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1. Torino F, Paragliola RM, Barnabei A, Corsello SM: Medullary thyroid cancer: a promising model for targeted therapy. Curr Mol Med; 2010 Oct;10(7):608-25
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  • [Title] Medullary thyroid cancer: a promising model for targeted therapy.
  • In recent years, the clinical validation of molecular targeted therapies inhibiting the action of pathogenic tyrosine kinase (TK) has been one of the most exciting developments in cancer research.
  • In this context, medullary thyroid carcinoma (MTC) represents a promising model.
  • However, although the inhibition of the RET pathway is actually one of the most studied for therapeutic purposes, other signal transduction pathways have been recognized to contribute to the growth and functional activity of MTC and are considered attractive therapeutic targets.
  • To date, surgery represents the only curative treatment of MTC.
  • Now, available mouse models bearing mutations of RET or other genes, which spontaneously develop MTC, promise to improve preclinical evaluation of activity of targeted compounds.
  • A major effort needs to be made by endocrinologists and oncologists to refer their patients for multi-institutional trials in order to optimize them, perform translational studies and expedite the availability of novel beneficial selective therapies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Medullary. Molecular Targeted Therapy
  • [MeSH-minor] Animals. Carcinoma / drug therapy. Carcinoma / genetics. Carcinoma / surgery. Carcinoma / therapy. Carcinoma, Neuroendocrine. Humans. Mice. Multiple Endocrine Neoplasia. Multiple Endocrine Neoplasia Type 2a. Neoplastic Syndromes, Hereditary / drug therapy. Neoplastic Syndromes, Hereditary / genetics. Neoplastic Syndromes, Hereditary / surgery. Neoplastic Syndromes, Hereditary / therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-ret / genetics. Proto-Oncogene Proteins c-ret / physiology. Signal Transduction / drug effects. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / genetics. Thyroid Neoplasms / surgery. Thyroid Neoplasms / therapy

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  • (PMID = 20712590.001).
  • [ISSN] 1875-5666
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human; Familial medullary thyroid carcinoma; Thyroid cancer, medullary
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2. Schiff BA, McMurphy AB, Jasser SA, Younes MN, Doan D, Yigitbasi OG, Kim S, Zhou G, Mandal M, Bekele BN, Holsinger FC, Sherman SI, Yeung SC, El-Naggar AK, Myers JN: Epidermal growth factor receptor (EGFR) is overexpressed in anaplastic thyroid cancer, and the EGFR inhibitor gefitinib inhibits the growth of anaplastic thyroid cancer. Clin Cancer Res; 2004 Dec 15;10(24):8594-602
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  • [Title] Epidermal growth factor receptor (EGFR) is overexpressed in anaplastic thyroid cancer, and the EGFR inhibitor gefitinib inhibits the growth of anaplastic thyroid cancer.
  • PURPOSE: No effective treatment options currently are available to patients with anaplastic thyroid cancer (ATC), resulting in high mortality rates.
  • Epidermal growth factor (EGF) has been shown to play a role in the pathogenesis of many types of cancer, and its receptor (EGFR) provides an attractive target for molecular therapy.
  • EXPERIMENTAL DESIGN: The expression of EGFR was determined in ATC in vitro and in vivo and in human tissue arrays of ATC.
  • In vitro studies showed that gefitinib greatly inhibited cellular proliferation and induced apoptosis in ATC cell lines and slowed tumor growth in a nude mouse model of thyroid carcinoma cells injected subcutaneously.
  • CONCLUSIONS: ATC cells consistently overexpress EGFR, rendering this receptor a potential target for molecular therapy.
  • Our in vivo results show that gefitinib has significant antitumor activity against ATC in a subcutaneous nude mouse tumor model and therefore is a potential candidate for human clinical trials.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Carcinoma / drug therapy. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Papillary / drug therapy. Carcinoma, Papillary / metabolism. Carcinoma, Papillary / prevention & control. Cell Proliferation / drug effects. Epidermal Growth Factor / metabolism. Epidermal Growth Factor / pharmacology. Humans. Mice. Mice, Nude. Paclitaxel / administration & dosage. Phosphorylation / drug effects. Transforming Growth Factor alpha / metabolism. Transforming Growth Factor alpha / pharmacology. Tumor Cells, Cultured


3. Wang Z, Chakravarty G, Kim S, Yazici YD, Younes MN, Jasser SA, Santillan AA, Bucana CD, El-Naggar AK, Myers JN: Growth-inhibitory effects of human anti-insulin-like growth factor-I receptor antibody (A12) in an orthotopic nude mouse model of anaplastic thyroid carcinoma. Clin Cancer Res; 2006 Aug 1;12(15):4755-65
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  • [Title] Growth-inhibitory effects of human anti-insulin-like growth factor-I receptor antibody (A12) in an orthotopic nude mouse model of anaplastic thyroid carcinoma.
  • PURPOSE: The insulin-like growth factor-I receptor (IGF-IR) and its ligands have been implicated in the pathogenesis and progression of various cancers, including those arising in the thyroid gland.
  • We therefore evaluated whether the IGF-IR could serve as a potential target for therapy of anaplastic thyroid carcinoma (ATC).
  • EXPERIMENTAL DESIGN: The expression and activation of the IGF-IR and some of its downstream signaling pathway components were evaluated in both human thyroid cancer specimens and thyroid cancer cell lines.
  • The therapeutic potential of a humanized monoclonal antibody (A12) directed against IGF-IR was assessed in vitro and in vivo in an orthotopic model of ATC.
  • Tumor volume and overall survival time were analyzed to evaluate the efficacy of A12 in vivo.
  • RESULTS: IGF-IR was overexpressed in 94% of the thyroid cancers.
  • However, the inhibitory effects of A12 on cell proliferation were cell line dependent, as those ATC cell lines that had detectable levels of pIGF-IR were more sensitive to A12 treatment.
  • Our results also highlighted a previously undefined IGF-IR-mediated antiangiogenic effect on tumor-associated endothelium in thyroid cancers.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Carcinoma / drug therapy. Receptor, IGF Type 1 / antagonists & inhibitors. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antigen-Antibody Reactions. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Humans. Insulin-Like Growth Factor I / pharmacology. Insulin-Like Growth Factor II / pharmacology. Male. Methylation. Mice. Mice, Nude. Neovascularization, Pathologic / drug therapy. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Signal Transduction / drug effects. Signal Transduction / immunology. Structure-Activity Relationship. Transplantation, Heterologous. Xenograft Model Antitumor Assays

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  • (PMID = 16899627.001).
  • [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 / CA016672; United States / NCI NIH HHS / CA / P50 CA097007
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 67763-96-6 / Insulin-Like Growth Factor I; 67763-97-7 / Insulin-Like Growth Factor II; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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4. Yalcin M, Bharali DJ, Lansing L, Dyskin E, Mousa SS, Hercbergs A, Davis FB, Davis PJ, Mousa SA: Tetraidothyroacetic acid (tetrac) and tetrac nanoparticles inhibit growth of human renal cell carcinoma xenografts. Anticancer Res; 2009 Oct;29(10):3825-31
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  • [Title] Tetraidothyroacetic acid (tetrac) and tetrac nanoparticles inhibit growth of human renal cell carcinoma xenografts.
  • Renal cell carcinoma is the most lethal of the common urologic malignancies, with no available effective therapeutics.
  • Tetrac (tetraiodothyroacetic acid) is a deaminated analogue of L-thyroxine (T(4)) that blocks the pro-angiogenesis actions of T(4) and 3, 5, 3'-triiodo-L-thyronine as well as other growth factors at the cell surface receptor for thyroid hormone on integrin alphavbeta3.
  • Since this integrin is expressed on cancer cells and also on endothelial and vascular smooth cells, the possibility exists that Tetrac may act on both cell types to block the proliferative effects of thyroid hormone on tumor growth and tumor-related angiogenesis.
  • To test this hypothesis, we determined the effect of Tetrac on tumor cell proliferation and on related angiogenesis of human renal cell carcinoma (RCC).
  • In the mouse xenograft model, Tetrac and Tetrac NP promptly reduced tumor volume (p<0.01) when administered daily for up to 20 days.
  • Animal weight gain was comparable in the control and treatment groups.
  • Overall, the findings presented here provide evidence for the anti-angiogenic, and anti-tumor actions of Tetrac and Tetrac NP and suggest their potential utility in the treatment of renal cell carcinoma.
  • [MeSH-major] Carcinoma, Renal Cell / drug therapy. Kidney Neoplasms / drug therapy. Nanoparticles / administration & dosage. Thyroxine / analogs & derivatives
  • [MeSH-minor] Animals. Cell Growth Processes / drug effects. Cell Line, Tumor. Chick Embryo. Chorioallantoic Membrane / blood supply. Chorioallantoic Membrane / drug effects. Humans. Lactic Acid / administration & dosage. Lactic Acid / chemistry. Lactic Acid / pharmacokinetics. Mice. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / pathology. Polyglycolic Acid / administration & dosage. Polyglycolic Acid / chemistry. Polyglycolic Acid / pharmacokinetics. Xenograft Model Antitumor Assays

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  • (PMID = 19846915.001).
  • [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 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid; PA7UX1FFYQ / tetraiodothyroacetic acid; Q51BO43MG4 / Thyroxine
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5. Quidville V, Segond N, Pidoux E, Cohen R, Jullienne A, Lausson S: Tumor growth inhibition by indomethacin in a mouse model of human medullary thyroid cancer: implication of cyclooxygenases and 15-hydroxyprostaglandin dehydrogenase. Endocrinology; 2004 May;145(5):2561-71
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  • [Title] Tumor growth inhibition by indomethacin in a mouse model of human medullary thyroid cancer: implication of cyclooxygenases and 15-hydroxyprostaglandin dehydrogenase.
  • Medullary thyroid cancer (MTC) is a C cell neoplasm-secreting calcitonin.
  • Surgery remains the only treatment as the primary tumor and metastases resist radio- and chemotherapies.
  • Nonsteroidal antiinflammatory drugs have an antitumoral effect, generally related to the decrease of PG levels.
  • We assessed the therapeutic potential of indomethacin in a model of human (TT cells) tumors in nude mice.
  • Immunological effector recruitment and vascular network was not modified by treatment.
  • [MeSH-major] Carcinoma, Medullary / pathology. Cyclooxygenase Inhibitors / therapeutic use. Hydroxyprostaglandin Dehydrogenases / physiology. Indomethacin / therapeutic use. Isoenzymes / physiology. Prostaglandin-Endoperoxide Synthases / physiology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Animals. Apoptosis. Calcitonin / blood. Cell Division / drug effects. Cyclooxygenase 1. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Female. Humans. In Situ Nick-End Labeling. Membrane Proteins. Mice. Mice, Nude. Neoplasm Transplantation. Tumor Cells, Cultured

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  • (PMID = 14736730.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 9007-12-9 / Calcitonin; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases; EC 1.1.1.141 / 15-hydroxyprostaglandin dehydrogenase; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.14.99.1 / Ptgs1 protein, mouse; XXE1CET956 / Indomethacin
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6. Dackiw AP, Ezzat S, Huang P, Liu W, Asa SL: Vitamin D3 administration induces nuclear p27 accumulation, restores differentiation, and reduces tumor burden in a mouse model of metastatic follicular thyroid cancer. Endocrinology; 2004 Dec;145(12):5840-6
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  • [Title] Vitamin D3 administration induces nuclear p27 accumulation, restores differentiation, and reduces tumor burden in a mouse model of metastatic follicular thyroid cancer.
  • We have previously demonstrated in vitro that 1alpha,25-dihydroxyvitamin D3 (calcitriol) treatment increases p27 expression and decreases cell proliferation in cultured thyroid carcinoma cell lines.
  • We hypothesized that in vivo treatment with calcitriol would have a beneficial effect on thyroid carcinoma growth and progression.
  • Five x 10(6) WRO (human thyroid follicular carcinoma derived) cells were implanted in the neck in 4- to 5-wk-old female SCID mice in an orthotopic xenograft model.
  • Animals (n = 15) were treated i.p. three times a week for 21 d with 0.75 microg/kg calcitriol or vehicle.
  • Mice were killed 21 d after tumor implantation, tumor volume was measured, and excised tumor tissue was examined by light microscopy and immunohistochemistry for p27 and thyroglobulin reactivity.
  • Average tumor volume in control mice after 21 d of vehicle treatment was 2002 +/- 207 mm3 compared with a mean tumor volume of 1241 +/- 115 mm3 in animals receiving calcitriol, reflecting a 38% reduction in tumor volume size (P < 0.003).
  • Tumors from vehicle-treated animals demonstrated morphological features of epithelial malignancies with characteristics of insular carcinoma and multiple metastases to the lungs.
  • These studies demonstrate that in vivo calcitriol administration can effectively restore p27 accumulation in thyroid carcinoma cells, an effect associated with appreciably enhanced cellular differentiation, reduction in tumor burden, and prevention of metastatic growth.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Cholecalciferol / pharmacology. Proliferating Cell Nuclear Antigen / metabolism. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Line, Tumor. Disease Models, Animal. Humans. Immunohistochemistry. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Mice. Thyroglobulin / metabolism. Xenograft Model Antitumor Assays


7. DeGroot LJ, Zhang R: Viral mediated gene therapy for the management of metastatic thyroid carcinoma. Curr Drug Targets Immune Endocr Metabol Disord; 2004 Sep;4(3):235-44
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  • [Title] Viral mediated gene therapy for the management of metastatic thyroid carcinoma.
  • Thyroid cancers are of special interest in gene therapy, since it is possible to direct gene expression specifically to the thyroid derived cells by using promoters with limited expression, and secondly, because destruction of the normal tissue by introduction of a toxic gene would have no important adverse effect.
  • Adenovirus is a well studied and widely used vector and is useful for targeting genes because it infects many cell types, including differentiated thyroid cancer and medullary thyroid cancer cells.
  • Combinations of vectors expressing thymidine kinase and IL-12 under control of a strong but non-tissue specific CMV promoter effectively destroy a model anaplastic thyroid tumor in Wistar rats.
  • Medullary thyroid cancer provides a target much like differentiated thyroid cancer because it is possible to address gene expression specifically to the medullary thyroid cells by the use of a modified calcitonin promoter.
  • Animal models of this tumor are available in a mouse and Wag/Rij rat model.
  • In the latter system, treatment with adenoviruses expressing genes under control of the modified calcitonin promoter and expressing thymidine kinase or IL-12 leads to destruction of growing medullary thyroid cancer tumors, destroy distant tumors after injection in one tumor, and cause induction of long lasting immunity to subsequent tumor development in the animals.
  • There are many ongoing studies of gene therapy in humans using various genes such as thymidine kinase, IL-2, and now IL-12.
  • Although none of these trials to date shows complete eradication of metastatic tumors in humans, there are reports showing distinctly that the viral mediated gene therapy approach can effectively destroy human tumors after in vivo administration.
  • Gene therapy using the adenoviral vectors appears to be safe in studies reported so far.
  • New genes and new vectors under development will certainly lead to the established use of these methods in the therapy of human thyroid carcinomas in the near future.
  • [MeSH-major] Adenoviridae / genetics. Carcinoma / drug therapy. Carcinoma / virology. Genetic Therapy / methods. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / virology


8. Yeung SC, Xu G, Pan J, Christgen M, Bamiagis A: Manumycin enhances the cytotoxic effect of paclitaxel on anaplastic thyroid carcinoma cells. Cancer Res; 2000 Feb 1;60(3):650-6
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  • [Title] Manumycin enhances the cytotoxic effect of paclitaxel on anaplastic thyroid carcinoma cells.
  • Despite the current multimodal approach to treatment of anaplastic thyroid cancer (ATC), the prognosis for patients with the disease is poor.
  • New effective therapy for ATC is desperately needed.
  • Thus, we investigated the effects of manumycin (a farnesyl:protein transferase inhibitor), alone and in combination with other drugs frequently used to treat ATC, in six human ATC cell lines: ARO, C643, DRO, Hth-74, KAT-4, and KAT-18.
  • The in vivo effect and toxicity of combined manumycin and paclitaxel treatments were evaluated in a nude mouse xenograft model using ARO and KAT-4 cells.
  • Drugs were injected i.p. on days 1 and 3 of a 7-day cycle for three cycles.
  • Combined manumycin and paclitaxel treatments seemed as effective as manumycin against ARO cells and more effective than either manumycin or paclitaxel alone against KAT-4 cells.
  • No significant morbidity or mortality was caused by the treatments.
  • Manumycin plus paclitaxel has enhanced cytotoxic effects and increased apoptotic cell death in ATC cells in vitro compared with either drug by itself.
  • The lack of synergy observed in this in vivo experiment may be due to a ceiling effect, and further experimentation is warranted to ascertain the optimal way to combine these two agents for maximal therapeutic effects.
  • [MeSH-major] Alkyl and Aryl Transferases / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Carcinoma / drug therapy. Enzyme Inhibitors / pharmacology. Paclitaxel / pharmacology. Polyenes / pharmacology. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cisplatin / pharmacology. Doxorubicin / pharmacology. Drug Synergism. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Polyunsaturated Alkamides. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 10676649.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Polyenes; 0 / Polyunsaturated Alkamides; 52665-74-4 / manumycin; 80168379AG / Doxorubicin; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.- / p21(ras) farnesyl-protein transferase; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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9. Pacifico F, Crescenzi E, Mellone S, Iannetti A, Porrino N, Liguoro D, Moscato F, Grieco M, Formisano S, Leonardi A: Nuclear factor-{kappa}B contributes to anaplastic thyroid carcinomas through up-regulation of miR-146a. J Clin Endocrinol Metab; 2010 Mar;95(3):1421-30
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  • [Title] Nuclear factor-{kappa}B contributes to anaplastic thyroid carcinomas through up-regulation of miR-146a.
  • Many human tumors show deregulated expression of miRNAs targeting oncogenes and/or tumor suppressors, thus identifying miRNAs as new molecular targets for cancer therapy.
  • OBJECTIVES: Nuclear factor (NF)-kappaB is strongly activated in human anaplastic thyroid carcinomas (ATCs).
  • Among others, the miR-146a showed a strong down-regulation that was confirmed by quantitative real time RT-PCR.
  • The expression of miR-146a was almost undetectable in mouse embryonic fibroblasts isolated from the RelA knockout mice and was restored after reexpression of RelA, thus indicating that miR-146a transcription was controlled by NF-kappaB.
  • The inhibition of miR-146a expression in FRO cells decreased their oncogenic potential and increased the susceptibility to chemotherapeutic drug-induced apoptosis.
  • Importantly, the miR-146a resulted in overexpression of human ATC specimens compared with the normal thyroid tissue.
  • CONCLUSIONS: Our results show that NF-kappaB contributes to anaplastic thyroid cancer up-regulating the expression of miR-146a.
  • [MeSH-major] Carcinoma / genetics. MicroRNAs / genetics. NF-kappa B / genetics. Thyroid Neoplasms / genetics. Up-Regulation / genetics
  • [MeSH-minor] Analysis of Variance. Animals. Apoptosis / drug effects. Apoptosis / genetics. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Cells, Cultured. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunohistochemistry. Mice. Microarray Analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20061417.001).
  • [ISSN] 1945-7197
  • [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 / MIRN146 microRNA, human; 0 / MicroRNAs; 0 / NF-kappa B
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10. Samadi AK, Mukerji R, Shah A, Timmermann BN, Cohen MS: A novel RET inhibitor with potent efficacy against medullary thyroid cancer in vivo. Surgery; 2010 Dec;148(6):1228-36; discussion 1236
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  • [Title] A novel RET inhibitor with potent efficacy against medullary thyroid cancer in vivo.
  • BACKGROUND: Most medullary thyroid carcinomas (MTC) recur or progress despite curative resection.
  • Current targeted therapies show promise but lack durable efficacy and tolerability.
  • Treatment with WA (8 mg/kg/day, intraperitoneally, for 21 days) was started for neoplasms > 100 mm(3).
  • Endpoints were survival, neoplasm > 15,00 mm(3), decreased body weight, or body score (all measured three times/wk).
  • Tumor cells treated with WA demonstrated inhibition of total and phospho-RET levels by Western blot analysis in a dose-dependent manner (almost complete inhibition with treatment of 5 μM WA) as well as potent inhibition of phospho-ERK and phospho-Akt levels.

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  • [Copyright] Copyright © 2010 Mosby, Inc. All rights reserved.
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  • (PMID = 21134556.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / L30 CA136330; United States / NCRR NIH HHS / RR / P20 RR015563-105577; United States / NCRR NIH HHS / RR / RR015563-105577; United States / NCRR NIH HHS / RR / P20 RR015563; United States / NCI NIH HHS / CA / L30 CA136330-02
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Withanolides; 9007-12-9 / Calcitonin; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / Ret protein, mouse; L6DO3QW4K5 / withaferin A
  • [Other-IDs] NLM/ NIHMS240003; NLM/ PMC3088305
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11. 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.
  • RESULTS: S100A4 expression was reduced by 71.3 +/- 4.7% in ARO/S100A4-shRNA by real-time RT-PCR analysis.
  • We also demonstrated significant induction of apoptosis in ARO/S100A4-shRNA after incubation with 15 nm paclitaxel, indicating that tumor cells were sensitized to chemotherapy as a result of S100A4 knockdown.
  • Given that S100A4 is overexpressed in many kinds of tumors, the current study provides the proof of concept in its therapeutic potential.
  • [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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12. Yuki K, Takahashi A, Ota I, Ohnishi K, Yasumoto J, Kanata H, Yane K, Hosoi H, Ohnishi T: Glycerol enhances CDDP-induced growth inhibition of thyroid anaplastic carcinoma tumor carrying mutated p53 gene. Oncol Rep; 2004 Apr;11(4):821-4
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  • [Title] Glycerol enhances CDDP-induced growth inhibition of thyroid anaplastic carcinoma tumor carrying mutated p53 gene.
  • To increase the chemo-sensitivity of anaplastic thyroid carcinoma, we examined the effects of glycerol on the tumor growth after CDDP treatment.
  • The cultured cells of an anaplastic thyroid carcinoma cell line (8305c) carrying a mutated p53 gene (mp53) were transplanted into the thighs of nude mice.
  • Therefore, glycerol might be useful for chemotherapy in patients with mp53 cancer cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / drug therapy. Cisplatin / therapeutic use. Genes, p53. Glycerol / therapeutic use. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspase 3. Caspases / metabolism. Cell Culture Techniques. Drug Synergism. Humans. Immunohistochemistry. Male. Mice. Mice, Inbred BALB C. Models, Animal. Neoplasm Transplantation. Point Mutation / genetics

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  • (PMID = 15010879.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; PDC6A3C0OX / Glycerol; Q20Q21Q62J / Cisplatin
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13. Nappi TC, Salerno P, Zitzelsberger H, Carlomagno F, Salvatore G, Santoro M: Identification of Polo-like kinase 1 as a potential therapeutic target in anaplastic thyroid carcinoma. Cancer Res; 2009 Mar 1;69(5):1916-23
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  • [Title] Identification of Polo-like kinase 1 as a potential therapeutic target in anaplastic thyroid carcinoma.
  • Anaplastic thyroid carcinoma (ATC) is one of the most aggressive and chemoresistant cancers.
  • Here, we used the BI 2536 PLK1 inhibitor on ATC and nontransformed thyroid follicular cell lines.
  • On treatment with nanomolar doses of BI 2536, ATC cells progressed normally through S phase but died thereafter, directly from mitotic arrest.
  • Nontransformed thyroid cells were 3.2- to 18.4-fold less susceptible to BI 2536-induced cell cycle effects compared with ATC cells.
  • These findings identify PLK1 as a promising target for the molecular therapy of ATC.
  • [MeSH-major] Carcinoma / drug therapy. Cell Cycle Proteins / antagonists & inhibitors. Protein Kinase Inhibitors / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins / antagonists & inhibitors. Pteridines / pharmacology. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin B / analysis. Cyclin B1. Female. Humans. Mice. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 19223553.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BI 2536; 0 / CCNB1 protein, human; 0 / Ccnb1 protein, mouse; 0 / Cell Cycle Proteins; 0 / Cyclin B; 0 / Cyclin B1; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Pteridines; 0 / Tumor Suppressor Protein p53; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / polo-like kinase 1
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14. Schmutzler C, Hoang-Vu C, Rüger B, Köhrle J: Human thyroid carcinoma cell lines show different retinoic acid receptor repertoires and retinoid responses. Eur J Endocrinol; 2004 Apr;150(4):547-56
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  • [Title] Human thyroid carcinoma cell lines show different retinoic acid receptor repertoires and retinoid responses.
  • DESIGN: To examine whether altered responses to retinoids may correlate with differences in RA receptor equipment, retinoid effects were examined in human thyroid carcinoma cell lines of various differentiation stages in culture and after xenotransplantation onto rodent models.
  • METHODS: Cell growth was assessed by the MTT test, mRNA expression was examined by Northern blot and quantitative competitive RT-PCR, and type I 5'-deiodinase (5'DI) activity was measured by in vitro deiodination assay.
  • RESULTS: All-trans-RA and RAR-selective synthetic retinoids stimulated activity and mRNA expression of the thyroid differentiation marker 5'DI in the follicular thyroid carcinoma cell line FTC-133.
  • In the anaplastic thyroid carcinoma cell lines HTh 74 and C 643, the activity of 5'DI was not increased by retinoids, and expression of RAR alpha mRNA was reduced.
  • Thus, retinoid therapy might be applied to treat follicular thyroid carcinomas.

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  • (PMID = 15080786.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 0 / retinoic acid receptor beta; 5688UTC01R / Tretinoin
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15. Das T, Cagan R: Drosophila as a novel therapeutic discovery tool for thyroid cancer. Thyroid; 2010 Jul;20(7):689-95
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  • [Title] Drosophila as a novel therapeutic discovery tool for thyroid cancer.
  • BACKGROUND: Multiple endocrine neoplasia type II (MEN2) is a rare but aggressive cancer for which no effective treatment currently exists.
  • A Drosophila model was developed to identify novel genetic modifier loci of oncogenic RET, as well as to provide a whole animal system to rapidly identify compounds that suppressed RET-dependent MEN2.
  • ZD6474 (Vandetanib), currently in phase III trials, suppressed tumorigenesis in MEN2 model flies, demonstrating for the first time the effectiveness of a Drosophila-based whole animal model for identifying therapeutically useful compounds.
  • SUMMARY: Clinical data suggest that drug mono-therapy for MEN2 and other cancers typically yield only moderate benefits as patients develop drug resistance and suffer from drug-induced pathway feedback.
  • Combinations of drugs that target different nodes of the oncogenic pathway are an effective way to prevent resistance as well as feedback.
  • Identifying the optimal drug-dose combinations for therapy poses a significant challenge in existing mouse models.
  • Fly models offer a means to quickly and effectively identify drug combinations that are well tolerated and potently suppress the MEN2 phenotype.
  • This approach may also identify differences in therapeutic responses between the two subtypes of MEN2--MEN2A and MEN2B--providing additional therapeutic insights.
  • CONCLUSIONS: Fly models have proven useful for identifying known drugs as well as novel compounds that, as single agents or in combinations, effectively suppress the MEN2 syndrome.
  • These findings validate the use of fly models for both drug discovery as well as identification of useful drug combinations.
  • In the future, rapid pairing of new genomic information with increasingly complex fly models will aid us in efforts to further tailor drug treatments toward personalized medicine.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Disease Models, Animal. Drosophila / drug effects. Drosophila / genetics. Drug Discovery / methods. Thyroid Neoplasms / drug therapy. Thyroid Nodule / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Medullary / drug therapy. Carcinoma, Medullary / genetics. Carcinoma, Medullary / metabolism. Carcinoma, Medullary / secondary. Humans. Multiple Endocrine Neoplasia Type 2a / drug therapy. Multiple Endocrine Neoplasia Type 2a / genetics. Multiple Endocrine Neoplasia Type 2a / metabolism. Multiple Endocrine Neoplasia Type 2b / drug therapy. Multiple Endocrine Neoplasia Type 2b / genetics. Multiple Endocrine Neoplasia Type 2b / metabolism. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Neoplasms, Experimental / secondary. Precision Medicine / methods. Proto-Oncogene Proteins c-ret / genetics. Signal Transduction / drug effects


16. Furuya F, Lu C, Willingham MC, Cheng SY: Inhibition of phosphatidylinositol 3-kinase delays tumor progression and blocks metastatic spread in a mouse model of thyroid cancer. Carcinogenesis; 2007 Dec;28(12):2451-8
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  • [Title] Inhibition of phosphatidylinositol 3-kinase delays tumor progression and blocks metastatic spread in a mouse model of thyroid cancer.
  • Aberrant activation of the phosphatidylinositol 3-kinase (PI3K)-AKT/protein kinase B-signaling pathway has been associated with multiple human cancers, including thyroid cancer.
  • Recently, we showed that, similar to human thyroid cancer, the PI3K-AKT pathway is overactivated in both the thyroid and metastatic lesions of a mouse model of follicular thyroid carcinoma (TRbeta(PV/PV) mice).
  • This TRbeta(PV/PV) mouse harbors a knockin mutant thyroid hormone receptor beta gene (TRbetaPV mutant) that spontaneously develops thyroid cancer and distant metastasis similar to human follicular thyroid cancer.
  • That the activation of the PI3K-AKT signaling contributes to thyroid carcinogenesis raised the possibility that this pathway could be a potential therapeutic target in follicular thyroid carcinoma.
  • The present study tested this possibility by treating TRbeta(PV/PV) mice with LY294002 (LY), a potent and specific PI3K inhibitor, and evaluating the effect of LY on the spontaneous development of thyroid cancer.
  • LY treatment inhibited the AKT-mammalian target of rapamycin (mTOR)-p70(S6K) signaling, and it decreased cyclin D1 and increased p27(Kip1) expression to inhibit thyroid tumor growth and reduce tumor cell proliferation.
  • LY treatment increased caspase 3 and decreased phosphorylated-BAD to induce apoptosis.
  • In addition, LY treatment reduced the AKT-matrix metalloproteinase 2 signaling to decrease cell motility to block metastatic spread of thyroid tumors.
  • No significant adverse effects were observed for wild-type mice treated similarly with LY.
  • The present study provides the first preclinical evidence for the in vivo efficacy for LY in the treatment of follicular thyroid cancer.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Chromones / therapeutic use. Morpholines / therapeutic use. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Thyroid Hormone Receptors beta / metabolism. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis. Caspase 3 / metabolism. Cell Movement / drug effects. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Matrix Metalloproteinase 2 / metabolism. Mice. Mice, Mutant Strains. Neoplasm Invasiveness. Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction. TOR Serine-Threonine Kinases. Tumor Cells, Cultured


17. Ezzat S, Huang P, Dackiw A, Asa SL: Dual inhibition of RET and FGFR4 restrains medullary thyroid cancer cell growth. Clin Cancer Res; 2005 Feb 1;11(3):1336-41
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  • [Title] Dual inhibition of RET and FGFR4 restrains medullary thyroid cancer cell growth.
  • Medullary thyroid cancer is frequently an aggressive form of carcinoma for which there are currently no effective forms of systemic therapy.
  • Treatment with STI571 resulted in inhibition of RET phosphorylation, cell proliferation, tumor growth and invasiveness.
  • These data highlight RET and FGFR4 as therapeutic targets and suggest a potential role for the combined use of tyrosine kinase inhibitors in the management of inoperable medullary thyroid cancers.
  • [MeSH-major] Carcinoma, Medullary / prevention & control. Oncogene Proteins / antagonists & inhibitors. Piperazines / pharmacology. Pyrimidines / pharmacology. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptors, Fibroblast Growth Factor / antagonists & inhibitors. Thyroid Neoplasms / prevention & control
  • [MeSH-minor] Animals. Apoptosis / drug effects. Benzamides. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Synergism. Female. Humans. Imatinib Mesylate. Mice. Phosphorylation / drug effects. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-ret. Receptor, Fibroblast Growth Factor, Type 4. Xenograft Model Antitumor Assays

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  • (PMID = 15709206.001).
  • [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 / Benzamides; 0 / Oncogene Proteins; 0 / PD 173074; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Receptors, Fibroblast Growth Factor; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FGFR4 protein, human; EC 2.7.10.1 / Fgfr4 protein, mouse; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 4
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18. Carlomagno F, Vitagliano D, Guida T, Napolitano M, Vecchio G, Fusco A, Gazit A, Levitzki A, Santoro M: The kinase inhibitor PP1 blocks tumorigenesis induced by RET oncogenes. Cancer Res; 2002 Feb 15;62(4):1077-82
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  • PP1 prevented the growth of two human papillary thyroid carcinoma cell lines that carry spontaneous RET/PTC1 rearrangements and blocked anchorage-independent growth and tumorigenicity in nude mice of NIH3T3 fibroblasts expressing the RET/PTC3 oncogene.
  • These findings suggest targeting RET oncogenes with PP1 or related compounds as a novel treatment strategy for RET-associated neoplasms.
  • [MeSH-major] Cell Transformation, Neoplastic / drug effects. Drosophila Proteins. Enzyme Inhibitors / pharmacology. Gonadotropin-Releasing Hormone / analogs & derivatives. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / genetics. Pyrazoles / pharmacology. Pyrimidines / pharmacology. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] 3T3 Cells / cytology. 3T3 Cells / drug effects. Animals. Gene Expression. Humans. Male. Mice. Mice, Inbred BALB C. Oncogenes. Phosphorylation / drug effects. Proto-Oncogene Proteins c-ret. Signal Transduction / drug effects. Signal Transduction / physiology. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / enzymology. Thyroid Neoplasms / genetics. Tumor Cells, Cultured

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  • (PMID = 11861385.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-amino-5-(4-methylphenyl)-7-(tert-butyl)pyrazolo(3,4-d)pyrimidine; 0 / Drosophila Proteins; 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Pyrazoles; 0 / Pyrimidines; 33515-09-2 / Gonadotropin-Releasing Hormone; 87565-51-3 / MI 1544; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Ret oncogene protein, Drosophila; EC 2.7.10.1 / Ret protein, mouse
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19. Kotchetkov R, Cinatl J, Krivtchik AA, Vogel JU, Matousek J, Pouckova P, Kornhuber B, Schwabe D, Cinatl J Jr: Selective activity of BS-RNase against anaplastic thyroid cancer. Anticancer Res; 2001 Mar-Apr;21(2A):1035-42
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  • [Title] Selective activity of BS-RNase against anaplastic thyroid cancer.
  • BACKGROUND: Anaplastic thyroid carcinoma is an aggressive solid tumor that fails to adequately respond to any known chemotherapeutic regimen.
  • The development of effective chemotherapy agents would provide the best chance for long-term survival of patients.
  • MATERIALS AND METHODS: The cytotoxic effects of bovine seminal ribonuclease (BS-RNase) against thyroid carcinoma cell lines with different degrees of differentiation in comparison to non-malignant cells, including human foreskin fibroblasts (HFF) and retinal pigment epithelial cells (RPE), were tested using the MTT dye reduction assay.
  • The antitumoral in vivo effects of BS-RNase were assessed on established xenografts of anaplastic thyroid carcinoma cell line 8505C in nude mice using subcutaneous injections of BS-RNase (12.5 mg/kg once a day, on 20 consecutive days).
  • The greatest growth inhibition was seen in the 8505C line, while IC50 values for papillary (B-CPAP) and poorly-differentiated thyroid carcinoma cells were about 6-fold higher.
  • In vivo treatment induced significant tumor regression after the course of 20 consecutive days.
  • No apparent toxic effects of BS-RNase toward non-malignant cells were observed during the in vivo treatment.
  • After cessation of therapy (day 20) tumor volume continued to decrease and the tumor was no longer detectable after 30 days of treatment induction in all animals.
  • CONCLUSION: BS-RNase may have beneficial effects for treatment of aggressive anaplastic thyroid cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Endoribonucleases / therapeutic use. Thyroid Neoplasms / drug therapy

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  • (PMID = 11396137.001).
  • [ISSN] 0250-7005
  • [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 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Fasl protein, mouse; 0 / Membrane Glycoproteins; 0 / Proto-Oncogene Proteins c-bcl-2; EC 3.1.- / Endoribonucleases; EC 3.1.27.- / ribonuclease SPL
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20. Haupt K, Siegel F, Lu M, Yang D, Hilken G, Mann K, Roggendorf M, Saller B: Induction of a cellular and humoral immune response against preprocalcitonin by genetic i: a potential new treatment for medullary thyroid carcinoma. Endocrinology; 2001 Mar;142(3):1017-23
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  • [Title] Induction of a cellular and humoral immune response against preprocalcitonin by genetic i: a potential new treatment for medullary thyroid carcinoma.
  • Currently, no effective therapy exists for patients suffering from progressive medullary thyroid carcinoma (MTC), a calcitonin (CT)-secreting C cell tumor.
  • Two groups were coinjected with mouse cytokine genes.
  • Our findings may have implications for the use of DNA immunization as a potential novel immunotherapeutic treatment for patients suffering from progressive MTC.
  • [MeSH-major] Calcitonin / immunology. Carcinoma, Medullary / therapy. Genetic Techniques. Immunization / methods. Protein Precursors / immunology. Thyroid Neoplasms / therapy
  • [MeSH-minor] Animals. Antibody Formation. Cell Division / drug effects. Female. Gene Expression. Humans. Immunity, Cellular. Mice. Mice, Inbred BALB C. Plasmids / genetics. Recombinant Proteins / genetics. Recombinant Proteins / immunology. Recombinant Proteins / pharmacology. T-Lymphocytes / cytology

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  • (PMID = 11181514.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Precursors; 0 / Recombinant Proteins; 80296-97-5 / preprocalcitonin; 9007-12-9 / Calcitonin
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21. Stein R, Goldenberg DM: A humanized monoclonal antibody to carcinoembryonic antigen, labetuzumab, inhibits tumor growth and sensitizes human medullary thyroid cancer xenografts to dacarbazine chemotherapy. Mol Cancer Ther; 2004 Dec;3(12):1559-64
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  • [Title] A humanized monoclonal antibody to carcinoembryonic antigen, labetuzumab, inhibits tumor growth and sensitizes human medullary thyroid cancer xenografts to dacarbazine chemotherapy.
  • The purpose of this study was to investigate the effect that an anti-CEA monoclonal antibody (MAb) may have on the growth of medullary thyroid cancer (MTC), a CEA-expressing tumor, alone and in combination with chemotherapy.
  • Antitumor effects were evaluated in a nude mouse-human MTC xenograft model.
  • The effects of time of administration post-tumor injection, MAb dose response, specificity of response, and combination with dacarbazine (DTIC) chemotherapy were studied.
  • In addition, labetuzumab sensitizes these tumor cells to chemotherapy with an effective drug in this model, DTIC, without increased toxicity.
  • Significant delays in tumor growth were caused by the MAb therapy or chemotherapy alone; however, the combination of these agents was significantly more effective than either agent given as a monotherapy or use of an irrelevant MAb in this model.
  • The superiority of the combined modality treatment argues for the integration of CEA MAb therapy into chemotherapeutic regimens for MTC management and possibly other CEA-expressing neoplasms.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents, Alkylating / therapeutic use. Carcinoembryonic Antigen / immunology. Carcinoma, Medullary / drug therapy. Dacarbazine / therapeutic use. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Mice. Mice, Nude. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 15634649.001).
  • [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 / Antibodies, Monoclonal; 0 / Antineoplastic Agents, Alkylating; 0 / Carcinoembryonic Antigen; 7GR28W0FJI / Dacarbazine
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22. Luong QT, O'Kelly J, Braunstein GD, Hershman JM, Koeffler HP: Antitumor activity of suberoylanilide hydroxamic acid against thyroid cancer cell lines in vitro and in vivo. Clin Cancer Res; 2006 Sep 15;12(18):5570-7
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  • [Title] Antitumor activity of suberoylanilide hydroxamic acid against thyroid cancer cell lines in vitro and in vivo.
  • EXPERIMENTAL DESIGN: We treated several anaplastic and papillary thyroid cancer cell lines with SAHA to determine if it could inhibit the growth of these cells in vitro and in vivo.
  • RESULTS: SAHA effectively inhibited 50% clonal growth of the anaplastic thyroid cancer cell lines, ARO and FRO, and the papillary thyroid cancer cell line, BHP 7-13, at 1.3x10(-7) to 5x10(-7) mol/L, doses that are achievable in patients.
  • Annexin V and cleavage of poly(ADP)ribose polymerase were both increased by exposure of the thyroid cancer cells to SAHA.
  • Of note, the combination of paclitaxel, doxorubicin, or paraplatin with SAHA enhanced cell killing of the thyroid cancer cells.
  • In addition, murine studies showed that SAHA administered daily by i.p. injection at 100 mg/kg inhibited the growth of human thyroid tumor cells.
  • CONCLUSION: Our data indicate that SAHA is a plausible adjuvant therapy for thyroid cancers.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Hydroxamic Acids / therapeutic use. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis Regulatory Proteins / metabolism. Carboplatin / therapeutic use. Carcinoma / drug therapy. Carcinoma / metabolism. Cell Cycle Proteins / metabolism. Cell Proliferation / drug effects. Cell Survival / drug effects. Doxorubicin / therapeutic use. Drug Therapy, Combination. Histone Deacetylase Inhibitors. Humans. Mice. Paclitaxel / therapeutic use. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. Signal Transduction / drug effects. Treatment Outcome. Tumor Cells, Cultured. Tumor Stem Cell Assay. Xenograft Model Antitumor Assays

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  • (PMID = 17000694.001).
  • [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 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Cell Cycle Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Tnfrsf10b protein, mouse; 58IFB293JI / vorinostat; 80168379AG / Doxorubicin; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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23. 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.
  • We hypothesized that PLX4720 (an inhibitor of B-Raf(V600E)) and thyroidectomy would extend survival and would decrease tumor burden in a mouse model.
  • METHODS: Orthotopic anaplastic thyroid tumors were induced in severe combined immunodeficient mice.
  • RESULTS: All 5 mice that received the vehicle developed cachexia, had invasive tumors (average 61 mm(3))and were sacrificed by day 35.
  • 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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24. Zhang R, DeGroot LJ: Genetic immunotherapy of established tumours with adenoviral vectors transducing murine interleukin-12 (mIL12) subunits in a rat medullary thyroid carcinoma model. Clin Endocrinol (Oxf); 2000 Jun;52(6):687-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic immunotherapy of established tumours with adenoviral vectors transducing murine interleukin-12 (mIL12) subunits in a rat medullary thyroid carcinoma model.
  • To reduce systemic toxicity and obtain local production of IL12, we developed a replication defective adenovirus transducing two subunits of the murine IL12 (AdCMVmIL12) gene.
  • Biological activity of virally expressed mIL12 was demonstrated in vitro through its ability to induce proliferation of mouse ConA blast cells.
  • RESULTS: Rat medullary thyroid carcinoma (MTC) cells infected with AdCMVmIL12 lost their tumorigenicity in their syngenic WAG/Rij rat hosts.
  • After intratumoural treatment with AdCMVmIL12, 86% of tumour bearing animals were apparently cured, and almost all remaining tumours were stabilized.
  • Challenge studies showed that most animals cured after the first treatment remained tumour free after reinjection of wild type rMTC cells, indicating that long-term antitumour immunity developed.
  • CONCLUSIONS: This study demonstrates the construction of an adenoviral vector expressing a functional heterodimeric mIL12 and its efficient antitumour activity after in vivo delivery in an animal model of medullary thyroid carcinoma.
  • [MeSH-major] Carcinoma, Medullary / therapy. Genetic Therapy / methods. Immunotherapy, Active / methods. Interleukin-12 / genetics. Thyroid Neoplasms / therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Concanavalin A / pharmacology. Cytomegalovirus / genetics. Gene Expression. Genetic Vectors / administration & dosage. Genetic Vectors / genetics. Humans. Mice. Rats. Rats, Inbred Strains. Spleen / drug effects. Transfection / methods. Tumor Cells, Cultured






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