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1. Friedman S, Lu M, Schultz A, Thomas D, Lin RY: CD133+ anaplastic thyroid cancer cells initiate tumors in immunodeficient mice and are regulated by thyrotropin. PLoS One; 2009;4(4):e5395
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  • [Title] CD133+ anaplastic thyroid cancer cells initiate tumors in immunodeficient mice and are regulated by thyrotropin.
  • BACKGROUND: Anaplastic thyroid cancer (ATC) is one of the most lethal human malignancies.
  • Its rapid onset and resistance to conventional therapeutics contribute to a mean survival of six months after diagnosis and make the identification of thyroid-cancer-initiating cells increasingly important.
  • METHODOLOGY/PRINCIPAL FINDINGS: In prior studies of ATC cell lines, CD133(+) cells exhibited stem-cell-like features such as high proliferation, self-renewal and colony-forming ability in vitro.
  • We also describe how the proportion of ATC cells that are CD133(+) increases dramatically over three months of culture, from 7% to more than 80% of the total.
  • They also express high levels of the stem cell antigen Oct4 and the receptor for thyroid stimulating hormone, TSHR.
  • Treating ATC cells with TSH causes a three-fold increase in the numbers of CD133(+) cells and elicits a dose-dependent up-regulation of the expression of TSHR and Oct4 in these cells.
  • More importantly, immunohistochemical analysis of tissue specimens from ATC patients indicates that CD133 is highly expressed on tumor cells but not on neighboring normal thyroid cells.
  • CONCLUSIONS/SIGNIFICANCE: To our knowledge, this is the first report indicating that CD133(+) ATC cells are solely responsible for tumor growth in immunodeficient mice.
  • These highly tumorigenic CD133(+) cells and the activated TSH signaling pathway may be useful targets for future ATC therapies.
  • [MeSH-major] Antigens, CD / analysis. Glycoproteins / analysis. Neoplasm Transplantation / methods. Peptides / analysis. Thyroid Neoplasms / pathology. Thyrotropin / pharmacology

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  • (PMID = 19404394.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK068057
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides; 9002-71-5 / Thyrotropin
  • [Other-IDs] NLM/ PMC2671400
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2. Nobuhara Y, Onoda N, Yamashita Y, Yamasaki M, Ogisawa K, Takashima T, Ishikawa T, Hirakawa K: Efficacy of epidermal growth factor receptor-targeted molecular therapy in anaplastic thyroid cancer cell lines. Br J Cancer; 2005 Mar 28;92(6):1110-6
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  • [Title] Efficacy of epidermal growth factor receptor-targeted molecular therapy in anaplastic thyroid cancer cell lines.
  • Anaplastic thyroid cancer is one of the most aggressive human malignancies and the outcomes of conventional therapy have been far from satisfactory.
  • Recently, epidermal growth factor receptor (EGFR)-targeted therapy has been introduced as an alternative therapeutic strategy for highly malignant cancers.
  • This study was undertaken to investigate the expression of EGFR in anaplastic thyroid cancer cell lines, and to explore the potential of therapies targeting EGFR as a new therapeutic approach.
  • EGFR was universally expressed in anaplastic cancer cell lines at a variety of levels.
  • Specific EGFR stimulation with epidermal growth factor showed significant phosphorylation of ERK1/2 and Akt, and resulted in marked growth stimulation in an anaplastic thyroid cancer cell line, which highly expressed EGFR.
  • This EGFR-transmitted proliferation effect of the cancer cell line was completely inhibited by gefitinib, an EGFR tyrosine kinase inhibitor.
  • Inhibition of EGFR-transmitted growth stimulation by gefitinib was clearly observed in anaplastic thyroid cancer cell lines.
  • Our results suggested that EGFR-targeted therapy, such as gefitinib, might be worth further investigation for the treatment of anaplastic thyroid cancer.
  • [MeSH-major] Carcinoma / drug therapy. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Thyroid Neoplasms / drug therapy


3. Patel KN, Shaha AR: Poorly differentiated and anaplastic thyroid cancer. Cancer Control; 2006 Apr;13(2):119-28
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  • [Title] Poorly differentiated and anaplastic thyroid cancer.
  • BACKGROUND: Poorly differentiated thyroid carcinoma (PDTC) and anaplastic (undifferentiated) thyroid carcinoma (ATC) comprise a small subset of thyroid tumors that are associated with a poor prognosis and account for a significant portion of the morbidity and mortality related to thyroid cancer.
  • Since management strategies vary between these two entities, it is important for clinicians to be able to differentiate PDTC from ATC.
  • METHODS: We reviewed the literature on PDTC and ATC and compared clinical and histopathologic features important in defining the disease process.
  • RESULTS: Both PDTC and ATC display aggressive behavior with increased locoregional and distant disease.
  • PDTC may represent an intermediate entity in the progression of well-differentiated thyroid carcinoma to ATC.
  • The use of surgical management may be curative or palliative and differs between PDTC and ATC.
  • CONCLUSIONS: PDTC and ATC are rare diseases that carry a poor prognosis.
  • [MeSH-major] Carcinoma / pathology. Thyroid Neoplasms / pathology


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4. Francipane MG, Eterno V, Spina V, Bini M, Scerrino G, Buscemi G, Gulotta G, Todaro M, Dieli F, De Maria R, Stassi G: Suppressor of cytokine signaling 3 sensitizes anaplastic thyroid cancer to standard chemotherapy. Cancer Res; 2009 Aug 1;69(15):6141-8
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  • [Title] Suppressor of cytokine signaling 3 sensitizes anaplastic thyroid cancer to standard chemotherapy.
  • We previously showed that cancer cells from papillary, follicular, and anaplastic thyroid carcinomas produce interleukin-4 and interleukin-10, which counteract the cytotoxic activity of conventional chemotherapy through the up-regulation of antiapoptotic molecules.
  • Here, we identify Janus kinase/signal transducers and activators of transcription (STAT) and phosphatidyl inositol 3-kinase (PI3K)/AKT as the down-stream pathways through which these cytokines confer resistance to cell death in thyroid cancer.
  • Exogenous expression of SOCS1, SOCS3, and SOCS5 in the highly aggressive anaplastic thyroid cancer cells reduces or abolishes STAT3 and 6 phosphorylation and PI3K/Akt pathway activation resulting in alteration in the balance of proapoptotic and antiapoptotic molecules and sensitization to chemotherapeutic drugs in vitro.
  • Our results indicate that SOCS3 regulation of cytokines-prosurvival programs might represent a new strategy to overcome the resistance to chemotherapy-induced cell death of thyroid cancer.
  • [MeSH-major] Suppressor of Cytokine Signaling Proteins / genetics. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / genetics

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  • (PMID = 19638576.001).
  • [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 / SOCS1 protein, human; 0 / SOCS3 protein, human; 0 / SOCS5 protein, human; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT6 Transcription Factor; 0 / STAT6 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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5. Onda M, Akaishi J, Asaka S, Okamoto J, Miyamoto S, Mizutani K, Yoshida A, Ito K, Emi M: Decreased expression of haemoglobin beta (HBB) gene in anaplastic thyroid cancer and recovery of its expression inhibits cell growth. Br J Cancer; 2005 Jun 20;92(12):2216-24
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  • [Title] Decreased expression of haemoglobin beta (HBB) gene in anaplastic thyroid cancer and recovery of its expression inhibits cell growth.
  • Anaplastic thyroid cancer (ATC) is one of the most fulminant and foetal diseases in human malignancies.
  • However, the genetic alterations and carcinogenic mechanisms of ATC are still unclear.
  • Recently, we investigated the gene expression profile of 11 anaplastic thyroid cancer cell lines (ACL) and significant decreased expression of haemoglobin beta (HBB) gene in ACL.
  • Haemoglobin beta is located at 11p15.5, where loss of heterozygosity (LOH) was reported in various kinds of cancers, including ATC, and it has been suggested that novel tumour suppressor genes might exist in this region.
  • In order to clarify the meaning of decreased expression of HBB in ATC, the expression status of HBB was investigated with ACL, ATC, papillary thyroid cancer (PTC) and normal human tissues.
  • Haemoglobin beta showed significant decreased expression in ACLs and ATCs; however, in PTC, HBB expressed equal to the normal thyroid gland.
  • The mechanism of downregulation of HBB in ATC is still unclear; however, our results suggested the possibility of HBB as a novel tumour-suppressor gene.
  • [MeSH-major] Carcinoma / genetics. Globins / genetics. Thyroid Neoplasms / genetics

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  • (PMID = 15956966.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hemoglobins; 9004-22-2 / Globins
  • [Other-IDs] NLM/ PMC2361827
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6. Jin N, Jiang T, Rosen DM, Nelkin BD, Ball DW: Dual inhibition of mitogen-activated protein kinase kinase and mammalian target of rapamycin in differentiated and anaplastic thyroid cancer. J Clin Endocrinol Metab; 2009 Oct;94(10):4107-12
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  • [Title] Dual inhibition of mitogen-activated protein kinase kinase and mammalian target of rapamycin in differentiated and anaplastic thyroid cancer.
  • CONTEXT: Differentiated thyroid cancer and anaplastic thyroid cancer tumors frequently have activation of the ras/raf /MAPK kinase (MEK)/ERK and phosphatidylinositol 3-kinase (PI-3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathways.
  • OBJECTIVE: The objective of the study was to investigate the efficacy of MEK and mTOR inhibitors in preclinical thyroid cancer treatment models with defined mutation status.
  • EXPERIMENTAL DESIGN: The MEK inhibitor AZD6244 (ARRY-142886) and mTOR inhibitor rapamycin were tested separately and in combination in 10 differentiated thyroid cancer and anaplastic thyroid cancer cell lines and in a xenograft model for evidence of pathway inhibition, growth inhibition, apoptosis, and long-range adaptation and resistance.
  • CONCLUSION: These preclinical results support the inclusion of thyroid cancer patients in early-phase clinical trials combining RAS/RAF/MEK/ERK and PI-3K/AKT/mTOR pathway inhibition.


7. Liu AH, Juan LY, Yang AH, Chen HS, Lin HD: Anaplastic thyroid cancer with uncommon long-term survival. J Chin Med Assoc; 2006 Oct;69(10):489-91
MedlinePlus Health Information. consumer health - Thyroid Cancer.

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  • [Title] Anaplastic thyroid cancer with uncommon long-term survival.
  • In general, most thyroid cancers are indolent and have a slowly progressive course.
  • The exception is anaplastic thyroid cancer.
  • Here, we present a patient with anaplastic thyroid cancer who survived for more than 10 years after diagnosis.
  • A 68-year-old man was incidentally found to have anaplastic thyroid cancer during operation for follicular neoplasm.
  • The patient also had chronic obstructive pulmonary disease and unfortunately died of pneumonia in a local hospital 10 years after thyroid operation.
  • [MeSH-major] Carcinoma / mortality. Thyroid Neoplasms / mortality

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  • (PMID = 17098674.001).
  • [ISSN] 1726-4901
  • [Journal-full-title] Journal of the Chinese Medical Association : JCMA
  • [ISO-abbreviation] J Chin Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
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8. 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.
  • Both ciglitazone and rosiglitazone showed complex biological effects in ATC cells, including inhibition of anchorage-dependent and -independent growth and migration, and increased apoptosis rate.
  • Finally, rosiglitazone increased the expression of thyroid-specific differentiation markers.
  • In conclusions, these data suggest that PPAR gamma agonists induce a partial reversion of the epithelial mesenchymal transition in ATC cells by multiple mechanisms.
  • PPAR gamma agonists may, therefore, have a role in the multimodal therapy currently used to slow down ATC growth and dissemination.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma / pathology. Epithelial Cells / pathology. Mesoderm / pathology. PPAR gamma / agonists. Thyroid Neoplasms / pathology


9. Catalano MG, Pugliese M, Poli R, Bosco O, Bertieri R, Fortunati N, Boccuzzi G: Effects of the histone deacetylase inhibitor valproic acid on the sensitivity of anaplastic thyroid cancer cell lines to imatinib. Oncol Rep; 2009 Feb;21(2):515-21
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  • [Title] Effects of the histone deacetylase inhibitor valproic acid on the sensitivity of anaplastic thyroid cancer cell lines to imatinib.
  • New therapeutic approaches are mandatory for anaplastic thyroid cancer.
  • We investigated the ability of a new combined treatment using valproic acid (VPA), the only clinically available histone deacetylase inhibitor, and the tyrosine-kinase inhibitor imatinib mesylate to control the cell growth of anaplastic thyroid cancer cell lines.
  • We showed that treatment with imatinib alone is unable to affect the cell growth of anaplastic thyroid cancer cells, whereas in ARO cells, the combined treatment resulted in a cytostatic effect, with clinically achievable doses of imatinib and VPA.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cell Proliferation / drug effects. Enzyme Inhibitors / administration & dosage. Thyroid Neoplasms / drug therapy

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  • (PMID = 19148530.001).
  • [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] 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 614OI1Z5WI / Valproic Acid; 8A1O1M485B / Imatinib Mesylate
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10. Haddad R, Mahadevan A, Posner MR, Sullivan C: Long term survival with adjuvant carboplatin, paclitaxel, and radiation therapy in anaplastic thyroid cancer. Am J Clin Oncol; 2005 Feb;28(1):104
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  • [Title] Long term survival with adjuvant carboplatin, paclitaxel, and radiation therapy in anaplastic thyroid cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / therapy. Thyroid Neoplasms / therapy

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  • (PMID = 15685044.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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11. Hogan T, Jing Jie Yu, Williams HJ, Altaha R, Xiaobing Liang, Qi He: Oncocytic, focally anaplastic, thyroid cancer responding to erlotinib. J Oncol Pharm Pract; 2009 Jun;15(2):111-7
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  • [Title] Oncocytic, focally anaplastic, thyroid cancer responding to erlotinib.
  • OBJECTIVE: To highlight the molecular findings and clinical response of a patient with rapidly progressing, focally anaplastic, oncocytic thyroid carcinoma (OTC) treated with erlotinib.Case Summary.
  • A 69-year-old woman with recurrent, focally anaplastic OTC was given a therapeutic trial of erlotinib, a small molecule inhibitor of epidermal growth factor receptor (EGFR).
  • CONCLUSION: Erlotinib or other novel protein kinase pathway inhibitors should be evaluated further in patients with aggressive thyroid cancer variants, who may exhibit these and perhaps other tyrosine kinase mutations.
  • [MeSH-major] Carcinoma / drug therapy. Carcinoma / pathology. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / pathology

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  • (PMID = 19276143.001).
  • [ISSN] 1078-1552
  • [Journal-full-title] Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners
  • [ISO-abbreviation] J Oncol Pharm Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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12. Podtcheko A, Ohtsuru A, Namba H, Saenko V, Starenki D, Palona I, Sedliarou I, Rogounovitch T, Yamashita S: Inhibition of ABL tyrosine kinase potentiates radiation-induced terminal growth arrest in anaplastic thyroid cancer cells. Radiat Res; 2006 Jan;165(1):35-42
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  • [Title] Inhibition of ABL tyrosine kinase potentiates radiation-induced terminal growth arrest in anaplastic thyroid cancer cells.
  • Gleevec, a selective tyrosine kinase inhibitor, retarded the growth of anaplastic thyroid cancer cell lines in vitro and in vivo through selective inhibition of ABL tyrosine kinase activity.
  • In the present study, we investigated the ability of Gleevec to modulate the in vitro and in vivo radiation response of anaplastic thyroid cancer cells.
  • Cell growth assays, colony formation assays and xenograft models were used to quantify the radiosensitizing effect of Gleevec in cells of the anaplastic thyroid cancer cell lines ARO and FRO.
  • Gleevec combined with radiation produced an increase in tumor growth inhibition compared to treatment with either modality alone in mice bearing anaplastic thyroid cancer xenografts.
  • The drug suppressed radiation-induced ABL activation and promoted CDKN1A (p21(cip1)) accumulation in irradiated anaplastic thyroid cancer cells.
  • [MeSH-major] Carcinoma / enzymology. Carcinoma / pathology. Piperazines / administration & dosage. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism. Pyrimidines / administration & dosage. Thyroid Neoplasms / enzymology. Thyroid Neoplasms / pathology

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  • (PMID = 16392960.001).
  • [ISSN] 0033-7587
  • [Journal-full-title] Radiation research
  • [ISO-abbreviation] Radiat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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13. She M, Yang H, Sun L, Yeung SC: Redox control of manumycin A-induced apoptosis in anaplastic thyroid cancer cells: involvement of the xenobiotic apoptotic pathway. Cancer Biol Ther; 2006 Mar;5(3):275-80
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  • [Title] Redox control of manumycin A-induced apoptosis in anaplastic thyroid cancer cells: involvement of the xenobiotic apoptotic pathway.
  • Our previous studies demonstrated that manumycin A, a farnesyltransferase inhibitor, induced apoptosis of anaplastic thyroid cancer cells via the intrinsic apoptosis pathway and induced reactive oxygen species (ROS), which mediated DNA damage.
  • In this study, we investigated the hypothesis that the mechanism of apoptosis induced by manumycin in anaplastic thyroid cancer cells fits the general pattern of the "xenobiotic apoptosis pathway," the hallmarks of which are induction of oxidative stress, mitogen-activated protein kinase (MAPK) signaling, and cytochrome c release, which activates the intrinsic apoptosis pathway.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Polyenes / metabolism. Polyenes / pharmacology. Polyunsaturated Alkamides / metabolism. Polyunsaturated Alkamides / pharmacology. Thyroid Neoplasms / metabolism. Thyroid Neoplasms / pathology

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  • (PMID = 16410725.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Polyenes; 0 / Polyunsaturated Alkamides; 0 / Reactive Oxygen Species; 31C4KY9ESH / Nitric Oxide; 52665-74-4 / manumycin; 9007-43-6 / Cytochromes c; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspase 3; GAN16C9B8O / Glutathione
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14. Larsson K, Kåreholt I, Thorslund M: Care utilisation in the last years of life in relation to age and time to death: results from a Swedish urban population of the oldest old. Eur J Ageing; 2008 Dec;5(4):349-357

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  • The proportion residing in institutional care facilities with around-the-clock care increased steadily with a sharper gradient 6 months before death.

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  • [Cites] J Aging Health. 2004 Nov;16(5):641-68 [15448276.001]
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  • (PMID = 28798585.001).
  • [ISSN] 1613-9372
  • [Journal-full-title] European journal of ageing
  • [ISO-abbreviation] Eur J Ageing
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Keywords] NOTNLM ; End-of-life care / Hospitalisation / Institutionalisation / Swedish elder care
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15. Bhatia A, Rao A, Ang KK, Garden AS, Morrison WH, Rosenthal DI, Evans DB, Clayman G, Sherman SI, Schwartz DL: Anaplastic thyroid cancer: Clinical outcomes with conformal radiotherapy. Head Neck; 2010 Jul;32(7):829-36
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  • [Title] Anaplastic thyroid cancer: Clinical outcomes with conformal radiotherapy.
  • BACKGROUND: The aim of this study was to review institutional outcomes for anaplastic thyroid cancer treated with conformal 3-dimensional radiotherapy (3DRT) or intensity-modulated radiotherapy (IMRT).
  • Patients without distant metastases receiving >or=50 Gy had superior survival outcomes; 5 such patients had no evidence of disease at last follow-up.
  • CONCLUSIONS: Outcomes for anaplastic thyroid cancer treated with 3DRT or IMRT remain equivalent to historical results.
  • Healthy patients with localized disease who tolerate full dose irradiation can potentially enjoy prolonged survival.
  • [MeSH-major] Radiotherapy, Intensity-Modulated. Thyroid Neoplasms / mortality. Thyroid Neoplasms / radiotherapy


16. 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.
  • When overexpressed, either exogenously or endogenously, DUSP26 promoted growth of the ATC cells.
  • DUSP26 effectively dephosphorylates p38 and has a little effect on extracellular signal-regulated kinase in ATC cells.
  • DUSP26 protein formed a physical complex with p38, and promoted survival of ATC cells by inhibiting p38-mediated apoptosis.
  • Our findings suggest that DUSP26 may act as an oncogene in ATC, and might be a useful diagnostic marker and therapeutic target of this disease.
  • [MeSH-major] Carcinoma / pathology. Gene Amplification. Protein Tyrosine Phosphatases / genetics. Thyroid Neoplasms / pathology. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors

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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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17. Abbosh PH, Li X, Li L, Gardner TA, Kao C, Nephew KP: A conditionally replicative, Wnt/beta-catenin pathway-based adenovirus therapy for anaplastic thyroid cancer. Cancer Gene Ther; 2007 Apr;14(4):399-408
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  • [Title] A conditionally replicative, Wnt/beta-catenin pathway-based adenovirus therapy for anaplastic thyroid cancer.
  • Thyroid cancer affects between 10,000 and 15,000 people per year in the US.
  • Typically, this disease can be controlled with surgical resection and radioiodide treatment.
  • However, resistance to these conventional therapies is observed in some patients, who develop intractable anaplastic thyroid cancer (ATC), for which no effective therapies exist.
  • Recently, a sizable fraction of undifferentiated or poorly differentiated thyroid cancers were shown to contain mutations in beta-catenin, an oncogenic protein involved in the etiology of cancers of many tissues.
  • We show that several thyroid cancer cell lines, derived from undifferentiated or anaplastic tissues and possessing an active Wnt/beta-catenin pathway, are susceptible to cell killing by HILMI.
  • Furthermore, viral replication in ATC cells as xenograft tumors in nude mice was observed, and prolonged survival of mice with ATC tumors was observed following administration of the HILMI therapeutic vector.
  • The results warrant further development of this therapeutic approach for ATC patients.
  • [MeSH-major] Adenoviridae / genetics. Genetic Therapy. Thyroid Neoplasms / therapy. Virus Replication / genetics. beta Catenin / genetics

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  • (PMID = 17218945.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA-85289
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin
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18. Akaishi J, Onda M, Okamoto J, Miyamoto S, Nagahama M, Ito K, Yoshida A, Shimizu K: Down-regulation of an inhibitor of cell growth, transmembrane protein 34 (TMEM34), in anaplastic thyroid cancer. J Cancer Res Clin Oncol; 2007 Apr;133(4):213-8
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  • [Title] Down-regulation of an inhibitor of cell growth, transmembrane protein 34 (TMEM34), in anaplastic thyroid cancer.
  • PURPOSE: Ansaplastic thyroid cancer (ATC) is one of the most lethal malignancies, but the carcinogenic mechanism of ATC has not been clarified.
  • Recently, we performed a cDNA microarray analysis and identified transmembrane protein 34 (TMEM34) that down-regulated in anaplastic thyroid cancer cell lines (ACL)s as compared to normal thyroid tissues.
  • METHODS: To investigate the role of TMEM34 in ATC carcinogenesis, we examined expression levels of TMEM34 in ACLs as well as differentiated thyroid cancers (DTC)s and normal human tissues.
  • To explore the effect of TMEM34 in ATC development, cell-growth assays with KTA2 cells were performed.
  • RESULTS: Expression of TMEM34 was down-regulated in all 11 ACLs, as compared to either normal thyroid tissues or cell lines derived from papillary or follicular thyroid cancers.
  • CONCLUSIONS: Our findings suggest that TMEM34 might be a tumor suppressor gene, associated with the development of ATC from DTC.
  • [MeSH-major] Carcinoma / genetics. Cell Growth Processes / genetics. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Membrane Proteins / metabolism. Thyroid Neoplasms / genetics. Tumor Suppressor Proteins / metabolism

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  • (PMID = 17072649.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Membrane Proteins; 0 / RNA, Neoplasm; 0 / Tumor Suppressor Proteins; 0 / transmembrane protein 34, human
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19. Kim TH, Lee SY, Rho JH, Jeong NY, Soung YH, Jo WS, Kang DY, Kim SH, Yoo YH: Mutant p53 (G199V) gains antiapoptotic function through signal transducer and activator of transcription 3 in anaplastic thyroid cancer cells. Mol Cancer Res; 2009 Oct;7(10):1645-54
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  • [Title] Mutant p53 (G199V) gains antiapoptotic function through signal transducer and activator of transcription 3 in anaplastic thyroid cancer cells.
  • In the present study, we identified a missense mutation (G199V) in KAT-18 cell line established from primary cultures of anaplastic thyroid cancer (ATC).
  • In addition, overexpression of STAT3 protected ATC cells against cell death induced by p53 knockdown.
  • Taken together, these data show that mt p53 (G199V) gains antiapoptotic function mediated by STAT3 in ATC cells.
  • Inhibition of the function of mt p53 (G199V) could be a novel and useful therapeutic strategy for decreasing the extent and severity of toxicity due to chemotherapeutic agents.
  • [MeSH-major] Apoptosis / genetics. Carcinoma / genetics. Mutation, Missense / genetics. STAT3 Transcription Factor / genetics. Thyroid Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 19825993.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Interleukin-6; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Tumor Suppressor Protein p53
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20. Meng Z, Mitsutake N, Nakashima M, Starenki D, Matsuse M, Takakura S, Namba H, Saenko V, Umezawa K, Ohtsuru A, Yamashita S: Dehydroxymethylepoxyquinomicin, a novel nuclear Factor-kappaB inhibitor, enhances antitumor activity of taxanes in anaplastic thyroid cancer cells. Endocrinology; 2008 Nov;149(11):5357-65
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  • [Title] Dehydroxymethylepoxyquinomicin, a novel nuclear Factor-kappaB inhibitor, enhances antitumor activity of taxanes in anaplastic thyroid cancer cells.
  • Nuclear factor kappaB (NF-kappaB), as an antiapoptotic factor, crucially affects the outcomes of cancer treatments, being one of the major culprits of resistance to chemotherapy.
  • In this study, we investigated whether dehydroxymethylepoxyquinomicin (DHMEQ), a novel NF-kappaB inhibitor, can enhance antitumor activities of taxanes in anaplastic thyroid cancer (ATC) cells.
  • Taxanes induced NF-kappaB activation in ATC cells, which could compromise the therapeutic effect of the drugs.
  • These findings suggest that taxanes are able to induce NF-kappaB activation in ATC cells, which could attenuate antitumor activities of the drugs, but inhibition of NF-kappaB by DHMEQ creates a chemosensitive environment and greatly enhances apoptosis in taxanes-treated ATC cells in vitro and in vivo.
  • Thus, DHMEQ may emerge as an attractive therapeutic strategy to enhance the response to taxanes in ATCs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Benzamides / pharmacology. Carcinoma / drug therapy. Cyclohexanones / pharmacology. NF-kappa B / antagonists & inhibitors. Taxoids / administration & dosage. Thyroid Neoplasms / drug therapy

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  • (PMID = 18653704.001).
  • [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 / Benzamides; 0 / Cyclohexanones; 0 / NF-kappa B; 0 / Peptides; 0 / SN50 peptide; 0 / Taxoids; 0 / dehydroxymethylepoxyquinomicin
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21. Green LD, Mack L, Pasieka JL: Anaplastic thyroid cancer and primary thyroid lymphoma: a review of these rare thyroid malignancies. J Surg Oncol; 2006 Dec 15;94(8):725-36
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  • [Title] Anaplastic thyroid cancer and primary thyroid lymphoma: a review of these rare thyroid malignancies.
  • BACKGROUND: To review the current literature on the treatment of anaplastic thyroid cancer (ATC) and thyroid lymphoma (TL).
  • RESULTS: Both anaplastic carcinoma (ATC) and TL represent rare forms of thyroid cancer.
  • ATC behaves in a highly aggressive manner, resulting in significant morbidity and mortality.
  • Although ATC has been relatively chemo resistant, newer agents such like taxotere show promise.
  • The role of surgery in the treatment of ATC continues to evolve, presently it should be reserved for patients who have shown an initial response to multimodality therapy and in patients in whom a complete macroscopic resection can be achieved with minimal morbidity.
  • DISCUSSION: Although both ATC and TL are rare, it is important for surgeons to be aware of the need for multimodality therapy when treating these patients and to understand the limited role surgery plays in diagnosis and treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma. Lymphoma. Thyroid Neoplasms. Thyroidectomy


22. Akaishi J, Onda M, Okamoto J, Miyamoto S, Nagahama M, Ito K, Yoshida A, Shimizu K: Down-regulation of transcription elogation factor A (SII) like 4 (TCEAL4) in anaplastic thyroid cancer. BMC Cancer; 2006;6:260
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  • [Title] Down-regulation of transcription elogation factor A (SII) like 4 (TCEAL4) in anaplastic thyroid cancer.
  • BACKGROUND: Anaplastic thyroid cancer (ATC) is one of the most aggressive human malignancies and appears to arise mainly from transformation of pre-existing differentiated thyroid cancer (DTC).
  • However, the carcinogenic mechanism of anaplastic transformation remains unclear.
  • Previously, we investigated specific genes related to ATC based on gene expression profiling using cDNA microarray analysis.
  • The detailed function of TCEAL4 has not been described nor has any association between this gene and human cancers been reported previously.
  • METHODS: To investigate the role of TCEAL4 in ATC carcinogenesis, we examined expression levels of TCEAL4 in ACLs as well as in other types of thyroid cancers and normal human tissue.
  • RESULTS: Expression of TCEAL4 was down-regulated in all 11 ACLs as compared to either normal thyroid tissues or papillary and follicular thyroid cancerous tissues.
  • CONCLUSION: To our knowledge, this is the first report of altered TCEAL4 expression in human cancers.
  • We suggest that loss of TCEAL4 expression might be associated with development of ATC from DTC.
  • [MeSH-major] Carcinoma / genetics. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / genetics. Thyroid Neoplasms / genetics. Transcriptional Elongation Factors / genetics
  • [MeSH-minor] Adenocarcinoma, Follicular / genetics. Adenocarcinoma, Follicular / metabolism. Adenocarcinoma, Follicular / pathology. Adult. Aged. Carcinoma, Papillary / genetics. Carcinoma, Papillary / metabolism. Carcinoma, Papillary / pathology. Cell Line, Tumor / metabolism. Cell Transformation, Neoplastic / genetics. DNA, Complementary / genetics. Disease Progression. Down-Regulation. Female. Gene Expression Profiling. Humans. Male. Middle Aged. Neoplasms / metabolism. Neoplasms / pathology. Organ Specificity. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Messenger / isolation & purification. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. RNA, Neoplasm / immunology. Reverse Transcriptase Polymerase Chain Reaction. Thyroid Gland / metabolism

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  • (PMID = 17076909.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / TCEAL4 protein, human; 0 / Transcriptional Elongation Factors
  • [Other-IDs] NLM/ PMC1635733
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23. Catalano MG, Fortunati N, Pugliese M, Poli R, Bosco O, Mastrocola R, Aragno M, Boccuzzi G: Valproic acid, a histone deacetylase inhibitor, enhances sensitivity to doxorubicin in anaplastic thyroid cancer cells. J Endocrinol; 2006 Nov;191(2):465-72
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  • [Title] Valproic acid, a histone deacetylase inhibitor, enhances sensitivity to doxorubicin in anaplastic thyroid cancer cells.
  • Multimodality treatments (i.e. surgery, chemotherapy, and radiotherapy) are recommended for anaplastic thyroid carcinoma (ATC), an extremely lethal human cancer, but to date there is little evidence that such approaches improve survival rates.
  • It is thus necessary to seek new therapeutic tools.
  • Using two ATC cell lines (CAL-62 and ARO), we show here that valproic acid (VPA), a clinically available HDAC inhibitor, enhances the activity of doxorubicin, whose anti-tumor properties involve binding to DNA and inhibiting topoisomerase II.
  • These results might offer a rationale for clinical studies of a new combined therapy in an effort to improve the outcome of patients with anaplastic thyroid cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma / drug therapy. Doxorubicin / therapeutic use. Histone Deacetylase Inhibitors. Thyroid Neoplasms / drug therapy. Valproic Acid / therapeutic use

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  • (PMID = 17088416.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / RNA, Messenger; 614OI1Z5WI / Valproic Acid; 80168379AG / Doxorubicin; EC 3.4.22.- / Caspase 3; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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24. O'Neill JP, Power D, Condron C, Bouchier-Hayes D, Walsh M: Anaplastic thyroid cancer, tumorigenesis and therapy. Ir J Med Sci; 2010 Mar;179(1):9-15
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  • [Title] Anaplastic thyroid cancer, tumorigenesis and therapy.
  • BACKGROUND: Anaplastic thyroid cancer (ATC) is a fatal endocrine malignancy.
  • Recent insights into thyroid tumorigenesis, post-malignant dedifferentiation and mode of metastatic activity offer new therapeutic strategies.
  • METHODS: An extensive literature search of Medline and Pubmed was conducted to include all published reports on ATC.
  • CONCLUSIONS: Significant progress, in the last 5 years, has been made outlining thyroid tumorigenesis and the progression to anaplasia.
  • [MeSH-major] Thyroid Neoplasms / surgery
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Cadherins. Cyclins. Disease Progression. Humans. Radiotherapy. Receptor, Epidermal Growth Factor. Vascular Endothelial Growth Factor A. beta Catenin

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  • (PMID = 19662494.001).
  • [ISSN] 1863-4362
  • [Journal-full-title] Irish journal of medical science
  • [ISO-abbreviation] Ir J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cadherins; 0 / Cyclins; 0 / Vascular Endothelial Growth Factor A; 0 / beta Catenin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 54
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25. Celano M, Schenone S, Cosco D, Navarra M, Puxeddu E, Racanicchi L, Brullo C, Varano E, Alcaro S, Ferretti E, Botta G, Filetti S, Fresta M, Botta M, Russo D: Cytotoxic effects of a novel pyrazolopyrimidine derivative entrapped in liposomes in anaplastic thyroid cancer cells in vitro and in xenograft tumors in vivo. Endocr Relat Cancer; 2008 Jun;15(2):499-510
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  • [Title] Cytotoxic effects of a novel pyrazolopyrimidine derivative entrapped in liposomes in anaplastic thyroid cancer cells in vitro and in xenograft tumors in vivo.
  • In this study, we evaluated the activity of two novel pyrazolopyrimidine derivatives (Si 34 and Si 35) against ARO cells, a human anaplastic thyroid cancer cell line.
  • When entrapped in unilamellar liposomes, Si 34 exerted its cytotoxic effects even at lower doses (maximal inhibition at 5 microM) and after shorter incubation time (48 h) either in ARO or other thyroid cancer cell lines.
  • In conclusion, the liposomal preparation of this novel pyrazolopyrimidine derivative appears to be a promising tool for the treatment of anaplasic thyroid cancer.
  • [MeSH-major] Liposomes / pharmacokinetics. Pyrazoles / pharmacokinetics. Pyrimidines / pharmacokinetics. Thyroid Neoplasms / drug therapy. Triazoles / pharmacokinetics


26. Yeung SC, She M, Yang H, Pan J, Sun L, Chaplin D: Combination chemotherapy including combretastatin A4 phosphate and paclitaxel is effective against anaplastic thyroid cancer in a nude mouse xenograft model. J Clin Endocrinol Metab; 2007 Aug;92(8):2902-9
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  • [Title] Combination chemotherapy including combretastatin A4 phosphate and paclitaxel is effective against anaplastic thyroid cancer in a nude mouse xenograft model.
  • CONTEXT: Anaplastic thyroid cancer (ATC) is extremely aggressive, and no effective treatment is available.
  • Combretastatin A4 phosphate (CA4P), a vascular disrupting agent, has limited activity against ATC in a clinical trial, and so does paclitaxel.
  • OBJECTIVE: We hypothesized that a triple-drug combination including CA4P and paclitaxel would improve efficacy against ATC.
  • CONCLUSIONS: Both triple-drug combinations demonstrated excellent antineoplastic activity against ATC.
  • These regimens warrant further investigation in clinical trials for ATC.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / drug therapy. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / metabolism. Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Phytogenic / administration & dosage. Bromodeoxyuridine / metabolism. Carboplatin / therapeutic use. Cell Line, Tumor. Cell Shape. Endothelial Cells / pathology. Endothelial Cells / ultrastructure. Humans. Immunohistochemistry. Mice. Mice, Nude. Microscopy, Electron, Transmission. Neoplasm Transplantation. Paclitaxel / administration & dosage. Polyenes / therapeutic use. Polyunsaturated Alkamides / therapeutic use. Stilbenes / administration & dosage. Transplantation, Heterologous

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  • (PMID = 17550961.001).
  • [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 / CA16672
  • [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 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Polyenes; 0 / Polyunsaturated Alkamides; 0 / Stilbenes; 52665-74-4 / manumycin; BG3F62OND5 / Carboplatin; G34N38R2N1 / Bromodeoxyuridine; I5590ES2QZ / fosbretabulin; P88XT4IS4D / Paclitaxel
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27. Schweppe RE, Kerege AA, French JD, Sharma V, Grzywa RL, Haugen BR: Inhibition of Src with AZD0530 reveals the Src-Focal Adhesion kinase complex as a novel therapeutic target in papillary and anaplastic thyroid cancer. J Clin Endocrinol Metab; 2009 Jun;94(6):2199-203
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  • [Title] Inhibition of Src with AZD0530 reveals the Src-Focal Adhesion kinase complex as a novel therapeutic target in papillary and anaplastic thyroid cancer.
  • CONTEXT: Focal adhesion kinase (FAK) and Src are overexpressed and activated in many cancers and have been associated with tumor progression.
  • The role of the Src-FAK complex has not been characterized in papillary and anaplastic thyroid cancer (PTC and ATC).
  • OBJECTIVE: The goal of this study was to determine the role of Src and FAK in the growth and invasion of PTC and ATC.
  • DESIGN: PTC and ATC cells were treated with the oral Src inhibitor, AZD0530, to determine the consequences of Src inhibition using growth and invasion assays.
  • RESULTS: AZD0530 treatment inhibited the growth and invasion in four of five thyroid cancer cell lines, and inhibition did not correlate with basal levels of phospho-Src.
  • Instead, we show for the first time that FAK, a critical substrate and effector of Src, is phosphorylated at tyrosine residue 861 (pY861) in PTC and ATC cells, and high levels of phospho-FAK correlate with AZD0530 sensitivity.
  • CONCLUSIONS: Inhibition of the Src-FAK complex represents a promising therapeutic strategy for patients with advanced thyroid cancer, and phospho-FAK represents a potential biomarker for response.

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  • (PMID = 19293266.001).
  • [ISSN] 1945-7197
  • [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 / CA100560; United States / NCI NIH HHS / CA / P30 CA 046934; United States / NCI NIH HHS / CA / P30 CA046934; United States / NCI NIH HHS / CA / R01 CA100560; United States / NCI NIH HHS / CA / K12 CA086913
  • [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 / Antineoplastic Agents; 0 / Benzodioxoles; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 9KD24QGH76 / saracatinib; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src)
  • [Other-IDs] NLM/ PMC2690419
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28. Haas V, Celakovský P, Brtková J, Hornychová H: Unusual manifestation of anaplastic thyroid cancer. Acta Medica (Hradec Kralove); 2008;51(4):233-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unusual manifestation of anaplastic thyroid cancer.
  • The diagnosis of anaplastic thyroid cancer was made after surgery and subsequent histological examination.
  • The histological examination of the lymph nodes identified metastasis of anaplastic thyroid cancer.
  • CONCLUSIONS: The differential diagnosis of diseases affecting deep neck structures can be very difficult.

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  • (PMID = 19453090.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Czech Republic
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29. Ha HT, Lee JS, Urba S, Koenig RJ, Sisson J, Giordano T, Worden FP: A phase II study of imatinib in patients with advanced anaplastic thyroid cancer. Thyroid; 2010 Sep;20(9):975-80
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  • [Title] A phase II study of imatinib in patients with advanced anaplastic thyroid cancer.
  • BACKGROUND: Currently, there is no standard treatment for metastatic anaplastic thyroid cancer (ATC).
  • DNA microarray analysis has shown platelet-dervived growth factor receptor (PDGFR) overexpression in ATC relative to well-differentiated thyroid cancer.
  • In p53-mutated/deficient ATC cell lines, cABL is overexpressed, and selective inhibition of cABL results in a cytostatic effect.
  • We hypothesize that patients with ATC that over-expresses PDGF receptors or cABL will respond to imatinib.
  • METHODS: Patients with histologically confirmed ATC who had measurable disease and whose disease expressed PDGF receptors by immunohistochemistry were eligible for study.
  • Patients with complete response, partial responses, or stable disease were treated until disease progression.
  • At baseline, 4/11 had locoregional disease, 5/11 had distant metastases, and 2/11 had both.
  • The overall response rates at 8 weeks were complete response 0/8, partial response 2/8, and stable disease 4/8.
  • CONCLUSIONS: Imatinib appears to have activity in advanced ATC and is well tolerated.
  • Due to difficulty of accruing patients with a rare malignancy at a single institution, further investigation of imatinib in ATC may be warranted in a multi-institutional setting.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Aged. Benzamides. Disease-Free Survival. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Receptors, Platelet-Derived Growth Factor / analysis. Receptors, Platelet-Derived Growth Factor / antagonists & inhibitors

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  • (PMID = 20718683.001).
  • [ISSN] 1557-9077
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
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30. Kumar V, Blanchon B, Gu X, Fowler M, Scarborough D, Nathan CO, Yaturu S: Anaplastic thyroid cancer and hyperthyroidism. Endocr Pathol; 2005;16(3):245-50
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  • [Title] Anaplastic thyroid cancer and hyperthyroidism.
  • We report a rare case of thyrotoxicosis in a patient with anaplastic thyroid cancer.
  • Physical examination revealed a large, hard thyroid mass and resting tachycardia.
  • Thyroid hormone levels were consistent with a hyperthyroid state.
  • CT scan of the neck and thorax showed a heterogeneous mass replacing the thyroid, bilateral pulmonary nodules, and a metastasis with pathological fracture at the level of T-8.
  • Technetium-pertechnetate scan failed to show any uptake in the region of the thyroid.
  • Fine needle aspiration of the thyroid revealed anaplastic thyroid cancer.
  • Brief surgical exploration of the thyroid revealed extensive local infiltration of adjacent neck tissues and marked tumor necrosis.
  • Immunohistochemical stains of the tumor were positive for p53, thyroglobulin, and thyroid transcription factor-1.
  • [MeSH-major] Carcinoma / complications. Thyroid Neoplasms / complications. Thyrotoxicosis / complications
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Bone Neoplasms / secondary. Bone Neoplasms / therapy. Fatal Outcome. Glucocorticoids / therapeutic use. Humans. Male. Radiotherapy, Adjuvant

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  • (PMID = 16299408.001).
  • [ISSN] 1046-3976
  • [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 / Biomarkers, Tumor; 0 / Glucocorticoids
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31. Behlendorf T, Voigt W, Mueller T, Jordan K, Arnold D, Schmoll H: Activity of mTOR-Inhibitor Rad001 (everolimus) in differentiated and anaplastic thyroid cancer cell lines. J Clin Oncol; 2009 May 20;27(15_suppl):e14608

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of mTOR-Inhibitor Rad001 (everolimus) in differentiated and anaplastic thyroid cancer cell lines.
  • : e14608 Background: Recent data suggest that aberrant activation of PIK3/AKT-pathway and mTOR are involved in the development of thyroid cancer, particularly of anaplastic (ATC) and follicular (FTC) subtype.
  • Therefore, mTOR could be a potential treatment target in thyroid cancer.
  • METHODS: To asses the potential role of mTOR as target for the treatment of thyroid cancer, two human ATC cell lines SW1736 and 8505C, the papillary thyroid cancer (PTC) cell line BCPAP and the FTC cell line FTC133 were exposed for 96h to increasing concentrations of the mTOR inhibitor RAD001 (Everolimus, kindly provided by Novartis, Switzerland).
  • CONCLUSION: RAD001 exerted interesting preclinical activity in two differentiated thyroid cancer cell lines.
  • Mainly additive drug interaction in thyroid cancer cell lines was observed for combinations with CDDP and DOX.
  • At least for differentiated thyroid cancer mTOR-inhibition appeared promising, further evaluation in thyroid cancer seems warranted.

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  • (PMID = 27964164.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Lee YJ, Chung JK, Kang JH, Jeong JM, Lee DS, Lee MC: Wild-type p53 enhances the cytotoxic effect of radionuclide gene therapy using sodium iodide symporter in a murine anaplastic thyroid cancer model. Eur J Nucl Med Mol Imaging; 2010 Feb;37(2):235-41
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  • [Title] Wild-type p53 enhances the cytotoxic effect of radionuclide gene therapy using sodium iodide symporter in a murine anaplastic thyroid cancer model.
  • PURPOSE: To evaluate the role of p53 in radionuclide gene therapy, we investigated the cytotoxic effect of (131)I and (188)Re following cotransfection of the sodium iodide symporter (NIS) and wild-type p53 (wt-p53) genes into cancer cells.
  • METHODS: The NIS gene was transfected to human anaplastic thyroid carcinoma cells (ARO) expressing mutant p53 (mt-p53) using liposomes.
  • Transfection of the NIS gene into human anaplastic thyroid cancer induced the accumulation of beta-emitter radionuclides, and cotransfection with a wt-p53 gene enhanced the cytotoxic effect.
  • [MeSH-major] Disease Models, Animal. Genetic Therapy / methods. Radioisotopes / therapeutic use. Symporters / therapeutic use. Thyroid Neoplasms / therapy. Tumor Suppressor Protein p53 / therapeutic use
  • [MeSH-minor] Animals. Cell Line, Tumor. Combined Modality Therapy. Humans. Mice. Mice, Nude. Radiopharmaceuticals / therapeutic use. Treatment Outcome

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  • (PMID = 19727716.001).
  • [ISSN] 1619-7089
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radioisotopes; 0 / Radiopharmaceuticals; 0 / Symporters; 0 / Tumor Suppressor Protein p53; 0 / sodium-iodide symporter
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33. Smallridge RC, Marlow LA, Copland JA: Anaplastic thyroid cancer: molecular pathogenesis and emerging therapies. Endocr Relat Cancer; 2009 Mar;16(1):17-44
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  • [Title] Anaplastic thyroid cancer: molecular pathogenesis and emerging therapies.
  • Anaplastic thyroid cancer (ATC) is a rare malignancy.
  • The objective of this study was to review the literature in order to identify potential new strategies for treating this highly lethal cancer.
  • The molecular pathogenesis of ATC includes mutations in BRAF, RAS, catenin (cadherin-associated protein), beta 1, PIK3CA, TP53, AXIN1, PTEN, and APC genes, and chromosomal abnormalities are common.
  • Several microarray studies have identified genes and pathways preferentially affected, and dysregulated microRNA profiles differ from differentiated thyroid cancers.
  • A variety of agents have been successful in controlling ATC cell growth both in vitro and in nude mice xenografts.
  • While many of these new compounds are in cancer clinical trials, there are few studies being conducted in ATC.
  • With the recent increased knowledge of the many critical genes and proteins affected in ATC, and the extensive array of targeted therapies being developed for cancer patients, there are new opportunities to design clinical trials based upon tumor molecular profiling and preclinical studies of potentially synergistic combinatorial novel therapies.

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  • (PMID = 18987168.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA015083-35; United States / NCI NIH HHS / CA / P30 CA015083; United States / NCI NIH HHS / CA / P30 CA015083-35; United States / NCI NIH HHS / CA / P30CA15083
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 227
  • [Other-IDs] NLM/ NIHMS175598; NLM/ PMC2829440
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34. Antonelli A, Ferrari SM, Fallahi P, Berti P, Materazzi G, Minuto M, Giannini R, Marchetti I, Barani L, Basolo F, Ferrannini E, Miccoli P: Thiazolidinediones and antiblastics in primary human anaplastic thyroid cancer cells. Clin Endocrinol (Oxf); 2009 Jun;70(6):946-53
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  • [Title] Thiazolidinediones and antiblastics in primary human anaplastic thyroid cancer cells.
  • OBJECTIVE: No study has evaluated the antiproliferative effects of thiazolidinediones and antiblastics in 'primary cultured human anaplastic thyroid cancer cells'.
  • DESIGN: Primary anaplastic cells proliferation was evaluated after incubation with increasing concentrations of rosiglitazone or pioglitazone or antiblastics (bleomycin, cisplatin, gemcitabine) by a proliferation assay (WST-1-tetrazolium reaction) and cell counting.
  • No significant thiazolidinediones effect was observed in normal thyroid follicular cells.
  • Bleomycin, cisplatin and gemcitabine significantly (P < 0.0001) inhibited (> 50%) anaplastic cells proliferation.
  • CONCLUSIONS: Thiazolidinediones exert an antiproliferative effect in primary cultured human anaplastic carcinoma cells in vitro, such as antiblastics.
  • [MeSH-major] Carcinoma / drug therapy. Cell Proliferation / drug effects. Growth Inhibitors / pharmacology. Thiazolidinediones / pharmacology. Thyroid Neoplasms / drug therapy

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  • (PMID = 18785992.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Growth Inhibitors; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; X4OV71U42S / pioglitazone
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35. Broome JT, Gauger PG, Miller BS, Doherty GM: Anaplastic thyroid cancer manifesting as new-onset Horner syndrome. Endocr Pract; 2009 Sep-Oct;15(6):563-6
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  • [Title] Anaplastic thyroid cancer manifesting as new-onset Horner syndrome.
  • OBJECTIVE: To report a case of Horner syndrome as the initial sign of locally advanced anaplastic thyroid cancer.
  • METHODS: We present a case report in conjunction with a retrospective review and evaluation of the English-language literature on Horner syndrome and thyroid pathologic conditions.
  • RESULTS: Horner syndrome is a rare complication of thyroid disease most often occurring in the postoperative setting after resections.
  • Malignant thyroid disease leading to Horner syndrome is less common than benign causes of the syndrome.
  • CONCLUSION: Horner syndrome is a rare complication of thyroid pathologic conditions.
  • [MeSH-major] Carcinoma / diagnosis. Horner Syndrome / diagnosis. Nerve Compression Syndromes / diagnosis. Thyroid Neoplasms / diagnosis
  • [MeSH-minor] Aged. Cervical Plexus. Chemotherapy, Adjuvant. Diagnosis, Differential. Female. Humans. Radiotherapy, Adjuvant. Thyroidectomy

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  • (PMID = 19491063.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 6
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36. Poisson T, Deandreis D, Leboulleux S, Bidault F, Bonniaud G, Baillot S, Aupérin A, Al Ghuzlan A, Travagli JP, Lumbroso J, Baudin E, Schlumberger M: 18F-fluorodeoxyglucose positron emission tomography and computed tomography in anaplastic thyroid cancer. Eur J Nucl Med Mol Imaging; 2010 Dec;37(12):2277-85
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  • [Title] 18F-fluorodeoxyglucose positron emission tomography and computed tomography in anaplastic thyroid cancer.
  • PURPOSE: Our aim was to evaluate in anaplastic thyroid carcinoma (ATC) patients the value of 18F-FDG PET/CT compared with total body computed tomography (CT) using intravenous contrast material for initial staging, prognostic assessment, therapeutic monitoring and follow-up.
  • METHODS: Twenty consecutive ATC patients underwent PET/CT for initial staging.
  • In three patients, the extent of disease was significantly changed with PET/CT that demonstrated unknown metastases.
  • CONCLUSION: FDG PET/CT appears to be the reference imaging modality for ATC at initial staging and seems promising in the early evaluation of treatment response and follow-up.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Radiopharmaceuticals. Reproducibility of Results. Sensitivity and Specificity. Thyroid Carcinoma, Anaplastic. Thyroid Neoplasms / radiography. Thyroid Neoplasms / radionuclide imaging

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  • (PMID = 20694463.001).
  • [ISSN] 1619-7089
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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37. García-Rostán G, Costa AM, Pereira-Castro I, Salvatore G, Hernandez R, Hermsem MJ, Herrero A, Fusco A, Cameselle-Teijeiro J, Santoro M: Mutation of the PIK3CA gene in anaplastic thyroid cancer. Cancer Res; 2005 Nov 15;65(22):10199-207
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutation of the PIK3CA gene in anaplastic thyroid cancer.
  • The phosphatidylinositol 3'-kinase (PI3K) pathway is frequently activated in thyroid carcinomas through the constitutive activation of stimulatory molecules (e.g., Ras) and/or the loss of expression and/or function of the inhibitory PTEN protein that results in Akt activation.
  • Recently, it has been reported that somatic mutations within the PI3K catalytic subunit, PIK3CA, are common (25-40%) among colorectal, gastric, breast, ovarian cancers, and high-grade brain tumors.
  • In this study, 13 thyroid cancer cell lines, 80 well-differentiated thyroid carcinomas of follicular (WDFC) and papillary (WDPC) type, and 70 anaplastic thyroid carcinomas (ATC) were investigated, by PCR-direct sequencing, for activating PIK3CA mutations at exons 9 and 20.
  • Nonsynonymous somatic mutations were found in 16 ATC (23%), two WDFC (8%), and one WDPC (2%).
  • In 18 of the 20 ATC cases showing coexisting differentiated carcinoma, mutations, when present, were restricted to the ATC component and located primarily within the kinase domain.
  • In addition, activation of Akt was observed in most of the ATC harboring PIK3CA mutations.
  • These findings indicate that mutant PIK3CA is likely to function as an oncogene among ATC and less frequently well-differentiated thyroid carcinomas.
  • The data also argue for a role of PIK3CA targeting in the treatment of ATC patients.
  • [MeSH-major] Carcinoma / genetics. Mutation, Missense. Phosphatidylinositol 3-Kinases / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma, Follicular / enzymology. Adenocarcinoma, Follicular / genetics. Adenocarcinoma, Follicular / pathology. Amino Acid Substitution. Carcinoma, Papillary / enzymology. Carcinoma, Papillary / genetics. Carcinoma, Papillary / pathology. Cell Growth Processes / genetics. Cell Line, Tumor. Enzyme Activation. Genes, p53 / genetics. Genes, ras / genetics. Humans. Oncogene Protein v-akt / metabolism. Proto-Oncogene Proteins B-raf / genetics


38. Lin SF, Price DL, Chen CH, Brader P, Li S, Gonzalez L, Zhang Q, Yu YA, Chen N, Szalay AA, Fong Y, Wong RJ: Oncolytic vaccinia virotherapy of anaplastic thyroid cancer in vivo. J Clin Endocrinol Metab; 2008 Nov;93(11):4403-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oncolytic vaccinia virotherapy of anaplastic thyroid cancer in vivo.
  • CONTEXT: Anaplastic thyroid carcinoma (ATC) is a fatal disease with a median survival of only 6 months.
  • OBJECTIVE: A mutated, replication-competent, vaccinia virus (GLV-1h68) has oncolytic effects on human ATC cell lines in vitro.
  • We assessed the utility of GLV-1h68 in treating anaplastic thyroid cancer in vivo.
  • CONCLUSIONS: GLV-1h68 efficiently infects, expresses transgenes within, and inhibits the growth of ATC in vivo.
  • These promising findings support future clinical trials for patients with ATC.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Carcinoma / immunology. Thyroid Neoplasms / immunology. Vaccinia virus / immunology. Viral Vaccines / therapeutic use

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  • (PMID = 18697871.001).
  • [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 / T32 CA009685
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Genetic Markers; 0 / Viral Vaccines
  • [Other-IDs] NLM/ PMC3728375
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39. Dackiw AP: Anaplastic thyroid cancer. Cancer Treat Res; 2010;153:75-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic thyroid cancer.
  • [MeSH-major] Carcinoma / therapy. Thyroid Neoplasms / therapy


40. Kawada K, Kitagawa K, Kamei S, Inada M, Mitsuma A, Sawaki M, Kikumori T, Fujimoto Y, Arima H, Imai T, Ando Y: The feasibility study of docetaxel in patients with anaplastic thyroid cancer. Jpn J Clin Oncol; 2010 Jun;40(6):596-9
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  • [Title] The feasibility study of docetaxel in patients with anaplastic thyroid cancer.
  • There is no established chemotherapy for anaplastic thyroid cancer.
  • We conducted a prospective feasibility study at a single center to explore the antitumor activity of docetaxel against anaplastic thyroid cancer.
  • Docetaxel was administered intravenously at a dose of 60 mg/m(2) over the course of 1 h every 3 weeks in patients with anaplastic thyroid cancer who had received no prior chemotherapy.
  • A total of seven patients with anaplastic thyroid cancer were enrolled over the course of 30 months and received docetaxel.
  • The treatment response was complete response in one patient, stable disease in two and progressive disease in four.
  • The response rate was 14%, and the disease control rate (complete response plus stable disease) was 43%.
  • Docetaxel could be an effective drug for the treatment of anaplastic thyroid cancer, with tolerable toxicity.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carcinoma / drug therapy. Taxoids / administration & dosage. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Aged. Disease Progression. Feasibility Studies. Female. Humans. Infusions, Intravenous. Lung Neoplasms / secondary. Male

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  • (PMID = 20200039.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel
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41. Catalano MG, Costantino L, Fortunati N, Bosco O, Pugliese M, Boccuzzi G, Berta L, Frairia R: High energy shock waves activate 5'-aminolevulinic Acid and increase permeability to Paclitaxel: antitumor effects of a new combined treatment on anaplastic thyroid cancer cells. Thyroid; 2007 Feb;17(2):91-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High energy shock waves activate 5'-aminolevulinic Acid and increase permeability to Paclitaxel: antitumor effects of a new combined treatment on anaplastic thyroid cancer cells.
  • OBJECTIVE: Multimodal treatments do not meaningfully improve survival of anaplastic thyroid cancer.
  • Consequently, new effective therapeutic modalities are needed.
  • The use of paclitaxel is under clinical investigation; it shows about a 50% response rate, but it is not able to alter the fatal outcome for patients with anaplastic carcinoma.
  • 5-Aminolevulinic acid (ALA) is used in the photodynamic therapy (PDT) of cancer, and HESW are under evaluation for their use as an activator in ALA-PDT.
  • DESIGN: We investigated the effect of HESW produced by a piezoelectric generator on the sensitivity to paclitaxel and ALA treatments of two different anaplastic thyroid cancer cell lines (ARO and CAL-62).
  • MAIN OUTCOME: Combined exposure to ALA, paclitaxel, and shock waves resulted in a significant enhancement of cytotoxicity and induction of apoptosis in thyroid cancer cells with respect to cells treated with paclitaxel alone.
  • CONCLUSIONS: These preliminary data suggest the possibility of using HESW and ALA in combination with paclitaxel as a promising new therapy in the treatment of anaplastic thyroid cancer.
  • [MeSH-major] Aminolevulinic Acid / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma / therapy. Cell Membrane Permeability. High-Energy Shock Waves. Paclitaxel / pharmacology. Photochemotherapy. Thyroid Neoplasms / therapy

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  • (PMID = 17316109.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 88755TAZ87 / Aminolevulinic Acid; P88XT4IS4D / Paclitaxel
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42. Nagaiah G, Fu P, Wasman JK, Cooney MM, Mooney C, Afshin D, Lavertu P, Bokar J, Savvides P, Remick SC, CTRU Research Nurses: Phase II trial of sorafenib (bay 43-9006) in patients with advanced anaplastic carcinoma of the thyroid (ATC). J Clin Oncol; 2009 May 20;27(15_suppl):6058

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of sorafenib (bay 43-9006) in patients with advanced anaplastic carcinoma of the thyroid (ATC).
  • We are conducting an open label, phase II study of sorafenib in patients with biopsy-proven ATC to evaluate if its objective response rate is >20% and to further characterize its safety profile.
  • METHODS: Patients with progressive ATC, after cytotoxic chemotherapy with or without radiation were given sorafenib, on a fixed dosing schedule of 400 mg PO bid on 28-day cycles.
  • Treatment was continued until disease progression, unacceptable toxicity or patient refusal.
  • Two of 15 evaluable patients (13%) have partial response (PR) and 4 patients (27%) have stable disease (SD).
  • One patient died on study with rapidly progressive disease.
  • CONCLUSIONS: Sorafenib demonstrates objective tumor response in the first 15 evaluable and pretreated patients with advanced ATC.

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  • (PMID = 27961935.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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43. Brose MS, Troxel AB, Redlinger M, Harlacker K, Redlinger C, Chalian AA, Flaherty KT, Loevner LA, Mandel SJ, O'Dwyer PJ: Effect of BRAF&lt;sup&gt;V600E&lt;/sup&gt; on response to sorafenib in advanced thyroid cancer patients. J Clin Oncol; 2009 May 20;27(15_suppl):6002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of BRAF<sup>V600E</sup> on response to sorafenib in advanced thyroid cancer patients.
  • : 6002 Background: We are conducting an open-label phase II study of sorafenib in patients with metastatic, iodine-refractory thyroid carcinoma.
  • Histological subtypes include papillary (PTC): 25 pts (47%); follicular/Hürthle Cell (FTC): 19 pts (36%); medullary: 4 pts (8%), and poorly differentiated/anaplastic: 5 pts (9%).
  • CONCLUSIONS: Sorafenib has activity in patients with advanced thyroid cancer with an overall PFS of 84 wks.

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  • (PMID = 27962409.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Zivaljevic VR, Vlajinac HD, Marinkovic JM, Kalezic NK, Paunovic IR, Diklic AD: Case-control study of anaplastic thyroid cancer: goiter patients as controls. Eur J Cancer Prev; 2008 Apr;17(2):111-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Case-control study of anaplastic thyroid cancer: goiter patients as controls.
  • Anaplastic thyroid cancer is very serious disease with bad prognosis and unknown etiology.
  • The aim of the study was to test some hypotheses about other factors in addition to goiter related to anaplastic thyroid cancer occurrence.
  • The case group comprised 126 patients with newly diagnosed anaplastic thyroid cancer.
  • The control group comprised 252 patients who had for the first time goiter operation, and had no malignancy of thyroid gland.
  • According to conditional multivariate logistic regression analysis, anaplastic thyroid cancer was significantly related to lower education (odds ratio=1.85, 95% confidence interval=1.21-2.82), other malignant tumors in personal history (odds ratio=4.37, 95% confidence interval=1.11-17.31), blood group B (odds ratio=3.69, 95% confidence interval=1.10-12.49), menarche at >or=15 years of age (odds ratio=2.63, 95% confidence interval=1.15-5.88), and first full-term pregnancy before 19 years of age (odds ratio=2.96, 95% confidence interval=1.26-6.96).
  • On the basis of the results obtained, risk factors for anaplastic thyroid cancer are similar to risk factors for differentiated thyroid cancers.
  • [MeSH-major] Carcinoma / epidemiology. Thyroid Neoplasms / epidemiology

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  • (PMID = 18287867.001).
  • [ISSN] 1473-5709
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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45. Flaherty K, Puzanov I, Sosman J, Kim K, Ribas A, McArthur G, Lee RJ, Grippo JF, Nolop K, Chapman P: Phase I study of PLX4032: Proof of concept for V600E BRAF mutation as a therapeutic target in human cancer. J Clin Oncol; 2009 May 20;27(15_suppl):9000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of PLX4032: Proof of concept for V600E BRAF mutation as a therapeutic target in human cancer.
  • V600E BRAF is the most common kinase mutation in melanoma (60%), also found in colorectal carcinomas (10%), most anaplastic and papillary thyroid carcinomas, and low-grade serous ovarian carcinomas.
  • RESULTS: 54 pts have been enrolled: metastatic melanoma (n=49), thyroid (n=3), rectal (n=1), or ovarian carcinoma (n=1).
  • 5 of the 7 BRAF V600E+ pts treated at ≥ 240 mg BID had tumor regression, up to 83%, with 1 confirmed partial response (PR) and 1 unconfirmed PR (too early); 2 of 4 pts with unknown V600E status had tumor regression, up to 50%, with 1 confirmed PR; 2 BRAF wild-type pts had progressive disease.
  • 3 thyroid cancer pts with V600E mutations have tumor regression (range 9-16%) and are progression-free (4-7 months).
  • These observations confirm that V600E BRAF is a valid therapeutic target in human cancer.

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  • (PMID = 27962338.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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46. Sherman EJ, Fury MG, Tuttle RM, Ghossein R, Stambuk H, Baum M, Lisa D, Su YB, Shaha A, Pfister DG: Phase II study of depsipeptide (DEP) in radioiodine (RAI)-refractory metastatic nonmedullary thyroid carcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):6059

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of depsipeptide (DEP) in radioiodine (RAI)-refractory metastatic nonmedullary thyroid carcinoma.
  • : 6059 Background: Historically, systemic therapy for radioactive iodine (RAI)-refractory thyroid cancer has been understudied.
  • In thyroid cancer cell lines, DEP increases expression of both thyroglobulin and the sodium/iodine symporter messenger RNAs, offering the possibility of improved iodine concentrating ability of radioactive iodine (RAI)-resistant tumors.
  • METHODS: Eligible patients (pts) must have progressive, RAI-refractory, recurrent/metastatic, non-medullary, non-anaplastic thyroid cancer; RECIST measurable disease; and adequate organ/marrow function.
  • Exclusionary criteria include prior chemotherapy in the recurrent/metastatic setting; cardiac disease or dysfunction; QTc prolongation or co-administration of drugs that prolong the QTc.
  • Evaluation of response: stable disease (10); progression (3); early death (1); unknown/inevaluable (6: 5 - temporary protocol suspension; 1 - withdrew consent).

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  • (PMID = 27961936.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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47. Catalano MG, Poli R, Pugliese M, Fortunati N, Boccuzzi G: Valproic acid enhances tubulin acetylation and apoptotic activity of paclitaxel on anaplastic thyroid cancer cell lines. Endocr Relat Cancer; 2007 Sep;14(3):839-45
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  • [Title] Valproic acid enhances tubulin acetylation and apoptotic activity of paclitaxel on anaplastic thyroid cancer cell lines.
  • The introduction of paclitaxel into multimodal therapy for anaplastic thyroid carcinoma has failed to improve overall survival.
  • We examined the effect of VPA on the sensitivity to paclitaxel of two anaplastic thyroid carcinoma cell lines (CAL-62 and ARO), and the ability of the drug to determine tubulin acetylation and enhance paclitaxel-induced acetylation.
  • [MeSH-major] Acetyltransferases / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Carcinoma / drug therapy. Paclitaxel / administration & dosage. Thyroid Neoplasms / drug therapy. Tubulin / metabolism. Valproic Acid / pharmacology

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  • (PMID = 17914112.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Enzyme Inhibitors; 0 / Tubulin; 614OI1Z5WI / Valproic Acid; EC 2.3.1.- / Acetyltransferases; P88XT4IS4D / Paclitaxel
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48. Stenner F, Liewen H, Zweifel M, Weber A, Tchinda J, Bode B, Samaras P, Bauer S, Knuth A, Renner C: Targeted therapeutic approach for an anaplastic thyroid cancer in vitro and in vivo. Cancer Sci; 2008 Sep;99(9):1847-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted therapeutic approach for an anaplastic thyroid cancer in vitro and in vivo.
  • Anaplastic thyroid carcinoma (ATC) is among the most aggressive human malignancies, being responsible for the majority of thyroid cancer-related deaths.
  • Despite multimodal therapy including surgery, chemotherapy, and radiotherapy, the outcome of ATC is poor.
  • The human ATC cell line MB1, derived from tumor tissue of a 57-year-old man with thyroid cancer and pronounced neutrophilia, was established from surgically excised tumor tissue.
  • Our observations together with previous data from preclinical models could serve as a rationale for selecting those patients suffering from ATC most likely to benefit from targeted therapy.
  • A prospective controlled randomized trial integrating kinase and proteasome inhibitors into a therapeutic regime for ATC is warranted.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Boronic Acids / therapeutic use. Carcinoma / drug therapy. Pyrazines / therapeutic use. Pyridines / therapeutic use. Thyroid Neoplasms / drug therapy


49. Arlot-Bonnemains Y, Baldini E, Martin B, Delcros JG, Toller M, Curcio F, Ambesi-Impiombato FS, D'Armiento M, Ulisse S: Effects of the Aurora kinase inhibitor VX-680 on anaplastic thyroid cancer-derived cell lines. Endocr Relat Cancer; 2008 Jun;15(2):559-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of the Aurora kinase inhibitor VX-680 on anaplastic thyroid cancer-derived cell lines.
  • Anaplastic thyroid cancers (ATC) are aggressive tumors, which exhibit cell cycle misregulations leading to uncontrolled cellular proliferation and genomic instability.
  • They fail to respond to chemotherapeutic agents and radiation therapy, and most patients die within a few months of diagnosis.
  • In the present study, we evaluated the in vitro effects on ATC cells of VX-680, an inhibitor of the Aurora serine/threonine kinases involved in the regulation of multiple aspects of chromosome segregation and cytokinesis.
  • The effects of VX-680 on proliferation, apoptosis, soft agar colony formation, cell cycle, and ploidy were tested on the ATC-derived cell lines CAL-62, 8305C, 8505C, and BHT-101.
  • Treatment of the different ATC cells with VX-680 inhibited proliferation in a time- and dose-dependent manner, with the IC50 between 25 and 150 nM.
  • In conclusion, our data demonstrated that VX-680 is effective in reducing cell growth of different ATC-derived cell lines and warrant further investigation to exploit its potential therapeutic value for ATC treatment.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Piperazines / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / pathology
  • [MeSH-minor] Agar. Apoptosis / drug effects. Aurora Kinases. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Histones / metabolism. Humans. Microtubule-Associated Proteins / metabolism. Phosphorylation / drug effects. Ploidies. Thyroid Gland / cytology

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  • (PMID = 18430894.001).
  • [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 / Enzyme Inhibitors; 0 / Histones; 0 / Microtubule-Associated Proteins; 0 / Piperazines; 0 / TACC3 protein, human; 639089-54-6 / VX680; 9002-18-0 / Agar; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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50. Rao AS, Kremenevskaja N, von Wasielewski R, Jakubcakova V, Kant S, Resch J, Brabant G: Wnt/beta-catenin signaling mediates antineoplastic effects of imatinib mesylate (gleevec) in anaplastic thyroid cancer. J Clin Endocrinol Metab; 2006 Jan;91(1):159-68
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  • [Title] Wnt/beta-catenin signaling mediates antineoplastic effects of imatinib mesylate (gleevec) in anaplastic thyroid cancer.
  • OBJECTIVE: Conflicting data are reported on the therapeutic effects of imatinib in anaplastic thyroid carcinomas (ATCs), but the molecular mechanism of action is unclear.
  • Here, we further delineated the antitumor effects and the potential efficacy of imatinib in dedifferentiated thyroid carcinomas.
  • Similarily, imatinib-sensitive TKs were detected in seven of 10 thyroid cancer cell lines derived from metastatic papillary, follicular, and ATCs.
  • It stabilized adherens junctions by increasing beta-catenin/E-cadherin binding and reduced the invasive potential of thyroid cancer.
  • CONCLUSION: Our data provide a molecular mechanism for the antitumor activity of imatinib that may help to develop it as a therapeutic option in a subset of ATC patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma / drug therapy. Carcinoma / pathology. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Signal Transduction / drug effects. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / pathology. beta Catenin / physiology

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  • [RetractionIn] J Clin Endocrinol Metab. 2006 Jun;91(6):2118 [16775851.001]
  • (PMID = 16263821.001).
  • [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; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Drug Combinations; 0 / Laminin; 0 / Piperazines; 0 / Proteoglycans; 0 / Pyrimidines; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / beta Catenin; 119978-18-6 / matrigel; 298-93-1 / thiazolyl blue; 8A1O1M485B / Imatinib Mesylate; 9007-34-5 / Collagen; EC 1.13.12.- / Luciferases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP7 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7; EC 3.4.22.- / Caspases; VC2W18DGKR / Thymidine
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51. Pushkarev VM, Starenki DV, Saenko VA, Pushkarev VV, Kovzun OI, Tronko MD, Popadiuk ID, Yamashita S: Differential effects of low and high doses of Taxol in anaplastic thyroid cancer cells: possible implication of the Pin1 prolyl isomerase. Exp Oncol; 2008 Sep;30(3):190-4
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  • [Title] Differential effects of low and high doses of Taxol in anaplastic thyroid cancer cells: possible implication of the Pin1 prolyl isomerase.
  • AIM: To study the molecular mechanisms of dose-dependent effects of an anticancer drug, Taxol, on the cell cycle machinery and apoptosis-related proteins in thyroid anaplastic cancer cell lines ARO and KTC-2.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / administration & dosage. Carcinoma / drug therapy. Paclitaxel / administration & dosage. Peptidylprolyl Isomerase / metabolism. Thyroid Neoplasms / drug therapy

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  • (PMID = 18806740.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / NIMA-interacting peptidylprolyl isomerase; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 5.2.1.8 / Peptidylprolyl Isomerase; P88XT4IS4D / Paclitaxel
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52. Troch M, Koperek O, Scheuba C, Dieckmann K, Hoffmann M, Niederle B, Raderer M: High efficacy of concomitant treatment of undifferentiated (anaplastic) thyroid cancer with radiation and docetaxel. J Clin Endocrinol Metab; 2010 Sep;95(9):E54-7
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  • [Title] High efficacy of concomitant treatment of undifferentiated (anaplastic) thyroid cancer with radiation and docetaxel.
  • CONTEXT: Anaplastic thyroid carcinoma (ATC) is a rare but aggressive solid tumor with a very short survival time even with multimodality treatment.
  • In view of in vitro data and the high rate of p53 mutations in ATC, we have used combined treatment with external beam radiation and docetaxel.
  • PATIENTS: A total of six patients with ATC were treated at our institution.
  • CONCLUSION: The preliminary data suggest that the combination of radiation and concomitant docetaxel is highly effective in patients with ATC.
  • However, a formal phase II study is needed to assess the therapeutic potential of this combination.
  • [MeSH-major] Carcinoma / drug therapy. Carcinoma / radiotherapy. Taxoids / therapeutic use. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / radiotherapy
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Cell Differentiation. Chemotherapy, Adjuvant. Combined Modality Therapy. Dose Fractionation. Female. Humans. Male. Middle Aged. Radiotherapy Dosage. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 20591979.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel
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53. Pudney D, Lau H, Ruether JD, Falck V: Clinical experience of the multimodality management of anaplastic thyroid cancer and literature review. Thyroid; 2007 Dec;17(12):1243-50
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  • [Title] Clinical experience of the multimodality management of anaplastic thyroid cancer and literature review.
  • Anaplastic Thyroid Carcinoma (ATC) is a rare thyroid tumor with a very aggressive clinical course.
  • The following is a report of five patients with inoperable locally advanced disease treated at our institution using multimodality management consisting of chemotherapy and hyperfractionated accelerated radiotherapy.
  • A flow diagram with management recommendations for inoperable ATC is suggested.
  • [MeSH-major] Carcinoma / therapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Combined Modality Therapy. Disease Progression. Female. Humans. Male. Treatment Outcome

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  • (PMID = 18177257.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 44
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54. 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.
  • Using a binary adenoviral vector system, we found that overexpression of Bax enhanced manumycin-induced apoptosis of ATC cells, and the combination of manumycin and overexpression of Bax increased inhibition of ATC xenograft growth in nude mice.
  • Thus, we concluded that manumycin-induced apoptosis in ATC cells was primarily mediated by Bax and that increasing Bax expression may sensitize ATC cells to manumycin.
  • [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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55. Hoffmann S, Maschuw K, Hassan I, Reckzeh B, Wunderlich A, Lingelbach S, Zielke A: Differential pattern of integrin receptor expression in differentiated and anaplastic thyroid cancer cell lines. Thyroid; 2005 Sep;15(9):1011-20
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  • [Title] Differential pattern of integrin receptor expression in differentiated and anaplastic thyroid cancer cell lines.
  • Adhesion of tumor cells to the extracellular matrix (ECM) is a crucial step for the development of metastatic disease and is mediated by specific integrin receptor molecules (IRM).
  • The pattern of metastatic spread differs substantially among the various histotypes of thyroid cancer (TC).
  • IRM expression was investigated in 10 differentiated (FTC133, 236, 238, HTC, HTC TSHr, XTC, PTC4.0/4.2, TPC1, Kat5) and two anaplastic TC cell lines (ATC, C643, Hth74), primary cultures of normal thyroid tissue (Thy1,3), and thyroid cancer specimens (TCS).
  • Thyroid tumor cell adhesion to ECM proteins and their IRM expression in response to thyrotropin (TSH) was assessed.
  • ATC mainly displayed integrins alpha2, alpha3, alpha5, alpha6, beta1 and low levels of alpha1, alpha4 and alphaV.
  • Thyroid carcinoma cell lines of different histogenetic background display profoundly different patterns of IRM expression that appear to correlate with tumor aggressiveness.
  • Finally, TSH-stimulated adhesion of thyroid tumor cell lines to ECM may not be associated with altered IRM expression.
  • [MeSH-major] Carcinoma / genetics. Integrins / biosynthesis. Integrins / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Cell Adhesion. Cell Differentiation / drug effects. Cell Differentiation / genetics. Cell Line, Tumor. Extracellular Matrix Proteins / metabolism. Flow Cytometry. Humans. Paraffin Embedding. Stimulation, Chemical. Thyrotropin / pharmacology


56. Pushkarev VM, Starenki DV, Saenko VA, Yamashita S, Kovzun OI, Popadiuk ID, Pushkarev VV, Tronko MD: Effects of low and high concentrations of antitumour drug taxol in anaplastic thyroid cancer cells. Exp Oncol; 2009 Mar;31(1):16-21
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  • [Title] Effects of low and high concentrations of antitumour drug taxol in anaplastic thyroid cancer cells.
  • AIM: To study the changes of cell cycle, mitochondrial membrane potential and caspase activation in response to an antitumour drug Taxol in ARO and KTC-2 cell lines of anaplastic thyroid carcinoma.
  • METHODS: Experiments were done on thyroid anaplastic cancer cell lines ARO and KTC-2 using Western blotting, flow cytometry, light and fluorescent microscopy.
  • CONCLUSION: Taxol induces bona fide apoptosis in thyroid cancer cell cultures at low (1-25 nM) concentrations.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma / drug therapy. Paclitaxel / pharmacology. Thyroid Neoplasms / drug therapy

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  • (PMID = 19300411.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.4.22.- / Caspases; P88XT4IS4D / Paclitaxel
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57. Koussis H, Maruzzo M, Scola A, Ide EC, Fassina A, Marioni G, Lora O, Corti L, Karachontziti P, Jirillo A: A case of anaplastic thyroid cancer with long-term survival. Anticancer Res; 2010 Apr;30(4):1273-8
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  • [Title] A case of anaplastic thyroid cancer with long-term survival.
  • Anaplastic thyroid carcinoma (ATC) (less than 10% of all thyroid cancer) is a high-grade neoplasm, characterized by an aggressive clinical course and refractoriness to currently available local and systemic modalities of treatment.
  • It is considered the most aggressive solid tumour, there is no adequate therapy for this disease and few patients with ATC live more than 1 year following diagnosis.
  • We report herein an unusual case of ATC in a 59-year-old woman.
  • She received many kinds of chemotherapeutical and multimodal treatment; we obtained a long period of localized disease (about two years) and an excellent response to therapy.
  • She is still alive 58 months from diagnosis.
  • [MeSH-major] Carcinoma / therapy. Thyroid Neoplasms / therapy

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  • (PMID = 20530439.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
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58. Shin HA, Cha YY, Park MS, Kim JM, Lim YC: Diallyl sulfide induces growth inhibition and apoptosis of anaplastic thyroid cancer cells by mitochondrial signaling pathway. Oral Oncol; 2010 Apr;46(4):e15-8
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  • [Title] Diallyl sulfide induces growth inhibition and apoptosis of anaplastic thyroid cancer cells by mitochondrial signaling pathway.
  • Anaplastic thyroid carcinoma (ATC) is one of the most lethal solid tumors arising thyroid gland with dismal prognosis.
  • This study examined whether DAS could induce growth inhibition and apoptosis in ATC cells.
  • Taken together, DAS decreased cell proliferation and induced apoptosis via mitochondrial signaling pathway in ATC cells.
  • [MeSH-minor] Blotting, Western. Caspase 3 / metabolism. Caspase 9 / metabolism. Cell Line, Tumor. Cell Proliferation. Female. Flow Cytometry. Garlic. Humans. Male. Mitochondria / metabolism. Thyroid Carcinoma, Anaplastic. Thyroid Neoplasms / diet therapy. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20219414.001).
  • [ISSN] 1879-0593
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Allyl Compounds; 0 / Anticarcinogenic Agents; 0 / Sulfides; 0 / Tumor Suppressor Protein p53; 60G7CF7CWZ / allyl sulfide; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
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59. Haas V, Čelakovský P, Brtková J, Hornychová H: Unusual Manifestation of Anaplastic Thyroid Cancer. Acta Medica (Hradec Kralove); 2008;51(4):233-236

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unusual Manifestation of Anaplastic Thyroid Cancer.
  • The diagnosis of anaplastic thyroid cancer was made after surgery and subsequent histological examination.
  • The histological examination of the lymph nodes identified metastasis of anaplastic thyroid cancer.
  • CONCLUSIONS: The differential diagnosis of diseases affecting deep neck structures can be very difficult.

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  • (PMID = 28113058.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
  • [Keywords] NOTNLM ; Anaplastic / Metastasis / Retropharyngeal abscess / Thyroid cancer
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60. Gomez-Rivera F, Santillan-Gomez AA, Younes MN, Kim S, Fooshee D, Zhao M, Jasser SA, Myers JN: The tyrosine kinase inhibitor, AZD2171, inhibits vascular endothelial growth factor receptor signaling and growth of anaplastic thyroid cancer in an orthotopic nude mouse model. Clin Cancer Res; 2007 Aug 1;13(15 Pt 1):4519-27
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  • [Title] The tyrosine kinase inhibitor, AZD2171, inhibits vascular endothelial growth factor receptor signaling and growth of anaplastic thyroid cancer in an orthotopic nude mouse model.
  • PURPOSE: Anaplastic thyroid cancer (ATC) is a locally aggressive type of thyroid tumor with high rate of distant metastases.
  • The objective of the study is to determine whether AZD2171 can inhibit VEGFR-2 signaling and decrease tumor growth and prolong survival of ATC in an orthotopic nude mouse model.
  • We assessed the antitumor effects of AZD2171 in a xenograft model of ATC using control, AZD2171, paclitaxel, and combination groups by measuring tumor size and survival.
  • In the ATC cell lines DRO and ARO, IC(50) was 7.5 micromol/L.
  • AZD2171 induced apoptosis in 50% of endothelial and ATC cells at 3 and 10 micromol/L concentrations, respectively.
  • CONCLUSIONS: AZD2171 effectively inhibits tumor growth and prolongs survival of ATC-bearing mice.
  • [MeSH-major] Carcinoma / pathology. Quinazolines / therapeutic use. Thyroid Neoplasms / pathology. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors

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  • (PMID = 17671138.001).
  • [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 / P60 CA097007A
  • [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 / Quinazolines; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; NQU9IPY4K9 / cediranib
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61. Kammori M, Onoda N, Nakamura K, Izumiyama N, Ogisawa K, Kurabayashi R, Ogawa T, Kaminishi M, Poon SS, Takubo K: Specific subtelomere loss on chromosome der(11)t(3;11)(q23;q23)x2 in anaplastic thyroid cancer cell line OCUT-1. Int J Mol Med; 2006 Jul;18(1):9-16
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  • [Title] Specific subtelomere loss on chromosome der(11)t(3;11)(q23;q23)x2 in anaplastic thyroid cancer cell line OCUT-1.
  • One of the most aggressive human malignancies, anaplastic thyroid carcinoma (ATC), has an extremely poor prognosis that may be explained by its genomic instability.
  • We hypothesized that the very rapid cell turnover observed in ATC might accelerate telomere shortening and chromosomal instability associated with tumor cell malignancy.
  • To compare and measure chromosomal aberrations and telomere shortening in the anaplastic thyroid cancer cell line OCUT-1, we applied quantitative fluorescence in situ hybridization (Q-FISH) techniques.
  • In all 15 metaphases studied, telomere length estimates from Q-FISH of chromosomes in ATC were shorter than those of a fibroblast cell line derived from the stroma adjacent to the carcinoma.
  • The karyotype showed 50, XX, +7, +11, der(11)t(3;11)(q23;q23)x2, del(12)(p11.2p12), +20, +1mar.
  • Telomere lengths in the q-arms of the abnormal chromosome del(12)(p11.2p12) were shorter than the average length in the q-arms of the normal chromosome 12 in OCUT-1.
  • Subtelomeres on the abnormal chromosome der(11)t(3;11)(q23;q23)x2 also showed loss of signals on 11p, but there was no loss of signals in the cytogenetically normal trisomies 7 and 20 or the abnormal chromosome del(12)(p11.2p12).
  • Our findings suggest that telomere shortening and subtelomere loss are correlated with genetic instability in this anaplastic thyroid carcinoma cell line.
  • [MeSH-minor] Cell Line, Tumor. Chromosome Banding. DNA-Binding Proteins / genetics. Humans. In Situ Hybridization, Fluorescence. Karyotyping. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Telomerase / genetics. Thyroid Neoplasms / genetics. Thyroid Neoplasms / pathology

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  • (PMID = 16786150.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; EC 2.7.7.49 / Telomerase
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62. Nahari D, Satchi-Fainaro R, Chen M, Mitchell I, Task LB, Liu Z, Kihneman J, Carroll AB, Terada LS, Nwariaku FE: Tumor cytotoxicity and endothelial Rac inhibition induced by TNP-470 in anaplastic thyroid cancer. Mol Cancer Ther; 2007 Apr;6(4):1329-37
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  • [Title] Tumor cytotoxicity and endothelial Rac inhibition induced by TNP-470 in anaplastic thyroid cancer.
  • Anaplastic thyroid carcinoma is an aggressive form of cancer with no treatment.
  • Angiogenesis inhibitors, such as TNP-470, a synthetic derivative of fumagillin, have been shown to reduce tumor size and increase survival in heterotopic animal models of thyroid cancer.
  • Our goals were to determine the effect of TNP-470 on anaplastic thyroid cancer using an orthotopic murine model, to identify the molecular pathways of TNP-470 actions on endothelial cells, and to determine the non-endothelial tumor effects of TNP-470.
  • We injected human anaplastic thyroid carcinoma cells (DRO'90) into the thyroid glands of nude mice.
  • TNP-470 had direct cytotoxic effects on anaplastic thyroid carcinoma cells in vitro and in vivo.

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  • (PMID = 17431111.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL061897; United States / NHLBI NIH HHS / HL / R01 HL067256; United States / NIGMS NIH HHS / GM / R01 GM067674-01A1; United States / NHLBI NIH HHS / HL / R01-HL61897; United States / NHLBI NIH HHS / HL / R01-HL67256; United States / NIGMS NIH HHS / GM / R01 GM067674
  • [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 / Angiogenesis Inhibitors; 0 / Cyclohexanes; 0 / Sesquiterpenes; 0 / Vascular Endothelial Growth Factor A; 129298-91-5 / O-(chloroacetylcarbamoyl)fumagillol; EC 3.6.5.2 / rac GTP-Binding Proteins
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63. 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.
  • 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.
  • In 3 of 6 clinical ATC samples, miR-17-3p and miR-17-5p were robustly overexpressed in cancer lesions compared to adjacent normal tissue.
  • To investigate the functional role of these miRNAs in ATC cells, ARO and FRO cells were transfected with miRNA inhibitors, antisense oligonucleotides containing locked nucleic acids.
  • Thus, we have clarified functional differences among the members of the cluster in ATC cells.
  • In conclusion, these findings suggest that the miR-17-92 cluster plays an important role in certain types of ATCs and could be a novel target for ATC treatment.
  • [MeSH-major] Carcinoma / genetics. Cell Transformation, Neoplastic. Gene Expression Regulation, Neoplastic / genetics. MicroRNAs / genetics. Oncogenes / genetics. Thyroid Neoplasms / genetics

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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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64. Zhong WB, Liang YC, Wang CY, Chang TC, Lee WS: Lovastatin suppresses invasiveness of anaplastic thyroid cancer cells by inhibiting Rho geranylgeranylation and RhoA/ROCK signaling. Endocr Relat Cancer; 2005 Sep;12(3):615-29
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  • [Title] Lovastatin suppresses invasiveness of anaplastic thyroid cancer cells by inhibiting Rho geranylgeranylation and RhoA/ROCK signaling.
  • Previously, we have reported that lovastatin treatment induced the occurrence of apoptosis and differentiation in ARO anaplastic thyroid cancer cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Lovastatin / pharmacology. Neoplasm Invasiveness / prevention & control. Signal Transduction / physiology. Thyroid Neoplasms / pathology. rho GTP-Binding Proteins / metabolism. rhoA GTP-Binding Protein / metabolism

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  • (PMID = 16172195.001).
  • [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 / Actins; 0 / Antineoplastic Agents; 0 / Drug Combinations; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Laminin; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; 9LHU78OQFD / Lovastatin; EC 3.6.5.2 / rho GTP-Binding Proteins; EC 3.6.5.2 / rhoA GTP-Binding Protein
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65. Kurebayashi J, Okubo S, Yamamoto Y, Ikeda M, Tanaka K, Otsuki T, Sonoo H: Additive antitumor effects of gefitinib and imatinib on anaplastic thyroid cancer cells. Cancer Chemother Pharmacol; 2006 Oct;58(4):460-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Additive antitumor effects of gefitinib and imatinib on anaplastic thyroid cancer cells.
  • PURPOSE: Anaplastic thyroid cancer (ATC) is one of the most aggressive malignancies.
  • Although multidisciplinary treatments have been introduced, patients with this disease rarely survive longer than 1 year.
  • These findings prompted us to investigate the antitumor activity of molecular targeting agents in thyroid cancer cells.
  • METHODS: Two tyrosine kinase inhibitors, gefitinib and imatinib, were tested in a poorly differentiated thyroid cancer cell line, KTC-1, and two ATC cell lines, KTC-2 and KTC-3.
  • CONCLUSIONS: These are the first findings to suggest that both gefitinib and imatinib have antitumor activity against ATC cells and that their combined use has greater activity than either drug alone.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Benzamides. Cell Line, Tumor. DNA Primers / genetics. Drug Synergism. Female. Humans. Imatinib Mesylate. Mice. Reverse Transcriptase Polymerase Chain Reaction. Thyroid Neoplasms / drug therapy


66. Papewalis C, Wuttke M, Schinner S, Willenberg HS, Baran AM, Scherbaum WA, Schott M: Role of the novel mTOR inhibitor RAD001 (everolimus) in anaplastic thyroid cancer. Horm Metab Res; 2009 Oct;41(10):752-6
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  • [Title] Role of the novel mTOR inhibitor RAD001 (everolimus) in anaplastic thyroid cancer.
  • Activation of the phosphatidylinositol-3-kinase (PI3K) signaling cascade is increasingly recognized as a common feature of thyroid follicular neoplasms.
  • The aim of the present study was to examine whether RAD001 (everolimus) can selectively suppress the proliferation of different anaplastic thyroid cancer (ATC) cells.
  • Five different human ATC cell lines were exposed to different concentrations of RAD001.
  • Importantly, we found a dose-dependent growth inhibition in two ATC cell lines at concentrations of 43.5 and 94.5 nM although not as intensive as within the RAD001 responding K562cell line.
  • In summary, we found a good responding effect in a part of ATC cell lines, which may have a clinical impact.
  • [MeSH-major] Carcinoma / metabolism. Immunosuppressive Agents / pharmacology. Protein Kinases / metabolism. Sirolimus / analogs & derivatives. Thyroid Neoplasms / metabolism

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  • [Copyright] Georg Thieme Verlag KG Stuttgart.New York.
  • (PMID = 19513966.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Proliferating Cell Nuclear Antigen; 63231-63-0 / RNA; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
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67. Straight AM, Oakley K, Moores R, Bauer AJ, Patel A, Tuttle RM, Jimeno J, Francis GL: Aplidin reduces growth of anaplastic thyroid cancer xenografts and the expression of several angiogenic genes. Cancer Chemother Pharmacol; 2006 Jan;57(1):7-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aplidin reduces growth of anaplastic thyroid cancer xenografts and the expression of several angiogenic genes.
  • BACKGROUND: Anaplastic thyroid cancer (ATC) is one of the most aggressive and highly lethal human cancers.
  • Median survival after diagnosis is 4-6 months despite available radiotherapy and chemotherapy.
  • Additional treatments are needed for ATC.
  • Vascular endothelial growth factor (VEGF) is a potent angiogenic stimulus, which is expressed by ATC.
  • Previously, anti-VEGF antibody was used to block VEGF-dependent angiogenesis in ATC xenografts.
  • We hypothesized that Aplidin, with its broad spectrum of action and antiangiogenic properties, would be a potentially effective drug against ATC.
  • METHODS: Thirty BALB/c nu/nu mice were injected with ATC cells (ARO-81, 1 x 10(6)) and allowed to implant for 3 weeks.
  • RESULTS: APLD significantly reduced ATC xenograft growth (low dose, 20% reduction, P = 0.01; high dose, 40% reduction, P < 0.001).
  • CONCLUSIONS: This data supports the hypothesis that APLD may be an effective adjunctive therapy against ATC.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma / drug therapy. Depsipeptides / therapeutic use. Gene Expression Regulation, Neoplastic / drug effects. Thyroid Neoplasms / drug therapy

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  • (PMID = 16001179.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Depsipeptides; Y76ID234HW / aplidine
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68. Neff RL, Farrar WB, Kloos RT, Burman KD: Anaplastic thyroid cancer. Endocrinol Metab Clin North Am; 2008 Jun;37(2):525-38, xi
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic thyroid cancer.
  • Anaplastic thyroid cancer is an uncommon, typically lethal malignancy of older adults with no effective systemic therapy.
  • The mean survival time is usually less than 6 months from the time of diagnosis and, unfortunately, this outcome is not fundamentally altered by available treatments.
  • Histologic tissue confirmation is recommended if the diagnosis is not absolutely certain to exclude tumors with better prognosis or that require different treatment.
  • Patency of the airway should be kept in mind throughout the patient's course and individuals with impending airway obstruction, in the absence of imminent death from other sites of disease, should be considered for a tracheostomy to secure the airway.
  • [MeSH-major] Carcinoma / epidemiology. Carcinoma / etiology. Thyroid Neoplasms / epidemiology. Thyroid Neoplasms / etiology

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  • (PMID = 18502341.001).
  • [ISSN] 0889-8529
  • [Journal-full-title] Endocrinology and metabolism clinics of North America
  • [ISO-abbreviation] Endocrinol. Metab. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 44
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69. Chiacchio S, Lorenzoni A, Boni G, Rubello D, Elisei R, Mariani G: Anaplastic thyroid cancer: prevalence, diagnosis and treatment. Minerva Endocrinol; 2008 Dec;33(4):341-57
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  • [Title] Anaplastic thyroid cancer: prevalence, diagnosis and treatment.
  • Anaplastic thyroid cancer (ATC) is a rare aggressive tumor arising from the follicular cells of the thyroid gland (as does well differentiated thyroid cancer, WDTC), but ATC cells do not retain any of the biological features of the original follicular cells, such as uptake of iodine and synthesis of thyroglobulin.
  • In this article the Authors review the pathology, epidemiology, clinical presentation, diagnosis and treatment options of ATC.
  • ATC incidence typically peaks at the 6-7th decade of life (mean age at diagnosis 55-65 years), women representing 55-77% of all patients.
  • ATC represents 2-5% of all thyroid tumors, with a decreasing trend with respect to the incidence of WDTC.
  • The histologic patterns of ATC include giant-cell, spindle-cell and squamoid-cell tumors; these subtypes frequently coexist and are not predictive of patients' outcome.
  • ATC may arise de novo, but in most cases it develops from a pre-existing WDTC, especially the follicular subtype.
  • Most ATC patients complain of local compressive symptoms, such as dysphagia, dysphonia, stridor and dyspnea in addition to neck pain and tenderness; in over 70% of the patients the tumor infiltrates surrounding tissues, such as fat, trachea, muscle, esophagus, and larynx.
  • The clinical course of a rapidly enlarging mass that is firm and fixed to surrounding structures in an elderly patient is quite suggestive for ATC.
  • Diagnosis can be confirmed by fine needle aspiration cytology or, in doubtful cases, by histology on core biopsy.
  • Computed tomography (CT) scan and magnetic resonance imaging (MRI) are useful for defining the local extent of disease and for identifying distant metastases, as is also positron-emission tomography (PET) with [(18)F]FDG.
  • Because of its aggressive behavior, the latest American Joint Committee on Cancer Staging Manual classifies all ATCs as T4 and Stage IV tumors, regardless of their actual overall tumor burden.
  • Treatment of ATC has not been standardized because it is not clear whether or not therapy is effective in prolonging survival; most patients die within six momths from diagnosis, primarily because of asphyxiation caused by local tumor invasion.
  • When employed alone, surgery, radiotherapy, or chemotherapy are seldom adequate to achieve overall control of the disease, but a combination of these treatments may improve local control.
  • Surgical treatment of local disease offers the best opportunity for prolonged survival if the tumor is intrathyroidal.
  • When the tumor is extrathyroidal, the surgical approach to ATC is controversial.
  • Tracheostomy should be performed in patients with impending airway obstruction when death is not imminent from other sites of disease, and if patients are not candidates for local resection or chemoradiation.
  • Interventional bronchoscopy, including Nd-YAG laser and airways stenting are alternatives to surgery in inoperable ATC-induced tracheal obstruction.
  • Although very rare, ATC is a highly aggressive tumor that belongs to the group of killer tumors with median survival time not longer than 6-8 months.
  • Surgery, chemotherapy and radiotherapy are the conventional therapeutic strategies performed in the attempt to improve survival.
  • Unfortunately, very often they do not succeed any clinical benefit but only palliative RESULTS: New therapeutic strategies based on molecular approaches are desirable.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma / therapy. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / therapy


70. Khairy G: Anaplastic transformation of differentiated thyroid carcinoma. Int J Health Sci (Qassim); 2009 Jan;3(1):93-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic transformation of differentiated thyroid carcinoma.
  • Anaplastic thyroid cancer (ATC) is one of the most aggressive malignancies that arise from transformation of pre-existing differentiated thyroid cancer (DTC).
  • However, the carcinogenic mechanism of anaplastic transformation remains unclear.
  • We describe a case for huge goiter diagnosed as papillary thyroid carcinoma, which underwent thyroidectomy.
  • The final histology showed anaplastic transformation.

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  • (PMID = 21475516.001).
  • [ISSN] 1658-3639
  • [Journal-full-title] International journal of health sciences
  • [ISO-abbreviation] Int J Health Sci (Qassim)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Saudi Arabia
  • [Other-IDs] NLM/ PMC3068789
  • [Keywords] NOTNLM ; anaplastic / thyroid cancer / transformation
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71. Shaha AR: Airway management in anaplastic thyroid carcinoma. Laryngoscope; 2008 Jul;118(7):1195-8
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  • [Title] Airway management in anaplastic thyroid carcinoma.
  • OBJECTIVES/HYPOTHESIS: In patients who present with advanced anaplastic thyroid cancer, airway management is difficult because of bilateral vocal cord paralysis or tracheal invasion by the tumor.
  • STUDY DESIGN: This is the author's 25 year experience with 30 patients who presented with anaplastic thyroid cancer and acute airway problems.
  • Airway management for these patients depended on the extent of distant disease and the family's understanding of the advanced nature of the disease and the palliative efforts.
  • CONCLUSIONS: Airway management was the most critical issue in patients who presented with anaplastic thyroid cancer and initial airway distress.
  • It is important to distinguish between poorly differentiated and anaplastic thyroid cancer and lymphoma for appropriate airway management.
  • [MeSH-major] Airway Obstruction / surgery. Carcinoma / surgery. Palliative Care. Thyroid Neoplasms / surgery
  • [MeSH-minor] Cricoid Cartilage / surgery. Humans. Neoplasm Invasiveness / pathology. Prognosis. Retrospective Studies. Survival Analysis. Thyroid Gland / surgery. Tomography, X-Ray Computed. Trachea / pathology. Vocal Cord Paralysis / etiology. Vocal Cord Paralysis / mortality

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  • (PMID = 18438260.001).
  • [ISSN] 1531-4995
  • [Journal-full-title] The Laryngoscope
  • [ISO-abbreviation] Laryngoscope
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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72. Ha HT, Lee JS, Urba S, Koenig RJ, Sisson J, Giordano T, Worden FP: Phase II trial evaluating imatinib (I) in patients (pts) with anaplastic thyroid carcinoma (ATC). J Clin Oncol; 2009 May 20;27(15_suppl):6057

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial evaluating imatinib (I) in patients (pts) with anaplastic thyroid carcinoma (ATC).
  • : 6057 Background: There is no standard treatment for ATC.
  • Affymetrix gene chip showed PDGFR overexpression in ATC.
  • In p53 mutated/deficient ATC cell lines, c-Abl is overexpressed, and selective inhibition of c-Abl resulted in cytostatic effect. (I) inhibits tyrosine kinase activity of Bcr-Abl and PDGF.
  • We hypothesize that ATC that overexpress PDGFR or Abl will respond to (I).
  • METHODS: Pts ≥ 18 years old with histologically confirmed ATC, overexpressing PDGFR or c-Abl by immunohistochemistry who had measurable disease were eligible.
  • Pts with complete response (CR)/partial responses (PR)/stable disease (SD) were treated until disease progression.
  • At baseline, 4/11 pts (36%) had locoregional disease, 5/11 pts (45%) had distant metastases, and 2/11 pts (18%) had both.
  • CONCLUSIONS: (I) appears to have activity in advanced ATC and is well tolerated.
  • Due to difficulty of accruing pts with a rare malignancy at a single institution, investigation of (I) in ATC may be warranted in a multi-institution setting.

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  • (PMID = 27961934.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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73. Brierley JD, Tsang RW: External beam radiation therapy for thyroid cancer. Endocrinol Metab Clin North Am; 2008 Jun;37(2):497-509, xi
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  • [Title] External beam radiation therapy for thyroid cancer.
  • This article discusses the role of external beam radiotherapy (XRT) in the management of well-differentiated thyroid cancer (WDTC), medullary thyroid cancer, and anaplastic thyroid cancer.
  • Although there are no randomized controlled studies on the use of XRT in thyroid cancer, evidence supports its use to treat gross disease after surgery or unresectable cancer and its use as an adjuvant after resection of a known high-risk disease in WDTC, and, to a lesser extent, in medullary thyroid cancer.
  • The use of XRT for the palliation of symptomatic disease and recent advances in the technology of radiation delivery also will be discussed.
  • [MeSH-major] Carcinoma, Papillary / radiotherapy. Thyroid Neoplasms / radiotherapy
  • [MeSH-minor] Carcinoma / mortality. Carcinoma / pathology. Carcinoma / radiotherapy. Carcinoma, Medullary / mortality. Carcinoma, Medullary / pathology. Carcinoma, Medullary / radiotherapy. Humans. Neoplasm Metastasis. Palliative Care. Radiotherapy, Adjuvant. Radiotherapy, Conformal. Survival Analysis. Treatment Outcome

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  • (PMID = 18502339.001).
  • [ISSN] 0889-8529
  • [Journal-full-title] Endocrinology and metabolism clinics of North America
  • [ISO-abbreviation] Endocrinol. Metab. Clin. North Am.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 56
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74. Phillips JS, Pledger DR, Hilger AW: Rapid thyrotoxicosis in anaplastic thyroid carcinoma. J Laryngol Otol; 2007 Jul;121(7):695-7
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  • [Title] Rapid thyrotoxicosis in anaplastic thyroid carcinoma.
  • We present the case of a 71-year-old man with anaplastic thyroid cancer.
  • On presentation, his thyroid function was normal, but he subsequently developed sudden, rapid thyrotoxicosis.
  • Thyrotoxicosis in anaplastic thyroid carcinoma is very rare, but in all previously reported cases the patient was thyrotoxic at presentation.
  • We challenge current ideas regarding the biochemical pathophysiology of rapid thyrotoxicosis in anaplastic thyroid carcinoma and provide an alternative explanation.
  • [MeSH-major] Carcinoma / complications. Thyroid Neoplasms / complications. Thyrotoxicosis / etiology
  • [MeSH-minor] Aged. Biopsy, Needle. Diagnosis, Differential. Fatal Outcome. Humans. Male. Thyroid Function Tests

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  • (PMID = 17156585.001).
  • [ISSN] 1748-5460
  • [Journal-full-title] The Journal of laryngology and otology
  • [ISO-abbreviation] J Laryngol Otol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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75. Won YS, Lee HH, Lee YS, Kim JS, Jeon HM, Jung SS, Lee JH, Park WC: A case of Riedel's thyroiditis associated with benign nodule: mimic of anaplastic transformation. Int J Surg; 2008 Dec;6(6):e24-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of Riedel's thyroiditis associated with benign nodule: mimic of anaplastic transformation.
  • Riedel's thyroiditis is a rare variant of thyroiditis and characterized by the replacement of thyroid parenchyma by extensive fibrosis.
  • Typically, the thyroid is diffusely involved and a painless, hard anterior neck mass shows clinical features similar to those of anaplastic thyroid carcinoma: a rapidly enlarging, hard, fixed thyroid mass and symptoms such as dysphagia, dysphonia, and dyspnea.
  • We experienced a case of Riedel's thyroiditis that had presented rapidly growing, hard, fixed, thyroid mass mimicking anaplastic thyroid cancer in a 41-year-old female patient with longstanding benign thyroid nodule for 6 years.
  • The clinical features were indistinguishable from that of anaplastic transformation and open biopsy could exclude anaplastic thyroid cancer.
  • After surgery final diagnosis of Riedel's thyroiditis could be made by typical microscopic findings and immunohistochemical studies.
  • [MeSH-major] Thyroid Gland / pathology. Thyroid Nodule / diagnosis. Thyroiditis / diagnosis
  • [MeSH-minor] Adult. Anaplasia. Diagnosis, Differential. Female. Humans. Thyroidectomy

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  • (PMID = 19059128.001).
  • [ISSN] 1743-9159
  • [Journal-full-title] International journal of surgery (London, England)
  • [ISO-abbreviation] Int J Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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76. Marlow LA, Reynolds LA, Cleland AS, Cooper SJ, Gumz ML, Kurakata S, Fujiwara K, Zhang Y, Sebo T, Grant C, McIver B, Wadsworth JT, Radisky DC, Smallridge RC, Copland JA: Reactivation of suppressed RhoB is a critical step for the inhibition of anaplastic thyroid cancer growth. Cancer Res; 2009 Feb 15;69(4):1536-44
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  • [Title] Reactivation of suppressed RhoB is a critical step for the inhibition of anaplastic thyroid cancer growth.
  • Anaplastic thyroid carcinoma (ATC) is a highly aggressive form of the disease for which new therapeutic options are desperately needed.
  • Previously, we showed that the high-affinity peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, RS5444, inhibits cell proliferation of ATC cells via induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) (p21).
  • Using multiple independently derived ATC cell lines, we found that treatment with RS5444 leads to the up-regulation of RhoB and subsequent activation of p21, and that silencing of RhoB by RNAi blocks the ability of RS5444 to induce p21 and to inhibit cell proliferation.
  • We further implicate RhoB as a key signaling effector for the growth inhibition of ATC, as treatment with a histone deacetylase inhibitor shown to increase RhoB expression in lung cancer cells caused the up-regulation of RhoB in ATC cells accompanied by increased expression of p21 and inhibition of cell proliferation; this effect occurred even in ATC cells that were unresponsive to RS5444 due to a lack of expression of PPARgamma.
  • Our results implicate RhoB as a novel intermediate in critical signaling pathways and as an additional target for therapeutic intervention in ATC.

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  • (PMID = 19208833.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA015083-34; United States / NCI NIH HHS / CA / P30 CA015083; United States / NCI NIH HHS / CA / P30 CA015083-34; United States / NCI NIH HHS / CA / P30CA15083
  • [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 / Antineoplastic Agents; 0 / PPAR gamma; 0 / Thiazolidinediones; EC 3.6.5.2 / rhoB GTP-Binding Protein; M17ILL71MC / efatutazone
  • [Other-IDs] NLM/ NIHMS83531; NLM/ PMC2644344
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77. 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.
  • Its rare and rapidly lethal disease course has made it challenging to study.
  • 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


78. Klopper JP, Berenz A, Hays WR, Sharma V, Pugazhenthi U, Janssen J, Singh M, Bissonnette RP, Haugen BR: In vivo and microarray analysis of rexinoid-responsive anaplastic thyroid carcinoma. Clin Cancer Res; 2008 Jan 15;14(2):589-96
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  • [Title] In vivo and microarray analysis of rexinoid-responsive anaplastic thyroid carcinoma.
  • PURPOSE: Anaplastic thyroid carcinoma is rare, yet lethal despite aggressive therapy.
  • In this report, we describe the efficacy of LGD1069 in anaplastic thyroid carcinoma in vitro and assess the in vivo treatment effects on a responsive cancer.
  • Additionally, we explore potential mediators of the rexinoid effect on a responsive anaplastic thyroid cancer using comparative microarray analysis.
  • EXPERIMENTAL DESIGN: Anaplastic thyroid cancer cell lines DRO, ARO, and FRO were treated with LGD1069 in vitro.
  • CONCLUSIONS: LGD1069 therapy decreases proliferation in an anaplastic thyroid cancer cell line that expresses retinoid X receptor-gamma, and this effect is confirmed with decreased tumor size in vivo in a nude mouse model.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma / drug therapy. Retinoid X Receptors / agonists. Tetrahydronaphthalenes / therapeutic use. Thyroid Neoplasms / drug therapy

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  • [ErratumIn] Clin Cancer Res. 2009 Jan 1;15(1):416
  • (PMID = 18223235.001).
  • [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 / CA100560
  • [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 / Antineoplastic Agents; 0 / Retinoid X Receptors; 0 / Tetrahydronaphthalenes; A61RXM4375 / bexarotene
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79. Zheng X, Cui D, Xu S, Brabant G, Derwahl M: Doxorubicin fails to eradicate cancer stem cells derived from anaplastic thyroid carcinoma cells: characterization of resistant cells. Int J Oncol; 2010 Aug;37(2):307-15
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  • [Title] Doxorubicin fails to eradicate cancer stem cells derived from anaplastic thyroid carcinoma cells: characterization of resistant cells.
  • Current chemotherapy with doxorubicin fails to eradicate anaplastic thyroid cancer or even to stop tumor progress which may be due to the failure of these drugs to effectively target putative cancer stem cells.
  • To test this hypothesis, anaplastic thyroid cell lines were characterized by FACS for their content of cancer stem cells, their in vitro sphere-forming capacity and their expression of multidrug resistance transporters of the ABC gene family which may confer drug resistance to the cells.
  • The survival of cancer and cancer stem cells and the differential expression of transporters were analyzed.
  • Anaplastic thyroid cancer cell lines that consisted of 0.4-0.8% side population cells, expressed ABCG2 and multi-drug-resistant 1 (MDR1) transporters.
  • Treatment with doxorubicin gradually killed the non-side population of cancer cells derived from anaplastic thyroid carcinoma cells.
  • This conferred a growth advantage to cancer stem cells which in turn overgrew the culture.
  • Resistant cell line consisted of a 70% side population fraction enriched with Oct4-positive cancer stem cells.
  • Inhibition of ABCG2 and/or MDR1 revealed that resistance of cancer stem cells to doxorubicin may be mainly due to the expression of these ABC transporters that were highly up-regulated in the resistant subline.
  • The poor outcome of chemotherapy with doxorubicin in anaplastic thyroid carcinoma may be partly explained by up-regulation of ABCG2 and MDR1 transporters that confers resistance to cancer stem cells.
  • Thus an effective treatment of anaplastic thyroid cancer has not only to destroy cancer cells that represent the bulk of tumor cell population but also cancer stem cells that may drive tumor progression.
  • [MeSH-major] Carcinoma / pathology. Doxorubicin / pharmacology. Drug Resistance, Neoplasm. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / pathology. Thyroid Neoplasms / pathology

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  • (PMID = 20596658.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Biomarkers, Tumor; 0 / Indoles; 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 80168379AG / Doxorubicin; CJ0O37KU29 / Verapamil; CW5S8OP3VO / tryptoquivaline
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80. Santarpia L, El-Naggar AK, Cote GJ, Myers JN, Sherman SI: Phosphatidylinositol 3-kinase/akt and ras/raf-mitogen-activated protein kinase pathway mutations in anaplastic thyroid cancer. J Clin Endocrinol Metab; 2008 Jan;93(1):278-84
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  • [Title] Phosphatidylinositol 3-kinase/akt and ras/raf-mitogen-activated protein kinase pathway mutations in anaplastic thyroid cancer.
  • CONTEXT: Anaplastic thyroid carcinoma (ATC) can occur in the setting of differentiated thyroid carcinoma (DTC), which suggests a continuum in malignant progression from DTC to ATC.
  • The Ras/Raf-MAPK and the phosphatidylinositol 3-kinase/Akt signaling pathways play critical roles in DTC tumorigenesis, but their roles in the pathogenesis of ATC are poorly defined.
  • OBJECTIVE: Our objective was to explore the potential contributions of these two pathways in ATC pathogenesis.
  • DESIGN, SETTING, AND SUBJECTS: The mutational status of BRAF, PIK3CA, PTEN, and RAS genes was analyzed in genomic DNA from microdissected tumor specimens of 36 cases of ATC, and in 16 samples of paired-matched lymph node metastases.
  • We performed immunohistochemistry for phospho-ERK and phospho-AKT in 26 cases of ATC.
  • BRAF V600E mutation was identified in nine of 36 (25%) ATCs; seven cases had identical mutations in both the ATC and DTC components.
  • PIK3CA kinase domain mutations were found in five (14%) ATCs, one of which had mutations in both differentiated and anaplastic areas.
  • PIK3CA alterations occur preferentially in the later stages of ATC and were the most relevant events during thyroid cancer progression.
  • The activation of both pathways suggests an important role in ATC dedifferentiation.
  • [MeSH-major] Carcinoma / enzymology. MAP Kinase Signaling System / genetics. Mutation. Phosphatidylinositol 3-Kinases / metabolism. Thyroid Neoplasms / enzymology. raf Kinases / metabolism


81. Antonelli A, Fallahi P, Ferrari SM, Carpi A, Berti P, Materazzi G, Minuto M, Guastalli M, Miccoli P: Dedifferentiated thyroid cancer: a therapeutic challenge. Biomed Pharmacother; 2008 Oct;62(8):559-63
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  • [Title] Dedifferentiated thyroid cancer: a therapeutic challenge.
  • Human papillary dedifferentiated thyroid cancer (HPDTC) represents a therapeutic dilemma.
  • In the future, the identification of patients who are likely to benefit from each therapeutic option will be important.
  • In this view particular importance should be given to development of primary cells from the single patient by fine needle aspiration samples, as recently observed in anaplastic thyroid cancer.
  • [MeSH-major] Thyroid Neoplasms / pathology. Thyroid Neoplasms / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Differentiation / physiology. Humans. Iodine Radioisotopes / pharmacokinetics. PPAR gamma / agonists

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  • (PMID = 18725177.001).
  • [ISSN] 0753-3322
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Iodine Radioisotopes; 0 / PPAR gamma
  • [Number-of-references] 43
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82. O'Neill JP, O'Neill B, Condron C, Walsh M, Bouchier-Hayes D: Anaplastic (undifferentiated) thyroid cancer: improved insight and therapeutic strategy into a highly aggressive disease. J Laryngol Otol; 2005 Aug;119(8):585-91
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  • [Title] Anaplastic (undifferentiated) thyroid cancer: improved insight and therapeutic strategy into a highly aggressive disease.
  • BACKGROUND: This review article discusses the clinical and diagnostic implications of anaplastic thyroid cancer, recognizing the aggressive nature of the disease and extensive disease progression upon diagnosis.
  • We question the pathological evolution of anaplasia as a 'de novo' disease or a post malignant transformation or dedifferentiation and the therapeutic implications of p53 mutation.
  • METHOD: An electronic search on Medline and Pubmed was performed under 'anaplastic thyroid carcinoma', 'anaplastic thyroid carcinogenesis', 'anaplastic thyroid carcinoma treatment reviews'.
  • [MeSH-major] Carcinoma / therapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Chemotherapy, Adjuvant. Combined Modality Therapy. Drug Resistance, Neoplasm. Humans. Neck Dissection. Neoadjuvant Therapy. Prognosis. Radiotherapy, Adjuvant. Thyroidectomy

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  • (PMID = 16102210.001).
  • [ISSN] 0022-2151
  • [Journal-full-title] The Journal of laryngology and otology
  • [ISO-abbreviation] J Laryngol Otol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 85
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83. Cornett WR, Sharma AK, Day TA, Richardson MS, Hoda RS, van Heerden JA, Fernandes JK: Anaplastic thyroid carcinoma: an overview. Curr Oncol Rep; 2007 Mar;9(2):152-8
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  • [Title] Anaplastic thyroid carcinoma: an overview.
  • Thyroid cancer is an uncommon malignancy that accounts for roughly 1% of all new cancers.
  • Although anaplastic lesions constitute fewer than 5% of thyroid cancers, they represent over half of thyroid cancer-related deaths.
  • The relative rarity of anaplastic thyroid cancer, its aggressive nature, and its rapidly fatal course have contributed to the difficulty in developing effective treatment for this disease.
  • [MeSH-major] Carcinoma / pathology. Thyroid Neoplasms / pathology

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  • (PMID = 17288883.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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84. Namba H, Yamashita S: [Gene abnormalities in thyroid cancer]. Nihon Rinsho; 2007 Nov;65(11):1967-72
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  • [Title] [Gene abnormalities in thyroid cancer].
  • A number of genetic abnormalities in oncogenes or anti-oncogenes have been identified in association with thyroid carcinogenesis.
  • Especially, oncogenes such as ras mutation, ret/PTC and Braf mutation that constitutively activate MAP kinase pathway a refrequently found in papillary thyroid cancer.
  • The p53 mutation aggravates differentiated thyroid cancers to anaplastic thyroid cancer.
  • These gene alterations are studied not only to understand basically the mechanisms of oncogenesis but also to develop clinically genetic diagnosis or molecular target therapy.
  • In this article, we review the genetic diagnostic methods and phenotype-genotype relationship of human thyroid cancers.
  • [MeSH-major] Adenocarcinoma, Follicular / genetics. Adenocarcinoma, Papillary / genetics. Thyroid Neoplasms / genetics

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  • (PMID = 18018556.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / PAX8 protein, human; 0 / PPAR gamma; 0 / Paired Box Transcription Factors; 0 / Receptors, G-Protein-Coupled; 0 / TRIM27 protein, human; 0 / taste receptors, type 2; 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
  • [Number-of-references] 22
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85. Paes JE, Ringel MD: Dysregulation of the phosphatidylinositol 3-kinase pathway in thyroid neoplasia. Endocrinol Metab Clin North Am; 2008 Jun;37(2):375-87, viii-ix
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  • [Title] Dysregulation of the phosphatidylinositol 3-kinase pathway in thyroid neoplasia.
  • These genetic abnormalities have been particularly associated with follicular thyroid neoplasia and anaplastic thyroid cancer, suggesting an important role for PI3K signaling in these disorders.
  • In this article, the role of PI3K pathway activation in thyroid cancer is discussed, with a focus on recent advances.

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  • (PMID = 18502332.001).
  • [ISSN] 0889-8529
  • [Journal-full-title] Endocrinology and metabolism clinics of North America
  • [ISO-abbreviation] Endocrinol. Metab. Clin. North Am.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA102572-04; United States / NCI NIH HHS / CA / R01 CA102572; United States / NCI NIH HHS / CA / 5 R01 CA102572-02; United States / NCI NIH HHS / CA / R01 CA102572-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Number-of-references] 72
  • [Other-IDs] NLM/ NIHMS55687; NLM/ PMC2446602
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86. Xu J, Filetti S, Hershman JM: Expression of hepatocyte nuclear factor-1alpha mRNA in human anaplastic thyroid cancer cell lines and tumors. Thyroid; 2008 May;18(5):533-9
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  • [Title] Expression of hepatocyte nuclear factor-1alpha mRNA in human anaplastic thyroid cancer cell lines and tumors.
  • Our previous study showed that HNF-1beta was highly expressed in papillary thyroid cancer cell lines and tumors.
  • HNF-1alpha mRNA, however, was not detected in differentiated thyroid cancer cell lines.
  • The objective of this study was to determine whether HNF-1alpha is expressed in dedifferentiated anaplastic thyroid cancer cells.
  • METHODS: Total RNA isolated from six anaplastic thyroid cancer cell lines and 38 surgical samples was analyzed for HNF-1alpha mRNA by conventional reverse-transcription polymerase chain reaction (RT-PCR) or real-time RT-PCR.
  • RESULTS: HNF-1alpha mRNA was expressed in four of the six anaplastic cell lines.
  • HNF-1alpha transcripts were also detected in five out of six anaplastic tumors, but not in the papillary tumors except one with weak PCR signal.
  • CONCLUSION: HNF-1alpha mRNA was detected in high frequency in anaplastic thyroid cancer cell lines and tumors.
  • HNF-1alpha might play a role in the pathogenesis of anaplastic thyroid cancer.
  • [MeSH-major] Carcinoma / metabolism. Carcinoma, Papillary / metabolism. Hepatocyte Nuclear Factor 1-alpha / metabolism. RNA, Messenger / metabolism. Thyroid Neoplasms / metabolism

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  • (PMID = 18399756.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / RNA, Messenger; 138674-15-4 / Hepatocyte Nuclear Factor 1-beta
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87. Wang TS, Ocal IT, Oxley K, Sosa JA: Primary leiomyosarcoma of the thyroid gland. Thyroid; 2008 Apr;18(4):425-8
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  • [Title] Primary leiomyosarcoma of the thyroid gland.
  • Primary leiomyosarcomas of the thyroid gland are rare.
  • The preoperative differential diagnosis included medullary thyroid cancer, anaplastic thyroid cancer, and primary versus metastatic sarcoma.
  • We review the literature on leiomyosarcoma of the thyroid, including the differential diagnoses, pathology, and alternative treatment strategies, including surgery and adjuvant therapy.
  • [MeSH-major] Leiomyosarcoma / diagnosis. Thyroid Neoplasms / diagnosis
  • [MeSH-minor] Aged. Biopsy, Fine-Needle. Female. Humans. Immunohistochemistry / methods. Necrosis. Neoplasm Metastasis. Thyroid Gland / metabolism. Thyroidectomy. Tomography, X-Ray Computed / methods. Treatment Outcome

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  • (PMID = 18346004.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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88. She M, Jim Yeung SC: Combining a matrix metalloproteinase inhibitor, a farnesyltransferase inhibitor, and a taxane improves survival in an anaplastic thyroid cancer model. Cancer Lett; 2006 Jul 18;238(2):197-201
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  • [Title] Combining a matrix metalloproteinase inhibitor, a farnesyltransferase inhibitor, and a taxane improves survival in an anaplastic thyroid cancer model.
  • We previously showed that the in vivo anticancer effects of a combination of manumycin (a farnesyltransferase inhibitor) and paclitaxel (a microtubule inhibitor) against anaplastic thyroid carcinoma (ATC) were partially due to inhibition of angiogenesis.
  • In this study, we investigated the effect of adding minocycline (a matrix metalloproteinase inhibitor) to manumycin and paclitaxel against human ATC cells xenografted in nude mice.
  • In conclusion, this novel combination deserves further investigation in the treatment of ATC.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Enzyme Inhibitors / administration & dosage. Farnesyltranstransferase / antagonists & inhibitors. Matrix Metalloproteinase Inhibitors. Thyroid Neoplasms / drug therapy

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  • (PMID = 16154259.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Matrix Metalloproteinase Inhibitors; 0 / Polyenes; 0 / Polyunsaturated Alkamides; 52665-74-4 / manumycin; EC 2.5.1.29 / Farnesyltranstransferase; FYY3R43WGO / Minocycline; P88XT4IS4D / Paclitaxel
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89. Hsieh YJ, Ke CC, Liu RS, Wang FH, Tang KT, Chi CW, Chen FD, Lee CH: Radioiodide imaging and treatment of ARO cancer xenograft in a mouse model after expression of human sodium iodide symporter. Anticancer Res; 2007 Jul-Aug;27(4B):2515-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radioiodide imaging and treatment of ARO cancer xenograft in a mouse model after expression of human sodium iodide symporter.
  • BACKGROUND: Most undifferentiated and anaplastic thyroid carcinomas are not sensitive to 131I therapy due to their lost ability for iodide accumulation.
  • This study aims to restore the iodide uptake by transferring and expressing human sodium iodide symporter (hNIS) in these cancer cells for 131I gene therapy.
  • MATERIALS AND METHODS: hNIS cDNA expression vector was transfected into wild-type anaplastic thyroid cancer cells (ARO-W) which do not concentrate iodide.
  • Administration of a therapeutic dose of 131I into mice bearing ARO-S tumors effectively inhibited tumor growth as compared to control mice.
  • CONCLUSION: Our results suggest the potential of hNIS-mediated 131I gene therapy on anaplastic thyroid cancer cells.
  • [MeSH-major] Iodine Radioisotopes. Radiopharmaceuticals. Symporters / biosynthesis. Thyroid Neoplasms / metabolism. Thyroid Neoplasms / radionuclide imaging
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Models, Animal. Gene Expression. Genetic Therapy. Humans. Immunohistochemistry. Mice. Neoplasm Transplantation. Reverse Transcriptase Polymerase Chain Reaction. Transplantation, Heterologous

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  • (PMID = 17695547.001).
  • [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 / Iodine Radioisotopes; 0 / Radiopharmaceuticals; 0 / Symporters; 0 / sodium-iodide symporter
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90. Goutsouliak V, Hay JH: Anaplastic thyroid cancer in British Columbia 1985-1999: a population-based study. Clin Oncol (R Coll Radiol); 2005 Apr;17(2):75-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic thyroid cancer in British Columbia 1985-1999: a population-based study.
  • AIMS: To review the outcome of patients diagnosed with anaplastic thyroid carcinoma in British Columbia between January 1985 and December 1999.
  • Survival curves were calculated using Kaplan-Meier estimates, and the charts of the 62 patients referred to a British Columbia Cancer Agency (BCCA) facility were reviewed.
  • The overall- and cancer-specific 5-year survival rates for the whole group were 5%.
  • non-referred cases: nine out of 13 patients were women; median age at diagnosis 84 years.
  • Eleven of the 13 patients died within 1 month of diagnosis.
  • Forty-eight patients presented with tumours that extended through the thyroid capsule, 10 presented with distant metastases.
  • CONCLUSION: Long-term, disease-free survival was achieved in a few patients who were able to receive high-dose radiotherapy, preferably after adequate surgery.
  • [MeSH-major] Thyroid Neoplasms / epidemiology. Thyroid Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. British Columbia / epidemiology. Carcinoma / epidemiology. Carcinoma / therapy. Female. Humans. Male. Middle Aged. Registries. Retrospective Studies. Survival Analysis

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  • (PMID = 15830567.001).
  • [ISSN] 0936-6555
  • [Journal-full-title] Clinical oncology (Royal College of Radiologists (Great Britain))
  • [ISO-abbreviation] Clin Oncol (R Coll Radiol)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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91. Dackiw A, Pan J, Xu G, Yeung SC: Modulation of parathyroid hormone-related protein levels (PTHrP) in anaplastic thyroid cancer. Surgery; 2005 Sep;138(3):456-63
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  • [Title] Modulation of parathyroid hormone-related protein levels (PTHrP) in anaplastic thyroid cancer.
  • BACKGROUND: Studies have demonstrated that manumycin, a farnesyltransferase inhibitor, enhances the cytotoxic effect of paclitaxel in anaplastic thyroid cancer cells and in xenografts, but the mechanism of this effect is unknown.
  • We hypothesized that this protein might have a novel role in anaplastic thyroid cancer.
  • METHODS: Five anaplastic thyroid cancer cell lines (ARO, DRO, KAT-4, Hth-74, C-643) were examined for PTHrP expression in vitro by immunohistochemistry (IHC), radioimmunoassay, and Western blot (IP/WB) analyses.
  • RESULTS: All 5 ATC cell lines were found to robustly express PTHrP by IHC of fixed cells and radioimmunoassay of cell lysates and conditioned culture media (range, 468 +/- 55 to 1410 +/- 195 pg/mg cellular protein).
  • CONCLUSIONS: Manumycin inhibits cell proliferation and decreases PTHrP levels in anaplastic thyroid cancer cells in vitro and in vivo and decreases the PTHrP level in the nucleus where PTHrP may function as an oncoprotein.
  • These data suggest that PTHrP has a novel role in anaplastic thyroid cancer and that modulation of PTHrP levels may be of therapeutic benefit in this lethal malignancy.
  • [MeSH-major] Carcinoma / metabolism. Parathyroid Hormone-Related Protein / metabolism. Thyroid Neoplasms / metabolism


92. 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.
  • 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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93. Younes MN, Kim S, Yigitbasi OG, Mandal M, Jasser SA, Dakak Yazici Y, Schiff BA, El-Naggar A, Bekele BN, Mills GB, Myers JN: Integrin-linked kinase is a potential therapeutic target for anaplastic thyroid cancer. Mol Cancer Ther; 2005 Aug;4(8):1146-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrin-linked kinase is a potential therapeutic target for anaplastic thyroid cancer.
  • We investigated integrin-linked kinase (ILK), a focal adhesion serine-threonine protein kinase, as a new molecular target for treating anaplastic thyroid cancer.
  • ILK mediates cell growth and survival signals and is overexpressed in a number of cancers.
  • Therefore, we hypothesized that inhibition of ILK leads to growth arrest and apoptosis of thyroid cancer cells.
  • According to Western blotting, the level of ILK protein was highly expressed in one papillary (NPA187) and four of five (Hth74, DRO, ARO, KAT4, and K4) anaplastic thyroid cancer cell lines.
  • Immunohistochemical analysis of a human tissue microarray revealed that ILK was highly expressed in anaplastic thyroid cancer but not in normal human thyroid tissue.
  • Treating thyroid cancer cell lines with a new ILK inhibitor, QLT0267, inhibited epidermal growth factor-induced phosphorylation of AKT, inhibited cell growth, and induced apoptosis in the NPA187, DRO, and K4 cell lines.
  • In immunohistochemical studies, QLT0267 suppressed phosphorylated p-AKT and angiogenesis (i.e., reduced mean vascular density) and induced apoptosis in both tumor cells and tumor-associated endothelial cells of the thyroid DRO xenografts.
  • In summary, we found that ILK expression and activity were elevated in human anaplastic thyroid cancer and ILK inhibition led to growth arrest and apoptosis in vitro and in vivo.
  • Our results provide preliminary evidence that ILK is a potential therapeutic target for treating anaplastic thyroid cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / enzymology


94. Kohlfuerst S, Igerc I, Gallowitsch HJ, Gomez I, Kresnik E, Matschnig S, Lind P: Is there a role for sandostatin treatment in patients with progressive thyroid cancer and iodine-negative but somatostatin-receptor-positive metastases? Thyroid; 2006 Nov;16(11):1113-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is there a role for sandostatin treatment in patients with progressive thyroid cancer and iodine-negative but somatostatin-receptor-positive metastases?
  • INTRODUCTION: The aim of our study was to determine whether treatment with a long-acting somatostatin-receptor analogue is effective in patients with (131)I-negative but somatostatin-receptor-positive metastases from dedifferentiated and anaplastic thyroid cancer.
  • All of them showed progressive disease confirmed by radiologic evaluation, increasing serum thyroglobulin (Tg), and negative diagnostic or posttherapeutic (131)I whole-body scans (WBS).
  • Eight of 12 patients (4 males and 4 females; age range, 57-89 years; 1 papillary thyroid cancer; 4 poorly differentiated follicular thyroid cancer; 1 follicular and anaplastic thyroid cancer; 2 anaplastic thyroid cancer) showed positive somatosatin-receptor expression in Tc-99m depreotide WBS/SPECT (Tc-99m Dep.WBS).
  • All patients showed progressive disease during the treatment: an increase of serum Tg on one hand and an increase in the number of lesions and extent in tumor size visible on FDG-PET-CT and Tc-99m Dep.WBS on the other.
  • CONCLUSION: Our data demonstrate that all of our patients treated with a somatostatin analogue showed clinical progression and that our attempt to achieve a stabilization of the disease failed.
  • [MeSH-major] Antineoplastic Agents, Hormonal / administration & dosage. Carcinoma, Papillary / drug therapy. Carcinoma, Papillary / secondary. Octreotide / administration & dosage. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Follicular / drug therapy. Adenocarcinoma, Follicular / radionuclide imaging. Adenocarcinoma, Follicular / secondary. Aged. Aged, 80 and over. Carcinoma / drug therapy. Carcinoma / radionuclide imaging. Carcinoma / secondary. Female. Fluorodeoxyglucose F18. Humans. Iodine Radioisotopes. Male. Middle Aged. Organotechnetium Compounds. Radiopharmaceuticals. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Tomography, Emission-Computed, Single-Photon. Treatment Failure

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  • (PMID = 17123338.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Iodine Radioisotopes; 0 / Organotechnetium Compounds; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 51110-01-1 / Somatostatin; 9M48M2SF02 / technetium Tc 99m depreotide; RWM8CCW8GP / Octreotide
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95. Xing M: BRAF mutation in thyroid cancer. Endocr Relat Cancer; 2005 Jun;12(2):245-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BRAF mutation in thyroid cancer.
  • Genetic alteration is the driving force for thyroid tumorigenesis and progression, based upon which novel approaches to the management of thyroid cancer can be developed.
  • A recent important genetic finding in thyroid cancer is the oncogenic T1799A transversion mutation of BRAF (the gene for the B-type Raf kinase, BRAF).
  • Since the initial report of this mutation in thyroid cancer 2 years ago, rapid advancements have been made.
  • BRAF mutation is the most common genetic alteration in thyroid cancer, occurring in about 45% of sporadic papillary thyroid cancers (PTCs), particularly in the relatively aggressive subtypes, such as the tall-cell PTC.
  • This mutation is mutually exclusive with other common genetic alterations, supporting its independent oncogenic role, as demonstrated by transgenic mouse studies that showed BRAF mutation-initiated development of PTC and its transition to anaplastic thyroid cancer.
  • BRAF mutation is mutually exclusive with RET/PTC rearrangement, and also displays a reciprocal age association with this common genetic alteration in thyroid cancer.
  • The T1799A BRAF mutation occurs exclusively in PTC and PTC-derived anaplastic thyroid cancer and is a specific diagnostic marker for this cancer when identified in cytological and histological specimens.
  • This mutation is associated with a poorer clinicopathological outcome and is a novel independent molecular prognostic marker in the risk evaluation of thyroid cancer.
  • Moreover, preclinical and clinical evaluations of the therapeutic value of novel specific mitogen-activated protein kinase pathway inhibitors in thyroid cancer are anticipated.
  • This newly discovered BRAF mutation may prove to have an important impact on thyroid cancer in the clinic.
  • [MeSH-major] Proto-Oncogene Proteins B-raf / genetics. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / genetics

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  • (PMID = 15947100.001).
  • [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; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins; 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 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Number-of-references] 134
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96. Lee JJ, Au AY, Foukakis T, Barbaro M, Kiss N, Clifton-Bligh R, Staaf J, Borg A, Delbridge L, Robinson BG, Wallin G, Höög A, Larsson C: Array-CGH identifies cyclin D1 and UBCH10 amplicons in anaplastic thyroid carcinoma. Endocr Relat Cancer; 2008 Sep;15(3):801-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Array-CGH identifies cyclin D1 and UBCH10 amplicons in anaplastic thyroid carcinoma.
  • Anaplastic thyroid cancer (ATC) is a rare but highly aggressive disease with largely unexplained etiology and molecular pathogenesis.
  • In this study, we analyzed genome-wide copy number changes, BRAF (V-raf sarcoma viral oncogene homolog B1) mutations, and p16 and cyclin D1 expressions in a panel of ATC primary tumors.
  • The effect of CCND1 on thyroid cell proliferation was assessed in vitro in ATC cells by means of siRNA and in thyroid cells after CCND1 transfection.
  • In summary, the recurrent chromosomal copy number changes and molecular alterations identified in this study may provide an insight into the pathogenesis and development of ATC.
  • [MeSH-major] Carcinoma / genetics. Comparative Genomic Hybridization / methods. Gene Amplification. Genes, bcl-1. Thyroid Neoplasms / genetics. Ubiquitin-Conjugating Enzymes / genetics


97. Bulgin D, Podtcheko A, Takakura S, Mitsutake N, Namba H, Saenko V, Ohtsuru A, Rogounovitch T, Palona I, Yamashita S: Selective pharmacologic inhibition of c-Jun NH2-terminal kinase radiosensitizes thyroid anaplastic cancer cell lines via induction of terminal growth arrest. Thyroid; 2006 Mar;16(3):217-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective pharmacologic inhibition of c-Jun NH2-terminal kinase radiosensitizes thyroid anaplastic cancer cell lines via induction of terminal growth arrest.
  • CONTEXT: The high radioresistance of anaplastic thyroid cancer (ATC) and cultured ATC cells stipulates for the means of increasing their radiosensitivity.
  • It has been shown that c-Jun NH(2)-terminal kinase (JNK) activation is one of the manifestations of radiation response in ATC cells.
  • OBJECTIVE: Assessment of the effect of selective JNK inhibition on ATC cell radiosensitivity and clarification of the associated mechanisms.
  • RESULTS: The JNK inhibitor markedly suppressed ATC cell growth in a reversible cytostatic manner.
  • CONCLUSIONS: JNK signaling is an essential component of ATC cell proliferation and survival after radiation therapy.
  • Hence, pharmacological interference with JNK pathway in combination with radiotherapy may be a promising treatment of ATC.
  • [MeSH-major] JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors. Radiation-Sensitizing Agents / pharmacology. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / radiotherapy
  • [MeSH-minor] Activating Transcription Factor 2 / metabolism. Anthracenes / pharmacology. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Apoptosis / radiation effects. Cell Aging / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Combined Modality Therapy. DNA Repair / drug effects. Humans. Signal Transduction / physiology

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  • (PMID = 16571083.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATF2 protein, human; 0 / Activating Transcription Factor 2; 0 / Anthracenes; 0 / Antineoplastic Agents; 0 / Radiation-Sensitizing Agents; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
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98. Song M, Park JE, Park SG, Lee DH, Choi HK, Park BC, Ryu SE, Kim JH, Cho S: NSC-87877, inhibitor of SHP-1/2 PTPs, inhibits dual-specificity phosphatase 26 (DUSP26). Biochem Biophys Res Commun; 2009 Apr 17;381(4):491-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Since DUSP26 is involved in survival of anaplastic thyroid cancer (ATC) cells, NSC-87877 could be a therapeutic reagent for treating ATC.

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  • (PMID = 19233143.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / NSC-87877; 0 / Quinolines; 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 Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6
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99. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • RESULTS: Knockdown of β4 integrin subunit expression by shRNA in ATC cells reduced the proliferation, migration, and anchorage-independent growth of ATC cells in vitro and xenograft tumor growth 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

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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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100. Pallante P, Visone R, Croce CM, Fusco A: Deregulation of microRNA expression in follicular-cell-derived human thyroid carcinomas. Endocr Relat Cancer; 2010 Mar;17(1):F91-104
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deregulation of microRNA expression in follicular-cell-derived human thyroid carcinomas.
  • Carcinoma of the thyroid gland is an uncommon cancer, but one of the most frequent malignancies of the endocrine system.
  • Most thyroid cancers are derived from the follicular cells.
  • Follicular carcinoma is considered more malignant than papillary thyroid carcinoma (PTC), and anaplastic thyroid cancer (ATC) is one of the most lethal human cancers.
  • Even though several genetic lesions have been already described in human thyroid cancer, particularly in the papillary histotype, the mechanisms underlying the development of these neoplasias are still far from being completely elucidated.
  • Some years ago, several studies were undertaken to analyze the expression of microRNAs (miRNAs or miRs) in thyroid carcinoma to evaluate a possible role of their deregulation in the process of carcinogenesis.
  • These studies showed an aberrant microRNA expression profile that distinguishes unequivocally among PTC, ATC, and normal thyroid tissue.
  • Here, other than summarizing the current findings on microRNA expression in human thyroid carcinomas, we discuss the mechanisms by which microRNA deregulation may play a role in thyroid carcinogenesis, and the possible use of microRNA knowledge in the diagnosis and therapy of thyroid neoplasms.
  • [MeSH-major] Adenocarcinoma, Follicular / genetics. Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Neoplastic. MicroRNAs / genetics. RNA, Neoplasm / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Animals. Biomarkers, Tumor / analysis. Carcinoma / diagnosis. Carcinoma, Papillary / diagnosis. Diagnosis, Differential. Gene Expression Profiling. Humans. Mice. Mice, Transgenic. Mutation. Neoplasms, Radiation-Induced / diagnosis. Neoplasms, Radiation-Induced / genetics. Neoplasms, Radiation-Induced / pathology. Oligonucleotide Array Sequence Analysis. Oncogenes

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  • (PMID = 19942715.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs; 0 / RNA, Neoplasm
  • [Number-of-references] 106
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