIN OUTCOME MEASURES: The main outcome measures were: analysis of BAG3 protein in NPA cells by Western blot and immunocytochemistry; analysis of apoptosis in TRAIL-stimulated NPA cells by flow cytometry; and evaluation of BAG3 expression in specimens from thyroid lesions by immunohistochemistry.
  • RESULTS: BAG3 was expressed in human thyroid carcinoma cell lines; small interfering RNA-mediated downmodulation of its levels significantly (P < 0.0195) enhanced NPA cell apoptotic response to TRAIL.
  • The protein was not detectable in 19 of 20 specimens of normal thyroid or goiters, whereas 54 of 56 analyzed carcinomas (15 follicular, 28 papillary, and 13 anaplastic) were clearly positive for BAG3 expression.
  • CONCLUSIONS: BAG3 downmodulates the apoptotic response to TRAIL in human neoplastic thyroid cells.
  • The protein is specifically expressed in thyroid carcinomas and not in normal thyroid tissue or goiter.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Adaptor Proteins, Signal Transducing / physiology. Apoptosis / drug effects. Carcinoma / metabolism. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Thyroid Neoplasms / metabolism
  • [MeSH-minor] Apoptosis Regulatory Proteins / metabolism. Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. Immunohistochemistry. RNA, Small Interfering / pharmacology

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  • (PMID = 17164298.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Apoptosis Regulatory Proteins; 0 / BAG3 protein, human; 0 / RNA, Small Interfering; 0 / TNF-Related Apoptosis-Inducing Ligand
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33. Liu Z, Liu D, Bojdani E, El-Naggar AK, Vasko V, Xing M: IQGAP1 plays an important role in the invasiveness of thyroid cancer. Clin Cancer Res; 2010 Dec 15;16(24):6009-18
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  • [Title] IQGAP1 plays an important role in the invasiveness of thyroid cancer.
  • PURPOSE: This study was designed to explore the role of IQGAP1 in the invasiveness of thyroid cancer and its potential as a novel prognostic marker and therapeutic target in this cancer.
  • EXPERIMENTAL DESIGN: We examined IQGAP1 copy gain and its relationship with clinicopathologic outcomes of thyroid cancer and investigated its role in cell invasion and molecules involved in the process.
  • RESULTS: We found IQGAP1 copy number (CN) gain ≥ 3 in 1 of 30 (3%), 24 of 74 (32%), 44 of 107 (41%), 8 of 16 (50%), and 27 of 41 (66%) of benign thyroid tumor, follicular variant papillary thyroid cancer (FVPTC), follicular thyroid cancer (FTC), tall cell papillary thyroid cancer (PTC), and anaplastic thyroid cancer, respectively, in the increasing order of invasiveness of these tumors.
  • The siRNA knockdown of IQGAP1 dramatically inhibited thyroid cancer cell invasion and colony formation.
  • This provided a mechanism for the invasive role of IQGAP1 in thyroid cancer.
  • CONCLUSIONS: IQGAP1, through genetic copy gain, plays an important role in the invasiveness of thyroid cancer and may represent a novel prognostic marker and therapeutic target for this cancer.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20959410.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA113507-05; United States / NCI NIH HHS / CA / R01 CA113507; United States / NCI NIH HHS / CA / R0-1 CA113507; United States / NCI NIH HHS / CA / R01 CA113507-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / IQ motif containing GTPase activating protein 1; 0 / RNA, Small Interfering; 0 / ras GTPase-Activating Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ NIHMS242709; NLM/ PMC3005072
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34. Ensinger C, Kremser R, Prommegger R, Spizzo G, Schmid KW: EpCAM overexpression in thyroid carcinomas: a histopathological study of 121 cases. J Immunother; 2006 Sep-Oct;29(5):569-73
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  • [Title] EpCAM overexpression in thyroid carcinomas: a histopathological study of 121 cases.
  • Epithelial cell adhesion molecule (EpCAM) is expressed by a broad variety of carcinoma cells.
  • It is recognized by the monoclonal antibody 17-1A, which has already been applied for immunotherapy of several carcinoma types in preclinical and small clinical studies.
  • In the present study the immunohistochemical properties of 17-1A were evaluated in 121 cases of thyroid carcinomas of follicular cell origin, comprising of 75 differentiated (DTC; 35 papillary and 40 follicular carcinomas), 24 poorly differentiated (PDTC) and 22 anaplastic thyroid carcinomas.
  • In contrast, all anaplastic thyroid carcinomas (0%) completely lacked EpCAM expression.
  • Normal thyroid tissue presented with weak and heterogeneous EpCAM staining.
  • [MeSH-major] Adenocarcinoma, Follicular / pathology. Antigens, Neoplasm / biosynthesis. Biomarkers, Tumor / biosynthesis. Carcinoma, Papillary / pathology. Cell Adhesion Molecules / biosynthesis. Thyroid Neoplasms / pathology

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  • (PMID = 16971812.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / EPCAM protein, human
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35. Sipos JA, Shah MH: Thyroid cancer: emerging role for targeted therapies. Ther Adv Med Oncol; 2010 Jan;2(1):3-16
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  • [Title] Thyroid cancer: emerging role for targeted therapies.
  • The histology and clinical behavior of thyroid cancer are highly diverse.
  • Although most are indolent tumors with a very favorable outcome with the current standard of care therapy, a small subset of tumors may be among the most lethal malignancies known to man.
  • While surgery and radioactive iodine are the standard of care for differentiated thyroid cancers (DTC) and are effective in curing a majority of such patients, those with iodine-resistant cancers pose a great challenge for clinicians, as these patients have limited treatment options and poor prognoses.
  • Medullary thyroid carcinoma (MTC) has no effective systemic therapy despite the genetic and signaling defects that have been well characterized for the last two decades.
  • Anaplastic thyroid cancer (ATC) is one of the most aggressive solid tumors that remains fatal despite conventional multimodality therapy.
  • Increased understanding of the pathogenesis of papillary thyroid carcinoma, the most common type of DTC, as well as ATC, has led to the development of targeted therapies aimed at signaling pathways and angiogenesis that are critical to the development and/or progression of such tumors.
  • Conduction of such trials in the last few years represents a major breakthrough in the field of thyroid cancer.
  • Several trials testing targeted therapies offer promise for setting new standards for the future of patients with progressive thyroid cancer.
  • The purpose of this paper is to outline the recent advances in understanding of the pathogenesis of thyroid cancer and to summarize the results of the clinical trials with these targeted therapies.

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  • (PMID = 21789122.001).
  • [ISSN] 1758-8359
  • [Journal-full-title] Therapeutic advances in medical oncology
  • [ISO-abbreviation] Ther Adv Med Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3126004
  • [Keywords] NOTNLM ; targeted therapy / thyroid cancer / tyrosine kinase inhibitors
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36. 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.
  • The ABCG2 expression in ARO and WRO cell lines was analyzed by Western blot analysis.
  • 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.
  • 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] 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 / 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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37. Zerilli M, Zito G, Martorana A, Pitrone M, Cabibi D, Cappello F, Giordano C, Rodolico V: BRAF(V600E) mutation influences hypoxia-inducible factor-1alpha expression levels in papillary thyroid cancer. Mod Pathol; 2010 Aug;23(8):1052-60
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  • [Title] BRAF(V600E) mutation influences hypoxia-inducible factor-1alpha expression levels in papillary thyroid cancer.
  • Hypoxia-inducible factor-1alpha is found frequently overexpressed in solid tumors cells, exerting an important role in angiogenesis, glucose metabolism, cell proliferation, survival and invasion.
  • In thyroid carcinomas, hypoxia-inducible factor-1alpha expression was found increased in differentiated, poorly differentiated, medullary and anaplastic variants.
  • Other nonhypoxic stimuli increase hypoxia-inducible factor-1alpha synthesis through the activation of phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways in a cell-type-specific manner.
  • We have previously shown the role of BRAF(V600E) mutation in papillary thyroid cancer cells as a factor that facilitates tumor cell growth and progression.
  • In this study, we tested the hypothesis that BRAF(V600E) mutation influences hypoxia-inducible factor-1alpha expression in papillary thyroid carcinoma cells.
  • We analyzed 27 papillary thyroid carcinomas, 13 of which presented BRAF(V600E) mutation.
  • A BRAF wild-type papillary thyroid carcinoma cell line and a BRAF(V600E) mutated papillary thyroid carcinoma cell line were selected to study the effects of BRAF mutation on hypoxia-inducible factor-1alpha expression in vitro.
  • Pharmacological inhibition of BRAF significantly reduces hypoxia-inducible factor-1alpha expression levels in papillary thyroid carcinoma cell line harboring BRAF(V600E) mutation.
  • Our results suggest that hypoxia-inducible factor-1alpha is expressed in papillary thyroid carcinomas and is regulated not only by hypoxia but also by BRAF(V600E)-mediated signaling pathway.
  • [MeSH-major] Adenocarcinoma, Papillary / genetics. Mutation. Proto-Oncogene Proteins B-raf / genetics. Repressor Proteins / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / metabolism. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic. Gene Knockdown Techniques. Gene Silencing. Humans. Male. Middle Aged. Mixed Function Oxygenases. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Thyroidectomy. Transfection. Young Adult

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  • (PMID = 20473281.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Small Interfering; 0 / Repressor Proteins; EC 1.- / Mixed Function Oxygenases; EC 1.14.11.- / HIF1AN protein, human; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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38. Shi H, Wang C, Wei L, Lu S, Cao D: Malignant mesenchymoma of the thyroid: case report and literature review. Tumori; 2010 Mar-Apr;96(2):345-8
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  • [Title] Malignant mesenchymoma of the thyroid: case report and literature review.
  • Malignant mesenchymoma of the thyroid is extremely rare.
  • We report such a tumor involving the bilateral lobes of the thyroid which showed simultaneous chondrosarcomatous, osteosarcomatous, fibrosarcomatous and rhabdomyosarcomatous differentiation.
  • Sonographic examination indicated a thyroid mass involving the bilateral lobes.
  • Microscopically, the tumor was composed of small primitive mesenchymal cells with osteoid formation resembling the small cell variant of osteosarcoma interspersed with multiple cartilaginous nodules that indicated chondrosarcomatous differentiation.
  • Immunohistochemically, the small primitive mesenchymal cells were positive for vimentin and CD99 and negative for CD56, Syn, CgA, CK, TG, TTF-1, calcitonin, and S-100.
  • Primary malignant mesenchymoma of the thyroid is a high-grade malignant tumor with a poor prognosis.
  • Its differerential diagnosis includes anaplastic carcinoma and other rare sarcomas with chondroid, osteoid, and other mesenchymal metaplasia.
  • [MeSH-major] Mesenchymoma / pathology. Thyroid Neoplasms / pathology


39. Laatikainen LE, Castellone MD, Hebrant A, Hoste C, Cantisani MC, Laurila JP, Salvatore G, Salerno P, Basolo F, Näsman J, Dumont JE, Santoro M, Laukkanen MO: Extracellular superoxide dismutase is a thyroid differentiation marker down-regulated in cancer. Endocr Relat Cancer; 2010 Sep;17(3):785-96
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  • [Title] Extracellular superoxide dismutase is a thyroid differentiation marker down-regulated in cancer.
  • Reactive oxygen species, specifically hydrogen peroxide (H(2)O(2)), have a significant role in hormone production in thyroid tissue.
  • Although recent studies have demonstrated that dual oxidases are responsible for the H(2)O(2) synthesis needed in thyroid hormone production, our data suggest a pivotal role for superoxide dismutase 3 (SOD3) as a major H(2)O(2)-producing enzyme.
  • According to our results, Sod3 is highly expressed in normal thyroid, and becomes even more abundant in rat goiter models.
  • We showed TSH-stimulated expression of Sod3 via phospholipase C-Ca(2+) and cAMP-protein kinase A, a pathway that might be disrupted in thyroid cancer.
  • In line with this finding, we demonstrated an oncogene-dependent decrease in Sod3 mRNA expression synthesis in thyroid cancer cell models that corresponded to a similar decrease in clinical patient samples, suggesting that SOD3 could be used as a differentiation marker in thyroid cancer.
  • Finally, the functional analysis in thyroid models indicated a moderate role for SOD3 in regulating normal thyroid cell proliferation being in line with our previous observations.
  • [MeSH-major] Antigens, Differentiation / metabolism. Cell Differentiation. Superoxide Dismutase / metabolism. Thyroid Neoplasms / enzymology
  • [MeSH-minor] Animals. Blotting, Western. Calcium / metabolism. Carcinoma. Cell Proliferation. Down-Regulation. Humans. Hydrogen Peroxide / metabolism. Male. RNA, Messenger / genetics. RNA, Small Interfering / pharmacology. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. Superoxides / metabolism. Thyroid Carcinoma, Anaplastic. Thyroid Gland / enzymology. Thyroid Gland / pathology. Tumor Cells, Cultured

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  • (PMID = 20576801.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 11062-77-4 / Superoxides; BBX060AN9V / Hydrogen Peroxide; EC 1.15.1.1 / SOD3 protein, human; EC 1.15.1.1 / Sod3 protein, rat; EC 1.15.1.1 / Superoxide Dismutase; SY7Q814VUP / Calcium; Thyroid cancer, papillary
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40. Chiang FY, Lin JC, Lee KW, Wang LF, Tsai KB, Wu CW, Lu SP, Kuo WR: Thyroid tumors with preoperative recurrent laryngeal nerve palsy: clinicopathologic features and treatment outcome. Surgery; 2006 Sep;140(3):413-7
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  • [Title] Thyroid tumors with preoperative recurrent laryngeal nerve palsy: clinicopathologic features and treatment outcome.
  • BACKGROUND: The aim of this present study is to define the significance of recurrent laryngeal nerve palsy (RLNP) detected before surgery for thyroid diseases with regard to the incidence of malignancy, histopathologic distribution, extrathyroidal invasion, management, and prognosis.
  • METHODS: Six hundred and twenty-two patients underwent operation for various thyroid disease and were treated by the same surgeon.
  • The study was confined to 16 (3%) patients who suffered from a thyroid tumor with preoperative RLNP.
  • RESULTS: Of these 16 patients, 1 had benign thyroid disease, while the other 15 had malignancy (94%).
  • The recurrent laryngeal nerve could be dissected from the thyroid neoplasm in 3 patients, 2 of whom experienced recovery of this nerve's function postoperatively.
  • CONCLUSIONS: Thyroid tumor associated with RLNP is strongly suggestive of malignancy.
  • Well-differentiated thyroid cancer accounts for only half of these patients who tend to present at an older age and feature a much higher incidence of upper aerodigestive tract invasion.
  • Radical excision of a resectable anaplastic or squamous cell carcinoma of the thyroid gland offers the chance, albeit small, of long-term survival in this study.
  • [MeSH-major] Thyroid Neoplasms / complications. Thyroid Neoplasms / surgery. Thyroidectomy / methods. Vocal Cord Paralysis / etiology. Vocal Cord Paralysis / surgery
  • [MeSH-minor] Aged. Carcinoma, Papillary / complications. Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / surgery. Carcinoma, Squamous Cell / complications. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / surgery. Female. Humans. Laryngeal Nerves / pathology. Laryngeal Nerves / physiology. Laryngeal Nerves / surgery. Male. Middle Aged. Prognosis. Retrospective Studies. Thyroid Gland / pathology. Thyroid Gland / surgery. Treatment Outcome

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  • (PMID = 16934603.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Pacifico F, Paolillo M, Chiappetta G, Crescenzi E, Arena S, Scaloni A, Monaco M, Vascotto C, Tell G, Formisano S, Leonardi A: RbAp48 is a target of nuclear factor-kappaB activity in thyroid cancer. J Clin Endocrinol Metab; 2007 Apr;92(4):1458-66
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  • [Title] RbAp48 is a target of nuclear factor-kappaB activity in thyroid cancer.
  • CONTEXT: We have recently shown that nuclear factor (NF)-kappaB activity is constitutively elevated in anaplastic human thyroid carcinomas.
  • The inhibition of NF-kappaB in the anaplastic thyroid carcinoma cell line (FRO) leads to increased susceptibility to apoptosis induced by chemotherapeutic drugs and to the block of oncogenic activity.
  • OBJECTIVES: To understand better the molecular mechanisms played by NF-kappaB in thyroid oncogenesis, we performed a differential proteomic analysis between FRO transfected with a superrepressor form of inhibitor of kappaBalpha (IkappaBalphaM) and the parental counterpart (FRO Neo cells).
  • Immunohistochemical analysis of normal and pathological human thyroid specimens confirmed that RbAp48 is strongly overexpressed in primary human carcinomas.
  • Reduction of RbAp48 expression using small interfering RNA determined the suppression of tumorigenicity, very likely due to the decrease of their growth rate rather than to an increased susceptibility to apoptosis.
  • CONCLUSION: Our results show that RbAp48 is a NF-kappaB-regulated gene playing an important role in thyroid cancer cell autonomous proliferation.
  • [MeSH-major] Carrier Proteins / genetics. NF-kappa B / metabolism. Nuclear Proteins / genetics. Thyroid Neoplasms / metabolism
  • [MeSH-minor] Blotting, Northern. Consensus Sequence. DNA, Neoplasm / genetics. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Mass Spectrometry. Promoter Regions, Genetic. RNA, Small Interfering / genetics. Retinoblastoma-Binding Protein 4. Thymidine / metabolism


42. Kojima M, Suzuki M, Shimizu K, Masawa N: Inflammatory pseudotumor of the thyroid gland showing prominent fibrohistiocytic proliferation. A case report. Endocr Pathol; 2009;20(3):186-90
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  • [Title] Inflammatory pseudotumor of the thyroid gland showing prominent fibrohistiocytic proliferation. A case report.
  • Inflammatory pseudotumor of the thyroid gland (IPT) appears to be exceedingly rare.
  • Histologically, 14 previously reported cases demonstrated plasma cell granuloma variant.
  • Histologically, the lesion was characterized by haphazardly arranged spindle cells, histiocytes having foamy cytoplasm containing intracytoplasmic brown pigments, and small lymphocytes.
  • Immunohistochemical study demonstrated that the spindle cells were vimentin+, desmin-, muscle-specific actin+, cytokeratin-, endomysial antibody-, anaplastic lymphoma kinase-, CD34-- CD68+/-, CD99-, cyclin D1-, bcl-2-, and antifollicular dendritic cell antibody-.
  • IPT showing a predominant fibrohistiocytic proliferation should be differentiated from various nonneoplastic or neoplastic disorders showing spindle cell proliferation and/or exuberant fibrosis.
  • They include Riedel's thyroiditis, fibrous variant of chronic thyroiditis, papillary carcinoma with exuberant nodular fasciitis-like stroma, paucicellular variant of anaplastic thyroid carcinoma, and solitary fibrous tumor.
  • [MeSH-major] Granuloma, Plasma Cell / pathology. Thyroid Diseases / pathology
  • [MeSH-minor] Aged. Antigens, CD / biosynthesis. Biomarkers, Tumor / analysis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Thyroid Neoplasms / pathology

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  • (PMID = 19444653.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor
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43. Burrows N, Resch J, Cowen RL, von Wasielewski R, Hoang-Vu C, West CM, Williams KJ, Brabant G: Expression of hypoxia-inducible factor 1 alpha in thyroid carcinomas. Endocr Relat Cancer; 2010 Mar;17(1):61-72
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  • [Title] Expression of hypoxia-inducible factor 1 alpha in thyroid carcinomas.
  • Its regulation and function in thyroid carcinomas are unknown.
  • We evaluated the regulation of HIF-1 alpha and target gene expression in primary thyroid carcinomas and thyroid carcinoma cell lines (BcPAP, WRO, FTC-133 and 8505c).
  • HIF-1 alpha was not detectable in normal tissue but was expressed in thyroid carcinomas.
  • Dedifferentiated anaplastic tumours (ATCs) exhibited high levels of nuclear HIF-1 alpha staining.
  • In vitro studies revealed a functionally active HIF-1 alpha pathway in thyroid cells with transcriptional activation observed after graded hypoxia (1% O(2), anoxia) or treatment with a hypoxia mimetic cobalt chloride.
  • Similarly, pharmacological inhibition of the phosphoinositide 3-kinase (PI3K) pathway using LY294002 inhibited HIF-1 alpha and HIF-1 alpha targets in all cell lines, including those with B-RAF mutations (BcPAP and 8505c).
  • HIF-1 is functionally expressed in thyroid carcinomas and is regulated not only by hypoxia but also via growth factor signalling pathways and, in particular, the PI3K pathway.
  • Given the strong association of HIF-1 alpha with an aggressive disease phenotype and therapeutic resistance, this pathway may be an attractive target for improved therapy in thyroid carcinomas.

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  • (PMID = 19808899.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / C7820/A8696
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Chromones; 0 / Glucose Transporter Type 1; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Morpholines; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 3G0H8C9362 / Cobalt; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases; EVS87XF13W / cobaltous chloride
  • [Other-IDs] NLM/ PMC2828807
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44. Knobel M, Medeiros-Neto G: Relevance of iodine intake as a reputed predisposing factor for thyroid cancer. Arq Bras Endocrinol Metabol; 2007 Jul;51(5):701-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relevance of iodine intake as a reputed predisposing factor for thyroid cancer.
  • Iodine is a trace element that is essential for the synthesis of thyroid hormone.
  • This may be associated to thyroid cancer risk, particularly in women.
  • Experimental studies have documented thyroid cancer induction by elevation of endogenous TSH, although in a small number of animals.
  • Iodine deficiency associated with carcinogenic agents and chemical mutagens will result in a higher incidence of thyroid malignancy.
  • Inadequate low iodine intake will result in increased TSH stimulation, increased thyroid cell responsiveness to TSH, increased thyroid cell EGF-induced proliferation, decreased TGFbeta 1 production and increased angiogenesis, all phenomena related to promotion of tumor growth.
  • Epidemiological studies associating iodine intake and thyroid cancer led to controversial and conflicting results.
  • There is no doubt that introduction of universal iodine prophylaxis in population previously in chronic iodine-deficiency leads to a changing pattern of more prevalent papillary thyroid cancer and declining of follicular thyroid cancer.
  • Also anaplastic thyroid cancer is practically not seen after years of iodine supplementation.
  • Iodine excess has also been indicated as a possible nutritional factor in the prevalence of differentiated thyroid cancer in Iceland, Hawaii and, more recently, in China.
  • IN CONCLUSION: available evidence from animal experiments, epidemiological studies and iodine prophylaxis has demonstrated a shift towards a rise in papillary carcinoma, but no clear relationship between overall thyroid cancer incidence and iodine intake.
  • [MeSH-major] Adenocarcinoma, Follicular / etiology. Adenocarcinoma, Papillary / etiology. Iodine. Thyroid Neoplasms / etiology
  • [MeSH-minor] Animals. Argentina / epidemiology. Diet. Disease Models, Animal. Epidemiologic Studies. Epidermal Growth Factor / metabolism. Female. Hawaii / epidemiology. Humans. Iceland / epidemiology. Italy / epidemiology. Male. Thyroid Gland / drug effects. Thyroid Gland / metabolism. Thyrotropin / drug effects. Thyrotropin / metabolism

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  • (PMID = 17891233.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 62229-50-9 / Epidermal Growth Factor; 9002-71-5 / Thyrotropin; 9679TC07X4 / Iodine
  • [Number-of-references] 89
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45. Iannetti A, Pacifico F, Acquaviva R, Lavorgna A, Crescenzi E, Vascotto C, Tell G, Salzano AM, Scaloni A, Vuttariello E, Chiappetta G, Formisano S, Leonardi A: The neutrophil gelatinase-associated lipocalin (NGAL), a NF-kappaB-regulated gene, is a survival factor for thyroid neoplastic cells. Proc Natl Acad Sci U S A; 2008 Sep 16;105(37):14058-63
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  • [Title] The neutrophil gelatinase-associated lipocalin (NGAL), a NF-kappaB-regulated gene, is a survival factor for thyroid neoplastic cells.
  • NF-kappaB is constitutively activated in primary human thyroid tumors, particularly in those of anaplastic type.
  • The inhibition of NF-kappaB activity in the human anaplastic thyroid carcinoma cell line, FRO, leads to an increased susceptibility to chemotherapeutic drug-induced apoptosis and to the blockage of their ability to form tumors in nude mice.
  • To identify NF-kappaB target genes involved in thyroid cancer, we analyzed the secretome of conditioned media from parental and NF-kappaB-null FRO cells.
  • NGAL is highly expressed in human thyroid carcinomas, and knocking down its expression blocks the ability of FRO cells to grow in soft agar and form tumors in nude mice.
  • Our data suggest that NF-kappaB contributes to thyroid tumor cell survival by controlling iron uptake via NGAL.
  • [MeSH-major] Acute-Phase Proteins / metabolism. Gene Expression Regulation, Neoplastic. Lipocalins / metabolism. NF-kappa B / metabolism. Proto-Oncogene Proteins / metabolism. Thyroid Neoplasms / enzymology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Cell Line, Tumor. Cell Survival. Health. Humans. I-kappa B Kinase / metabolism. Immunohistochemistry. Proteomics. RNA, Small Interfering / genetics

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  • (PMID = 18768801.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / LCN2 protein, human; 0 / Lipocalins; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; EC 2.7.11.10 / I-kappa B Kinase
  • [Other-IDs] NLM/ PMC2544578
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46. Hirokawa M, Haba R, Kushida Y, Bando K, Kuma S, Kihara M, Miyauchi A: Benign nodular goiter with spindle cell component. Pathol Int; 2010 Aug;60(8):586-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Benign nodular goiter with spindle cell component.
  • We report three benign nodular goiters associated with spindle cell component.
  • The spindle cells were bland, and showed short fascicular pattern or formed small nests.
  • Immunohistochemically, they were positive for thyroglobulin and thyroid transcription factor-1.
  • We thought that the spindle cells are derived from follicular cell and non-neoplastic, and it is important to recognize this lesion to distinguish from aggressive and lethal components seen in papillary carcinoma or anaplastic carcinoma.
  • [MeSH-major] Carcinoma, Papillary / pathology. Goiter, Nodular / pathology. Thyroid Neoplasms / pathology

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  • (PMID = 20618737.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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47. Zitzmann S, Krämer S, Mier W, Hebling U, Altmann A, Rother A, Berndorff D, Eisenhut M, Haberkorn U: Identification and evaluation of a new tumor cell-binding peptide, FROP-1. J Nucl Med; 2007 Jun;48(6):965-72

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification and evaluation of a new tumor cell-binding peptide, FROP-1.
  • Because currently known peptides are restricted to a small number of tumors, new molecules and their corresponding receptors have to be identified to enlarge the spectrum of malignancies that can be diagnosed or treated using tumor-targeting peptides.
  • METHODS: A 12-amino-acid peptide phage display system was applied to identify a new peptide binding to follicular thyroid carcinoma cells.
  • The properties of the radiolabeled peptide were assessed in binding, competition, and internalization experiments in a variety of tumor cell lines including FRO82-2 and MCF-7 cells, and the pharmacokinetic behavior of the radiolabeled peptide was evaluated in tumor-bearing mice.
  • It showed binding to follicular thyroid carcinoma as well as anaplastic thyroid carcinoma, mammary carcinoma, cervix carcinoma, prostate carcinoma, and cell lines derived from head and neck tumors, and low affinity could be observed to control cells such as human umbilical vein endothelial cells or immortalized keratinocytes.
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Humans. Iodine Radioisotopes. Mammary Neoplasms, Experimental / metabolism. Mammary Neoplasms, Experimental / radionuclide imaging. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Peptide Library. Thyroid Neoplasms / metabolism. Thyroid Neoplasms / radionuclide imaging. Tissue Distribution

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  • (PMID = 17504878.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FROP-1 peptide; 0 / Iodine Radioisotopes; 0 / Oligopeptides; 0 / Peptide Library; 0 / Radiopharmaceuticals
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48. Voigt W, Pickan V, Pfeiffer C, Mueller T, Simon H, Arnold D: Preclinical evaluation of ZD1839 alone or in combination with oxaliplatin in a panel of human tumor cell lines -- implications for clinical use. Onkologie; 2005 Oct;28(10):482-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preclinical evaluation of ZD1839 alone or in combination with oxaliplatin in a panel of human tumor cell lines -- implications for clinical use.
  • However, in non-small cell lung cancer (NSCLC), addition of ZD1839 (Iressa) to combination chemotherapy did not improve the therapeutic outcome.
  • MATERIALS AND METHODS: In the present study, the activity of ZD1839 alone or in combination with oxaliplatin (Eloxatin) was evaluated in 12 human cancer cell lines including colon, testicular, anaplastic thyroid and epidermoid carcinoma cells.
  • RESULTS: The EGF-receptor protein was overexpressed in line A431 (epidermoid carcinoma) and near the minimum detection limit in all other cell lines.
  • The single agent activity of ZD1839 was highest in cell line A431.
  • In the other cell lines, it was lower and appeared to be independent of EGF-receptor expression levels.
  • Combined exposure to oxaliplatin and ZD1839 (IC30) resulted in significant synergy in 4 out of 6 colorectal cancer (CRC) cell lines and significant antagonism in 4 out of 6 non-colorectal cancer cell lines.
  • Continuous exposure to ZD1839 (IC30) induced a marked G1-phase arrest and dephosphorylation of EGF-receptor in A431, whereas no significant cell cycle perturbation could be detected in the low-expression cell lines.
  • Other factors than cell cycle perturbation seem to determine the mode of drug interaction between oxaliplatin and ZD1839.
  • CONCLUSION: Based on RAA, the single agent activity of ZD1839 in the investigated cell line panel appeared to be low.
  • Combined exposure to ZD1839 and oxaliplatin exerted synergy in colorectal cancer cell lines, warranting further evaluation in this type of cancer.
  • However, based on the observed antagonism in non-colorectal cancer cell lines, combined treatment with ZD1839 and oxaliplatin is not recommended for other types of cancer.
  • [MeSH-minor] Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Survival / drug effects. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Humans. Lethal Dose 50. Organoplatinum Compounds / administration & dosage. Quinazolines / administration & dosage

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  • (PMID = 16160394.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; 0 / Quinazolines; 04ZR38536J / oxaliplatin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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49. Liptak JM, Kamstock DA, Dernell WS, Ehrhart EJ, Rizzo SA, Withrow SJ: Cranial mediastinal carcinomas in nine dogs. Vet Comp Oncol; 2008 Mar;6(1):19-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Based on histological and immunohistochemical analysis, four dogs were diagnosed with ectopic follicular cell thyroid carcinomas, one dog with ectopic medullary cell thyroid carcinoma, two dogs with neuroendocrine carcinomas and two dogs with anaplastic carcinomas.
  • Local invasion, pleural effusion and metastasis did not have a negative impact on survival time in this small case series.
  • [MeSH-major] Carcinoma / veterinary. Dog Diseases / diagnosis. Dog Diseases / surgery. Mediastinal Neoplasms / veterinary
  • [MeSH-minor] Animals. Carcinoma, Medullary / diagnosis. Carcinoma, Medullary / mortality. Carcinoma, Medullary / surgery. Carcinoma, Medullary / veterinary. Carcinoma, Neuroendocrine / diagnosis. Carcinoma, Neuroendocrine / mortality. Carcinoma, Neuroendocrine / surgery. Carcinoma, Neuroendocrine / veterinary. Dogs. Female. Male. Neoplasm Invasiveness. Neoplasm Recurrence, Local / veterinary. Prognosis. Survival Analysis. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / mortality. Thyroid Neoplasms / surgery. Thyroid Neoplasms / veterinary. Treatment Outcome

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  • (PMID = 19178660.001).
  • [ISSN] 1476-5829
  • [Journal-full-title] Veterinary and comparative oncology
  • [ISO-abbreviation] Vet Comp Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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50. Fury MG, Solit DB, Su YB, Rosen N, Sirotnak FM, Smith RP, Azzoli CG, Gomez JE, Miller VA, Kris MG, Pizzo BA, Henry R, Pfister DG, Rizvi NA: A phase I trial of intermittent high-dose gefitinib and fixed-dose docetaxel in patients with advanced solid tumors. Cancer Chemother Pharmacol; 2007 Mar;59(4):467-75
Hazardous Substances Data Bank. DOCETAXEL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: 18 patients were enrolled in this study with the most frequent tumor types being non-small cell lung cancer and head and neck squamous cell cancer.
  • Partial responses were observed in one patient with head and neck squamous cell carcinoma and one patient with anaplastic thyroid cancer.

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  • (PMID = 16896930.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Quinazolines; 0 / Taxoids; 15H5577CQD / docetaxel; S65743JHBS / gefitinib
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