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1. Tulloch-Reid M, Skarulis MC, Sherman SI, Sarlis NJ, Santarpia L: Long-term eradication of locally recurrent invasive follicular thyroid carcinoma after taxane-based concomitant chemoradiotherapy. Anticancer Res; 2009 Nov;29(11):4665-71
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  • [Title] Long-term eradication of locally recurrent invasive follicular thyroid carcinoma after taxane-based concomitant chemoradiotherapy.
  • A 46-year-old woman with history of radioiodine-refractory follicular thyroid carcinoma (FTC) presented with locally recurrent, high-risk, invasive disease.
  • This case highlights the possibility of combining taxane-based chemotherapy with definitive radiotherapy (as CRT) for the management of locally aggressive recurrences in poorly differentiated thyroid carcinoma, thereby resulting in rapid and persistent disease eradication.
  • Even in the light of recent data on the potential benefit of novel targeted therapy agents in poorly differentiated thyroid carcinoma, this approach in similar clinical settings deserves future investigation.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Adenocarcinoma, Follicular / radiotherapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / radiotherapy. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / radiotherapy
  • [MeSH-minor] Adult. Carboplatin / administration & dosage. Combined Modality Therapy. Female. Humans. Middle Aged. Paclitaxel / administration & dosage

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  • (PMID = 20032418.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA DK047053-04
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS294986; NLM/ PMC3109502
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2. Cherk MH, Moore M, Serpell J, Swain S, Topliss DJ: Metastatic colorectal cancer to a primary thyroid cancer. World J Surg Oncol; 2008;6:122
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  • [Title] Metastatic colorectal cancer to a primary thyroid cancer.
  • BACKGROUND: Metastatic malignancy to the thyroid gland is generally uncommon due to an unfavourable local thyroid micro-environment which impairs the ability of metastatic cells to settle and thrive.
  • Metastases to the thyroid gland have however been reported to occur occasionally particularly if there has been disruption to normal thyroid tissue architecture.
  • CASE PRESENTATION: We report a patient with a history of surgically resected rectal adenocarcinoma who presents with a rising serum CEA level and an 18F-FDG PET scan positive thyroid nodule which was subsequently confirmed at surgery to be a focus of metastatic rectal adenocarcinoma within a primary poorly differentiated papillary thyroid carcinoma.Subsequent treatment involved right hemi-thyroidectomy, pulmonary wedge resection of oligometastatic metastatic colorectal cancer and chemotherapy.
  • CONCLUSION: Metastatic rectal carcinoma to the thyroid gland and in particular to a primary thyroid malignancy is rare and unusual.
  • Prognosis is likely to be more dependent on underlying metastatic disease rather than the primary thyroid malignancy hence primary treatments should be tailored towards treating and controlling metastatic disease and less emphasis placed on the primary thyroid malignancy.
  • [MeSH-major] Colorectal Neoplasms / pathology. Thyroid Neoplasms / secondary
  • [MeSH-minor] Fluorodeoxyglucose F18. Humans. Male. Middle Aged. Positron-Emission Tomography


3. Graf H: [Poorly differentiated thyroid carcinomas: new therapeutic considerations]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):711-8
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  • [Title] [Poorly differentiated thyroid carcinomas: new therapeutic considerations].
  • [Transliterated title] Carcinoma de tireóide pouco diferenciado: novas considerações terapêuticas.
  • For most differentiated thyroid carcinomas, as papillary and follicular carcinomas, following total thyroidectomy and 131I therapy for thyroid remnant ablation, treatment with thyroid hormones to suppress TSH levels will reduce the growth of any remaining thyroid cancer cells, and thyroid cell-specific radiation therapy will either cure or control the disease.
  • Thyroid carcinomas are considered poorly differentiated when they start to lose such functions as iodine uptake and thyrotropin-dependence for growth and production of thyroid proteins like NIS, thyroglobulin and desiodases.
  • One of the greatest challenges in the management of patients with follicular cell-derived thyroid cancer is the treatment of tumors that progressed despite surgery, (131)I and T4 suppression of TSH.
  • With the better knowledge of the abnormal molecular signaling in thyroid cancer cells, actually known targeted cancer therapies, directed against molecules involved in neoplastic transformation, are being used.
  • As the critical molecular requirements for tumor initiation, maintenance and progression are identified, combination therapies with targeted agents acting on each of them will improve the treatment of poorly differentiated thyroid carcinoma.
  • [MeSH-major] Adenocarcinoma, Follicular / therapy. Antineoplastic Agents / therapeutic use. Carcinoma, Papillary / therapy. Iodine Radioisotopes / therapeutic use. Proto-Oncogene Proteins / drug effects. Thyroid Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Humans

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  • (PMID = 16444353.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Iodine Radioisotopes; 0 / Proto-Oncogene Proteins
  • [Number-of-references] 53
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4. Ruangpratheep C, Lohachittranond C, Poonpracha T, Punyarit P: OCT4 expression on a case of poorly differentiated (insular) carcinoma of the thyroid gland and minireview. J Med Assoc Thai; 2005 Nov;88 Suppl 3:S281-9
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  • [Title] OCT4 expression on a case of poorly differentiated (insular) carcinoma of the thyroid gland and minireview.
  • Poorly differentiated (insular) carcinoma of the thyroid gland is rare and defined as follicular-cell neoplasms that show limited evidence of structural follicular cell differentiation and occupy both morphologically and behaviourally an intermediate position between differentiated (follicular and papillary carcinomas) and undifferentiated (anaplastic) carcinomas.
  • The authors report a case of a 37-year-old Thai woman who presented with a prolonged left thyroid nodule.
  • Final pathological diagnoses of her mass were poorly differentiated (insular) carcinoma with lymphovascular invasion and nodular goiter.
  • The tumor cell arrangements were nest (insular) and trabecular patterns with some follicular formations.
  • The authors believe that poorly differentiated (insular) carcinoma of the thyroid gland probably develops from the remnant of thyroid stem cells and is not associated with dedifferentiation (anaplasia or loss of cellular differentiation) from nodular goiter or cells of other thyroid carcinomas.
  • Although there was negative immunostain for OCT4 in the presented case, the authors assumed that the tumor cells behave with an intermediate position between thyroid stem cells and prothyrocytes Also they do not behave with thyroblasts.
  • However, there is only one case of immunohistochemistry of OCT4 in poorly differentiated (insular) carcinoma of the thyroid gland.
  • Further research on expression of OCT4 gene on thyroid cancers and other malignant tumors relating to tumorigenic cancer cells (cancer stem cells) may be useful to prognostic evaluation and administration of a new chemotherapy and/or radiotherapy that is specific for tumor-initiating cells.
  • [MeSH-major] Carcinoma / metabolism. Octamer Transcription Factor-3 / metabolism. Thyroid Neoplasms / metabolism

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  • (PMID = 16858970.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Octamer Transcription Factor-3
  • [Number-of-references] 14
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5. Landriscina M, Maddalena F, Fabiano A, Piscazzi A, La Macchia O, Cignarelli M: Erlotinib enhances the proapoptotic activity of cytotoxic agents and synergizes with paclitaxel in poorly-differentiated thyroid carcinoma cells. Anticancer Res; 2010 Feb;30(2):473-80
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  • [Title] Erlotinib enhances the proapoptotic activity of cytotoxic agents and synergizes with paclitaxel in poorly-differentiated thyroid carcinoma cells.
  • BACKGROUND: The therapeutic role of EGFR inhibitors in thyroid malignancies is still controversial even though the full activation of EGF signaling has recently been proposed as involved in the dedifferentiation of human thyroid cancers.
  • MATERIALS AND METHODS: Agents which target EGFR signaling (erlotinib, cetuximab and panitumumab) were evaluated at preclinical level in a panel of thyroid tumor cell lines.
  • RESULTS: Erlotinib induced a dose-dependent inhibition of cell proliferation together with inhibition of EGF-induced AKT and ERK1/2 signaling only in poorly-differentiated thyroid carcinoma FRO cells.
  • Of note, erlotinib enhanced the proapoptotic activity of doxorubicin and paclitaxel and exhibited synergy with paclitaxel in poorly-differentiated thyroid carcinoma cells.
  • CONCLUSION: EGFR signaling may represent a molecular target only in poorly-differentiated thyroid carcinoma cells, and agents that inhibit EGFR tyrosine kinase may be more effective than monoclonal antibodies which target the extracellular domain of the receptor.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Blotting, Western. Drug Synergism. Erlotinib Hydrochloride. Humans. Paclitaxel / administration & dosage. Quinazolines / administration & dosage. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 20332457.001).
  • [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 / Antineoplastic Agents; 0 / Quinazolines; 0 / RNA, Messenger; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; P88XT4IS4D / Paclitaxel
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6. Walczyk A, Kowalska A, Sygut J: The clinical course of poorly differentiated thyroid carcinoma (insular carcinoma) - own observations. Endokrynol Pol; 2010 Sep-Oct;61(5):467-73
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  • [Title] The clinical course of poorly differentiated thyroid carcinoma (insular carcinoma) - own observations.
  • INTRODUCTION: Poorly differentiated thyroid carcinoma (PDTC, insular carcinoma) occurs rarely.
  • It is described with more aggressive behaviour, poorer prognosis, and higher mortality than well differentiated thyroid carcinoma (WDTC).
  • The aim of this study was to evaluate the clinical course of patients with PDTC, in addition to frequency, clinical stage at the time of diagnosis and the possibility of radical surgical resection, the necessity and kind of complementary treatment, occurrence of distant metastases, and the survival of patients.
  • RESULTS: PDTC was diagnosed in 14 among 801 patients with thyroid carcinoma (1.75%).
  • Clinical stages (UICC 2002) at the time of diagnosis were as follows: 3 patients - pT(₁-₂)N(o-x)M(x) (21.5%); 10 patients - pT(₃ ₄)N(x o ₁)M(x-₁)(71.4%); and 1 was unresectable - T(x)N₁M₁ (7.1%).
  • Complementary radioiodine treatment was given to 12 patients (85.8%).
  • Radiation therapy of the neck was applied to 7 patients, palliative radiotherapy of the brain to 1 patient, and chemotherapy to 1 patient.
  • CONCLUSIONS: Poorly differentiated thyroid carcinoma is still a challenge both for pathologists and clinicians.
  • [MeSH-major] Adenocarcinoma, Follicular / secondary. Adenocarcinoma, Follicular / therapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / therapeutic use. Brain Neoplasms / secondary. Cell Differentiation. Chemotherapy, Adjuvant. Disease Progression. Disease-Free Survival. Female. Follow-Up Studies. Humans. Iodine Radioisotopes. Lung Neoplasms / secondary. Lymph Node Excision. Male. Middle Aged. Neoplasm Staging. Palliative Care. Radiotherapy, Adjuvant. Retrospective Studies. Thyroidectomy

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  • (PMID = 21049460.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Iodine Radioisotopes
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7. 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.
  • PDTC may represent an intermediate entity in the progression of well-differentiated thyroid carcinoma to ATC.
  • The roles of radiotherapy and chemotherapy have not been well described.
  • [MeSH-major] Carcinoma / pathology. Thyroid Neoplasms / pathology


8. Ghofrani M, Sosa JA, Ocal IT, Angeletti C: Fine needle aspiration of poorly differentiated oxyphilic (Hürthle cell) thyroid carcinoma: a case report. Acta Cytol; 2006 Sep-Oct;50(5):560-2
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  • [Title] Fine needle aspiration of poorly differentiated oxyphilic (Hürthle cell) thyroid carcinoma: a case report.
  • BACKGROUND: Poorly differentiated oxyphilic (Hürthle cell) carcinomas are a more recently described variant of poorly differentiated thyroid carcinoma and are characterized by a prominent Hürthle cell component in a solid or trabecular arrangement.
  • Clinically, poorly differentiated oxyphilic carcinomas behave more aggressively as compared to classic Hürthle cell carcinomas, which have a predominantly follicular pattern.
  • Although the histology of these rare thyroid tumors has been reported in the literature, the cytologic features on fine needle aspiration biopsy have not been described before.
  • CASE: A 73-year-old man with a long history of radioactive iodine and levothyroxine therapy for multinodular goiter presented with a painful, rapidly expanding, 6-cm, left thyroid mass with aggressive radiologic features.
  • Fine needle aspiration biopsy of the mass yielded extremely cellular smears with a dual population of medium-sized follicular cells and numerous Hürthle cells.
  • Subsequent thyroidectomy confirmed the malignant nature of this Hürthle cell-rich tumor, warranting a diagnosis of poorly differentiated oxyphilic (Hürthle cell) thyroid carcinoma.
  • CONCLUSION: Poorly differentiated oxyphilic thyroid carcinoma is an aggressive variant of Hürthle cell carcinomas and must enter the differential diagnosis when fine needle aspiration biopsy of a radiologically aggressive thyroid mass yields extremely hypercellular smears with a prominent Hürthle cell component.
  • [MeSH-major] Adenocarcinoma / diagnosis. Epithelial Cells / pathology. Lung Neoplasms / diagnosis. Thyroid Gland / pathology. Thyroid Neoplasms / diagnosis
  • [MeSH-minor] Aged. Biopsy, Fine-Needle. Diagnosis, Differential. Disease Progression. Goiter, Nodular / complications. Goiter, Nodular / drug therapy. Goiter, Nodular / radiotherapy. Humans. Iodine Radioisotopes / therapeutic use. Male. Neoplasm Invasiveness. Thyroidectomy. Thyroxine / therapeutic use

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  • (PMID = 17017447.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; Q51BO43MG4 / Thyroxine
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9. Siironen P, Hagström J, Mäenpää HO, Louhimo J, Heikkilä A, Heiskanen I, Arola J, Haglund C: Anaplastic and poorly differentiated thyroid carcinoma: therapeutic strategies and treatment outcome of 52 consecutive patients. Oncology; 2010;79(5-6):400-8
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  • [Title] Anaplastic and poorly differentiated thyroid carcinoma: therapeutic strategies and treatment outcome of 52 consecutive patients.
  • Anaplastic thyroid carcinoma (ATC) is one of the most lethal malignancies; poorly differentiated thyroid carcinoma (PDTC) is a new diagnosis for rare aggressive thyroid tumours.
  • Surgery is often considered the only chance for survival, but the benefit of surgery and subsequent multimodal therapy is unclear.
  • Multimodal therapy was successful for 9 (20%) ATC patients, and their median survival was the longest (11.6 months) among treatment groups.
  • Most PDTC patients (88%) underwent total thyroidectomy followed by radioiodine ablation; the only 2 who received chemotherapy survived longest.
  • Although ATC and PDTC are both aggressive thyroid carcinomas, multimodal therapy for both can provide a chance of prolonged survival in patients with locoregional disease.
  • [MeSH-major] Antineoplastic Agents / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Disease-Free Survival. Doxorubicin / therapeutic use. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Paclitaxel / therapeutic use. Prognosis. Retrospective Studies. Thyroid Carcinoma, Anaplastic. Thyroid Neoplasms / pathology. Thyroid Neoplasms / therapy. Treatment Outcome

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  • [Copyright] Copyright © 2011 S. Karger AG, Basel.
  • (PMID = 21455012.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel
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10. Ringel MD, Greenberg M, Chen X, Hayre N, Suzuki K, Priebat D, Saji M, Burman KD: Cytotoxic activity of 2',2'-difluorodeoxycytidine (gemcitabine) in poorly differentiated thyroid carcinoma cells. Thyroid; 2000 Oct;10(10):865-9
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  • [Title] Cytotoxic activity of 2',2'-difluorodeoxycytidine (gemcitabine) in poorly differentiated thyroid carcinoma cells.
  • Poorly differentiated and anaplastic thyroid cancers are aggressive and usually fatal neoplasms, despite aggressive treatment.
  • We performed an in vitro study to assess the activity of gemcitabine (2',2' difluorodeoxycytidine), a new fluorinated nucleoside analogue, against three poorly differentiated human thyroid carcinoma cell lines (ARO, WRO, and NPA).
  • In summary, gemcitabine has activity against poorly differentiated thyroid cancer cell lines in vitro.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Carcinoma / drug therapy. Deoxycytidine / pharmacology. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Cell Differentiation. Cell Division / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Humans. Mutation. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 11081253.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Tumor Suppressor Protein p53; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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11. Tauchmanovà L, Pensabene M, Capuano I, Spagnoletti I, Zeppa P, Del Vecchio S, Mainenti M, De Rosa G, Colao A, Contegiacomo A: Poorly differentiated small cell neuroendocrine carcinoma localized in three different endocrine glands: response to chemotherapy and octreotide LAR. J Endocrinol Invest; 2005 Apr;28(4):371-8
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  • [Title] Poorly differentiated small cell neuroendocrine carcinoma localized in three different endocrine glands: response to chemotherapy and octreotide LAR.
  • Neuroendocrine tumors represent a heterogeneous category of neoplasm, with conflicting diagnostic and therapeutic demands.
  • We here describe the case of a 72-yr-old woman with evidence of a poorly differentiated small-cell neuroendocrine carcinoma (NEC) localized in different endocrine glands and other non-endocrine organs.
  • In particular, a large ovarian mass, multinodular thyroid goiter, right adrenal mass, cystic liver metastases and anterior mediastinum lymph node metastasis were present.
  • The largest thyroid nodule caused tracheal restriction and dyspnea.
  • Diagnosis of poorly differentiated metastasized NEC of unknown origin was made on the basis of histological and immunohistochemical findings, and treatment with etoposide (100 mg/m2 in days 1, 2 and 3) and cisplatinum (45 mg/m2 in days 2 and 3) was initiated.
  • Rapid improvement of dyspnea and a reduction of the largest thyroid nodule, liver metastases and adrenal mass by 50% were observed after 3 months of treatment; the dimensions remained stable thereafter, while the pericardial lymph node disappeared.
  • In conclusion, poorly differentiated NEC of unknown primary site is a well-recognized category, usually with an aggressive behavior, rapid growth rate and wide dissemination.
  • Our patient is alive 18 months after beginning the treatment, reporting good general condition and quality of life over the whole follow-up period.
  • [MeSH-major] Adrenal Gland Neoplasms / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Small Cell / drug therapy. Liver Neoplasms / secondary. Neoplasms, Unknown Primary / drug therapy. Neuroendocrine Tumors / drug therapy. Octreotide / therapeutic use. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Aged. Female. Humans. Immunohistochemistry. Lymphatic Metastasis. Treatment Outcome

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  • (PMID = 15966513.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
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12. Kitazono M, Robey R, Zhan Z, Sarlis NJ, Skarulis MC, Aikou T, Bates S, Fojo T: Low concentrations of the histone deacetylase inhibitor, depsipeptide (FR901228), increase expression of the Na(+)/I(-) symporter and iodine accumulation in poorly differentiated thyroid carcinoma cells. J Clin Endocrinol Metab; 2001 Jul;86(7):3430-5
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  • [Title] Low concentrations of the histone deacetylase inhibitor, depsipeptide (FR901228), increase expression of the Na(+)/I(-) symporter and iodine accumulation in poorly differentiated thyroid carcinoma cells.
  • Thyroid carcinoma accounts for the majority of deaths from endocrine cancers.
  • A major cause of treatment failure is the inability to trap iodine.
  • We examined the ability of the novel histone deacetylase (HDAC) inhibitor, depsipeptide (FR901228), to modulate the expression of thyroid-specific genes.
  • Four cell lines, two derived from follicular thyroid carcinomas (FTC 133 and FTC 236) and two derived from anaplastic thyroid carcinomas (SW-1736 and KAT-4) were used.
  • After 3 days, messenger RNA levels approached those of a normal thyroid control.
  • These in vitro results suggest that depsipeptide or other histone deacetylase inhibitors might be used clinically in thyroid carcinomas that are unable to trap iodine as an adjunct to radioiodine therapy.
  • [MeSH-major] Anti-Bacterial Agents / administration & dosage. Carrier Proteins / metabolism. Depsipeptides. Enzyme Inhibitors / administration & dosage. Gene Expression / drug effects. Histone Deacetylase Inhibitors. Membrane Proteins / metabolism. Peptides, Cyclic. Symporters. Thyroid Neoplasms / metabolism
  • [MeSH-minor] Acetylation. Adenocarcinoma, Follicular / metabolism. Antibiotics, Antineoplastic / administration & dosage. Blotting, Western. Carcinoma / metabolism. Histones / metabolism. Humans. Iodine Radioisotopes / metabolism. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Thyroglobulin / genetics. Tumor Cells, Cultured

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  • (PMID = 11443220.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antibiotics, Antineoplastic; 0 / Carrier Proteins; 0 / Depsipeptides; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Iodine Radioisotopes; 0 / Membrane Proteins; 0 / Peptides, Cyclic; 0 / RNA, Messenger; 0 / Symporters; 0 / sodium-iodide symporter; 9010-34-8 / Thyroglobulin; CX3T89XQBK / romidepsin
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13. Schoenberger J, Grimm D, Kossmehl P, Infanger M, Kurth E, Eilles C: Effects of PTK787/ZK222584, a tyrosine kinase inhibitor, on the growth of a poorly differentiated thyroid carcinoma: an animal study. Endocrinology; 2004 Mar;145(3):1031-8
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  • [Title] Effects of PTK787/ZK222584, a tyrosine kinase inhibitor, on the growth of a poorly differentiated thyroid carcinoma: an animal study.
  • Vascular endothelial growth factor (VEGF) plays a key role in tumor angiogenesis including thyroid carcinomas.
  • The principal aim of this study was to test the hypothesis that inhibition of VEGF activity by PTK787/ZK222584 (PTK/ZK), a specific blocker of both VEGF-receptor tyrosine kinases, could inhibit the growth of a poorly differentiated thyroid cancer.
  • Human follicular thyroid tumor xenografts were implanted sc into nude mice.
  • Treatment was orally administered using a gastric tube.
  • Treatment with PTK/ZK induced a 41.4% reduction in tumor volumes.
  • These results showed that VEGF receptor blockade is a rational approach to the therapy of thyroid cancer.
  • The combination of radioiodine or external radiation with VEGF receptor tyrosine kinase inhibitors might be a new option, especially for poorly differentiated thyroid cancers with limited or no response to conventional therapy.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Angiogenesis Inhibitors / pharmacology. Phthalazines / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyridines. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Differentiation. Cell Line, Tumor. Extracellular Matrix Proteins / metabolism. Humans. Mice. Mice, Nude. Neovascularization, Pathologic / drug therapy. Thyroglobulin / metabolism. Vascular Endothelial Growth Factor A / metabolism. Xenograft Model Antitumor Assays

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  • [CommentIn] Endocrinology. 2004 Mar;145(3):1027-30 [14976150.001]
  • (PMID = 14607854.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Extracellular Matrix Proteins; 0 / Phthalazines; 0 / Pyridines; 0 / Vascular Endothelial Growth Factor A; 5DX9U76296 / vatalanib; 9010-34-8 / Thyroglobulin; EC 2.7.10.1 / Protein-Tyrosine Kinases
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14. Nabeshima S, Kishihara Y, Nabeshima A, Yamaga S, Kinjo M, Kashiwagi S, Hayashi J: Poorly differentiated adenocarcinoma with signet-ring cells of the Vater's ampulla, without jaundice but with disseminated carcinomatosis. Fukuoka Igaku Zasshi; 2003 Jul;94(7):235-40
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  • [Title] Poorly differentiated adenocarcinoma with signet-ring cells of the Vater's ampulla, without jaundice but with disseminated carcinomatosis.
  • To reduce tumor cells in number and improve DIC, 11 cycles of 5-Fluorouracil and leucovorin therapy were done, and the patient survived for 12 months.
  • Autopsy showed a 0.8 cm diameter, poorly differentiated adenocarcinoma with the signet-ring cell type in the lamina propria of the Vater's ampulla.
  • The sections of the stomach, the gallbladder, urinary bladder, prostate, and thyroid gland showed no malignant cells.
  • This is a rare case of an ampullary tumor of poorly differentiated adenocarcinoma with the signet-ring cell type, without jaundice but with multiple metastasis.
  • 5-Fluorouracil and leucovorin were effective for increasing survival time and improving quality of life.
  • [MeSH-major] Ampulla of Vater. Bone Marrow Neoplasms / secondary. Carcinoma, Signet Ring Cell / pathology. Common Bile Duct Neoplasms / pathology. Lung Neoplasms / secondary
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disseminated Intravascular Coagulation / complications. Disseminated Intravascular Coagulation / drug therapy. Fatal Outcome. Fluorouracil / administration & dosage. Humans. Jaundice. Leucovorin / administration & dosage. Male. Middle Aged. Neoplastic Cells, Circulating / pathology. Quality of Life

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  • (PMID = 14509231.001).
  • [ISSN] 0016-254X
  • [Journal-full-title] Fukuoka igaku zasshi = Hukuoka acta medica
  • [ISO-abbreviation] Fukuoka Igaku Zasshi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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15. Kurebayashi J, Tanaka K, Otsuki T, Moriya T, Kunisue H, Uno M, Sonoo H: All-trans-retinoic acid modulates expression levels of thyroglobulin and cytokines in a new human poorly differentiated papillary thyroid carcinoma cell line, KTC-1. J Clin Endocrinol Metab; 2000 Aug;85(8):2889-96
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  • [Title] All-trans-retinoic acid modulates expression levels of thyroglobulin and cytokines in a new human poorly differentiated papillary thyroid carcinoma cell line, KTC-1.
  • A new human thyroid carcinoma cell line, KTC-1, was established from the malignant pleural effusion of a recurrent thyroid carcinoma patient.
  • Histological findings by light and electron microscopy, such as the absence of follicular structures and the existence of intranuclear cytoplasmic inclusions and psammoma bodies, indicated transplanted tumors to be a poorly differentiated papillary thyroid carcinoma.
  • Messenger ribonucleic acid (mRNA) expression of thyroid transcription factor-1 and PAX-8 was also detected.
  • No mRNA expression of TSH receptors, thyroid peroxidase, or Na+/I- symporter was detected.
  • These findings suggest this cell line to be functionally poorly differentiated.
  • This cell line may be useful for studying redifferentiation therapy for thyroid carcinoma.
  • [MeSH-major] Carcinoma, Papillary / genetics. Cytokines / genetics. Gene Expression Regulation, Neoplastic / drug effects. Thyroglobulin / genetics. Thyroid Neoplasms / genetics. Transcription, Genetic. Tretinoin / pharmacology
  • [MeSH-minor] Animals. Cell Differentiation. Cell Division. DNA-Binding Proteins / genetics. Genes, p53. Growth Inhibitors / genetics. Humans. Interleukin-6 / genetics. Leukemia Inhibitory Factor. Lymphokines / genetics. Mice. Mice, Nude. Nuclear Proteins / genetics. Paired Box Transcription Factors. Polymorphism, Single-Stranded Conformational. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Thyroid Gland / metabolism. Trans-Activators / genetics. Transcription Factors / genetics. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 10946899.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / Growth Inhibitors; 0 / Interleukin-6; 0 / LIF protein, human; 0 / Leukemia Inhibitory Factor; 0 / Lif protein, mouse; 0 / Lymphokines; 0 / Nuclear Proteins; 0 / PAX8 protein, human; 0 / Paired Box Transcription Factors; 0 / Pax8 protein, mouse; 0 / RNA, Messenger; 0 / Trans-Activators; 0 / Transcription Factors; 0 / thyroid nuclear factor 1; 5688UTC01R / Tretinoin; 9010-34-8 / Thyroglobulin
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16. Santini F, Bottici V, Elisei R, Montanelli L, Mazzeo S, Basolo F, Pinchera A, Pacini F: Cytotoxic effects of carboplatinum and epirubicin in the setting of an elevated serum thyrotropin for advanced poorly differentiated thyroid cancer. J Clin Endocrinol Metab; 2002 Sep;87(9):4160-5
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  • [Title] Cytotoxic effects of carboplatinum and epirubicin in the setting of an elevated serum thyrotropin for advanced poorly differentiated thyroid cancer.
  • Chemotherapy represents the only therapeutic option in most poorly differentiated thyroid carcinomas, although its effect is limited and short lasting.
  • The aim of this study was to evaluate whether increasing the metabolic rate of thyroid cancer cells by TSH stimulation might result in higher response rate to chemotherapy.
  • Fourteen patients with poorly differentiated thyroid carcinoma and nonfunctioning diffuse lung metastases detected at computed tomography scan, entered this study.
  • Two additional patients did not complete the therapeutic protocol due to severe hematological side effects.
  • Results were evaluated by comparison of lung computed tomography scans before and after therapy.
  • Serum thyroglobulin after chemotherapy declined more than 50% in six patients, with respect to basal levels.
  • At the time of this analysis, among the patients who completed the treatment courses, 9 of 14 patients (64.3%) are still alive (median survival from start of chemotherapy = 21 months, range: 15-34).
  • Six of these patients did not show progression of lung disease, whereas regrowth of lung metastases was observed in three patients after 19, 20, and 21 months from chemotherapy, respectively.
  • Five patients died of their disease, including the one who had progression of lung disease during chemotherapy, three who died for brain or bone metastases, and one who died for refractory local tumor invasion.
  • In conclusion, the response rate of poorly differentiated thyroid cancer to chemotherapy observed in this study was favorable and promising.
  • [MeSH-major] Carboplatin / adverse effects. Epirubicin / adverse effects. Thyroid Neoplasms / drug therapy. Thyrotropin / blood
  • [MeSH-minor] Adult. Antineoplastic Agents / adverse effects. Female. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / radiography. Lung Neoplasms / secondary. Male. Middle Aged. Thyroxine / blood

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  • (PMID = 12213865.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 3Z8479ZZ5X / Epirubicin; 9002-71-5 / Thyrotropin; BG3F62OND5 / Carboplatin; Q51BO43MG4 / Thyroxine
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17. Catalano MG, Fortunati N, Pugliese M, Costantino L, Poli R, Bosco O, Boccuzzi G: Valproic acid induces apoptosis and cell cycle arrest in poorly differentiated thyroid cancer cells. J Clin Endocrinol Metab; 2005 Mar;90(3):1383-9
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  • [Title] Valproic acid induces apoptosis and cell cycle arrest in poorly differentiated thyroid cancer cells.
  • Poorly differentiated thyroid carcinoma is an aggressive human cancer that is resistant to conventional therapy.
  • Histone deacetylase inhibitors are a promising class of drugs, acting as antiproliferative agents by promoting differentiation, as well as inducing apoptosis and cell cycle arrest.
  • Valproic acid (VPA), a class I selective histone deacetylase inhibitor widely used as an anticonvulsant, promotes differentiation in poorly differentiated thyroid cancer cells by inducing Na(+)/I(-) symporter and increasing iodine uptake.
  • Here, we show that it is also highly effective at suppressing growth in poorly differentiated thyroid cancer cell lines (N-PA and BHT-101).
  • Both apoptosis and cell cycle arrest are induced by treatment with 1 mm VPA, a dose that promotes cell redifferentiation and that is slightly above the serum concentration reached in patients treated for epilepsy.
  • These multifaceted properties make VPA of clinical interest as a new approach to treating poorly differentiated thyroid cancer.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma, Papillary. Enzyme Inhibitors / pharmacology. Thyroid Neoplasms. Valproic Acid / pharmacology
  • [MeSH-minor] Cell Cycle / drug effects. Cell Cycle Proteins / genetics. Cell Differentiation. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / drug effects. Histone Deacetylase Inhibitors. Humans

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  • (PMID = 15585556.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 614OI1Z5WI / Valproic Acid
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18. Broecker-Preuss M, Sheu SY, Worm K, Feldkamp J, Witte J, Scherbaum WA, Mann K, Schmid KW, Schott M: Expression and mutation analysis of the tyrosine kinase c-kit in poorly differentiated and anaplastic thyroid carcinoma. Horm Metab Res; 2008 Oct;40(10):685-91
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  • [Title] Expression and mutation analysis of the tyrosine kinase c-kit in poorly differentiated and anaplastic thyroid carcinoma.
  • Poorly differentiated and anaplastic thyroid carcinoma are aggressive tumors failing to res-pond to conventional therapy.
  • Imatinib mesylate offers an effective therapeutic option in patients with various types of malignancies by inhibiting tyrosine kinases such as c-kit.
  • In this study we investigated c-kit expression in anaplastic and poorly differentiated thyroid carcinoma compared to differentiated carcinoma and adenoma and the presence of c-kit mutations.
  • In total, 224 thyroid tissues were analyzed by immunohistochemistry.
  • Mutation analysis of exon 9, 11, 13, and 17 of the c-kit gene was performed in anaplastic and poorly differentiated carcinoma. c-Kit expression was negative in all anaplastic thyroid carcinoma, while c-kit expression of poorly differentiated carcinoma showed a high variability with a more intense staining in tumors showing obvious differentiated malignant follicular tumor areas.
  • Differentiated carcinoma showed a slight, but not significantly stronger c-kit expression than poorly differentiated carcinoma.
  • All tumors revealed wild type sequences of c-kit gene in exons 9, 11, 13, and 17.
  • The low or lacking c-kit expression in undifferentiated thyroid carcinoma together with the lack of mutations argue against a crucial role of c-kit in thyroid carcinoma cell proliferation.
  • Further molecular targets of imatinib mesylate have to be analyzed to estimate a potential benefit of this drug for patients with dedifferentiated thyroid carcinoma.
  • [MeSH-major] Carcinoma / enzymology. Carcinoma / pathology. Cell Differentiation. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / metabolism. Thyroid Neoplasms / enzymology. Thyroid Neoplasms / pathology

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  • (PMID = 18622894.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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19. Elisei R, Vivaldi A, Agate L, Ciampi R, Molinaro E, Piampiani P, Romei C, Faviana P, Basolo F, Miccoli P, Capodanno A, Collecchi P, Pacini F, Pinchera A: All-trans-retinoic acid treatment inhibits the growth of retinoic acid receptor beta messenger ribonucleic acid expressing thyroid cancer cell lines but does not reinduce the expression of thyroid-specific genes. J Clin Endocrinol Metab; 2005 Apr;90(4):2403-11
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  • [Title] All-trans-retinoic acid treatment inhibits the growth of retinoic acid receptor beta messenger ribonucleic acid expressing thyroid cancer cell lines but does not reinduce the expression of thyroid-specific genes.
  • Conventional chemotherapy and radiotherapy are ineffective for the treatment of advanced thyroid tumors like poorly differentiated papillary, anaplastic, and medullary thyroid cancer.
  • In the attempt to evaluate the possibility of using retinoic acid (RA) in the treatment of thyroid cancer refractory to conventional therapy, we studied the effect of all-trans-RA treatment on five human thyroid cancer cell lines.
  • We found that WRO and NPA, derived from follicular and poorly differentiated human thyroid carcinoma, respectively, showed a growth inhibition after 25 and 21 d of RA treatment.
  • On the contrary, we did not observe any recovery of mRNA expression of thyroid-specific genes and in particular of the sodium iodide symporter gene.
  • The lack of recovery of radioiodide uptake after all-trans-RA treatment confirmed the inability to reexpress sodium iodide symporter mRNA.
  • The main difference between the all-trans-RA responding cells (WRO and NPA) and the nonresponding cells [ARO, FRO (derived from human anaplastic thyroid tumors) and TT (derived from human medullary thyroid tumor)] was the basal and all-trans-RA induced RA receptor (RAR)beta mRNA expression.
  • Interestingly, 14 thyroid tumors (10 papillary and four anaplastic) showed a significant lower expression of RARbeta mRNA when compared with normal thyroid tissues.
  • In agreement with this result, only 30% of papillary thyroid carcinomas analyzed were positive for RARbeta protein expression with a degree of expression that was much lower than that found in normal thyroid tissue.
  • In conclusion we found that all-trans-RA treatment can determine a significant in vitro growth inhibition especially in differentiated thyroid tumor-derived cell lines but it seems unable to reinduce the expression of thyroid-specific genes and in particular to reinduce the ability to take up iodine.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / drug effects. RNA, Messenger / analysis. Receptors, Retinoic Acid / genetics. Thyroid Gland / metabolism. Thyroid Neoplasms / drug therapy. Tretinoin / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Immunohistochemistry

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  • (PMID = 15623821.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor beta; 5688UTC01R / Tretinoin
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20. Heron DE, Karimpour S, Grigsby PW: Anaplastic thyroid carcinoma: comparison of conventional radiotherapy and hyperfractionation chemoradiotherapy in two groups. Am J Clin Oncol; 2002 Oct;25(5):442-6
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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 carcinoma: comparison of conventional radiotherapy and hyperfractionation chemoradiotherapy in two groups.
  • Anaplastic thyroid carcinoma (ATC) is a highly aggressive neoplasm with a poor prognosis.
  • Treatment modalities including surgery and fractionated radiotherapy have had limited success in controlling these tumors.
  • Median survival time is often measured in months.
  • A review of all patients treated between 1952 and 1999 identified 32 patients with anaplastic or poorly differentiated thyroid carcinoma.
  • Most group 1 patients received once-daily radiotherapy and most group 2 patients received twice-daily radiotherapy with concurrent chemotherapy.
  • Chemotherapy consisted of doxorubicin, paclitaxel, vincristine, or cisplatin.
  • In group 2, 1 patient was treated with surgery only; 3 with surgery and radiotherapy; 10 with radiotherapy and chemotherapy; 5 with surgery, radiotherapy, and chemotherapy; and 5 with radiotherapy alone.
  • Among patients with ATC surgery, hyperfractionated radiotherapy in conjunction with chemotherapy is associated with better survival but not PFS compared to conventional radiotherapy.
  • [MeSH-major] Carcinoma / radiotherapy. Thyroid Neoplasms / radiotherapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Radiation Dosage. Survival Analysis. Thyroidectomy

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  • (PMID = 12393980.001).
  • [ISSN] 0277-3732
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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21. Haugen BR: Redifferentiation therapy in advanced thyroid cancer. Curr Drug Targets Immune Endocr Metabol Disord; 2004 Sep;4(3):175-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Redifferentiation therapy in advanced thyroid cancer.
  • Thyroid cancer is a relatively common malignancy with an estimated prevalence of 250,000 in the U.S.
  • A minority of patients have poorly differentiated thyroid carcinoma that is unresponsive to radioiodine therapy.
  • Redifferentiation agents that 'reprogram' these tumors to concentrate radioiodine would be of great value in treating patients with advanced thyroid cancer.
  • It appears that 20-40% of patients respond to isotretinoin treatment by concentration of radioiodine in metastatic tumors, but the clinical utility of this redifferentiation is still unclear.
  • Abnormal DNA methylation may be an early event in thyroid tumorigenesis and methylation of the sodium iodide symporter (NIS) may play a role in the loss of iodine concentration in these tumors.
  • Histone acetylation is required for efficient transcription of genes necessary for differentiated function.
  • Proteins that cause histone deacetylation inhibit gene transcription and differentiated function.
  • Inhibitors of histone deacetylation (depsipeptide, trichostatin A) have been shown to increase NIS expression and iodine uptake in poorly differentiated and undifferentiated cell lines.
  • Finally, commonly used agents such as thiazolidinediones (diabetes) and HMG-CoA reductase inhibitors (hypercholesterolemia) have shown promise in preliminary in vitro studies in advanced thyroid cancer cell lines.
  • Development of these and other novel agents for the treatment of advanced thyroid cancer is critical for us to treat an uncommon progression of a common malignancy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Transformation, Neoplastic / drug effects. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / pathology
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Differentiation / physiology. Humans

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  • (PMID = 15379720.001).
  • [ISSN] 1568-0088
  • [Journal-full-title] Current drug targets. Immune, endocrine and metabolic disorders
  • [ISO-abbreviation] Curr. Drug Targets Immune Endocr. Metabol. Disord.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 56
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22. Kaltsas GA, Besser GM, Grossman AB: The diagnosis and medical management of advanced neuroendocrine tumors. Endocr Rev; 2004 Jun;25(3):458-511
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Neuroendocrine tumors (NETs) constitute a heterogeneous group of neoplasms that originate from endocrine glands such as the pituitary, the parathyroids, and the (neuroendocrine) adrenal, as well as endocrine islets within glandular tissue (thyroid or pancreatic) and cells dispersed between exocrine cells, such as endocrine cells of the digestive (gastroenteropancreatic) and respiratory tracts.
  • Conventionally, NETs may present with a wide variety of functional or nonfunctional endocrine syndromes and may be familial and have other associated tumors.
  • Imaging modalities include endoscopic ultrasonography, computed tomography and magnetic resonance imaging, and particularly, scintigraphy with somatostatin analogs and metaiodobenzylguanidine.
  • Successful treatment of disseminated NETs requires a multimodal approach; radical tumor surgery may be curative but is rarely possible.
  • Well-differentiated and slow-growing gastroenteropancreatic tumors should be treated with somatostatin analogs or alpha-interferon, with chemotherapy being reserved for poorly differentiated and progressive tumors.
  • Therapy with radionuclides may be used for tumors exhibiting uptake to a diagnostic scan, either after surgery to eradicate microscopic residual disease or later if conventional treatment or biotherapy fails.
  • [MeSH-major] Interferon-alpha / therapeutic use. Neuroendocrine Tumors / diagnosis. Neuroendocrine Tumors / drug therapy. Somatostatin / therapeutic use
  • [MeSH-minor] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / therapy. Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Carcinoma, Neuroendocrine / diagnosis. Carcinoma, Neuroendocrine / drug therapy. Gastrointestinal Neoplasms / diagnosis. Gastrointestinal Neoplasms / therapy. Humans. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy. Parathyroid Neoplasms / diagnosis. Parathyroid Neoplasms / therapy. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy. Prognosis. Quality of Life. Sensitivity and Specificity. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / therapy. Tomography, X-Ray Computed

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  • (PMID = 15180952.001).
  • [ISSN] 0163-769X
  • [Journal-full-title] Endocrine reviews
  • [ISO-abbreviation] Endocr. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Interferon-alpha; 51110-01-1 / Somatostatin
  • [Number-of-references] 620
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23. Kotchetkov R, Cinatl J, Krivtchik AA, Vogel JU, Matousek J, Pouckova P, Kornhuber B, Schwabe D, Cinatl J Jr: Selective activity of BS-RNase against anaplastic thyroid cancer. Anticancer Res; 2001 Mar-Apr;21(2A):1035-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective activity of BS-RNase against anaplastic thyroid cancer.
  • BACKGROUND: Anaplastic thyroid carcinoma is an aggressive solid tumor that fails to adequately respond to any known chemotherapeutic regimen.
  • The development of effective chemotherapy agents would provide the best chance for long-term survival of patients.
  • MATERIALS AND METHODS: The cytotoxic effects of bovine seminal ribonuclease (BS-RNase) against thyroid carcinoma cell lines with different degrees of differentiation in comparison to non-malignant cells, including human foreskin fibroblasts (HFF) and retinal pigment epithelial cells (RPE), were tested using the MTT dye reduction assay.
  • The antitumoral in vivo effects of BS-RNase were assessed on established xenografts of anaplastic thyroid carcinoma cell line 8505C in nude mice using subcutaneous injections of BS-RNase (12.5 mg/kg once a day, on 20 consecutive days).
  • The greatest growth inhibition was seen in the 8505C line, while IC50 values for papillary (B-CPAP) and poorly-differentiated thyroid carcinoma cells were about 6-fold higher.
  • In vivo treatment induced significant tumor regression after the course of 20 consecutive days.
  • No apparent toxic effects of BS-RNase toward non-malignant cells were observed during the in vivo treatment.
  • After cessation of therapy (day 20) tumor volume continued to decrease and the tumor was no longer detectable after 30 days of treatment induction in all animals.
  • CONCLUSION: BS-RNase may have beneficial effects for treatment of aggressive anaplastic thyroid cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Endoribonucleases / therapeutic use. Thyroid Neoplasms / drug therapy

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  • (PMID = 11396137.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Fasl protein, mouse; 0 / Membrane Glycoproteins; 0 / Proto-Oncogene Proteins c-bcl-2; EC 3.1.- / Endoribonucleases; EC 3.1.27.- / ribonuclease SPL
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24. Grosse J, Grimm D, Westphal K, Ulbrich C, Moosbauer J, Pohl F, Koelbl O, Infanger M, Eilles C, Schoenberger J: Radiolabeled annexin V for imaging apoptosis in radiated human follicular thyroid carcinomas--is an individualized protocol necessary? Nucl Med Biol; 2009 Jan;36(1):89-98
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiolabeled annexin V for imaging apoptosis in radiated human follicular thyroid carcinomas--is an individualized protocol necessary?
  • INTRODUCTION: Induction of apoptosis is a widely used strategy for cancer therapy, but evaluating the degree and success of this therapy still poses a problem.
  • Radiolabeled annexin V has been proposed to be a promising candidate for detecting apoptotic cells in tumors following chemotherapy in vivo.
  • In order to see whether radiolabeled annexin V could be a suitable substance for the noninvasive in vivo detection of apoptosis in thyroid tissue and to establish an optimized study protocol, we investigated two poorly differentiated thyroid carcinoma cell lines: ML-1 and FTC-133.
  • METHODS: Apoptosis was evaluated before as well as 2 and 4 days after in vitro irradiation with 30 Gy X-rays.
  • A reliable evaluation of apoptosis induced by radiotherapy in thyroid tumors was possible 48 h after irradiation, when binding of radiolabeled annexin V is most significantly enhanced.
  • Using two poorly differentiated cell lines of thyroid carcinoma, one may expect to find a nearly similar response to external irradiation.
  • However, an individualized study protocol for each type of tumor and probably within each type is necessary.
  • [MeSH-major] Annexin A5 / analysis. Annexin A5 / metabolism. Apoptosis / radiation effects. Thyroid Neoplasms / pathology. Thyroid Neoplasms / radiotherapy

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  • (PMID = 19181273.001).
  • [ISSN] 0969-8051
  • [Journal-full-title] Nuclear medicine and biology
  • [ISO-abbreviation] Nucl. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antigens, CD95; 0 / Biomarkers, Tumor; 0 / FAS protein, human; 0 / Iodine Radioisotopes; 0 / bcl-2-Associated X Protein; EC 3.4.22.- / Caspase 3; I223NX31W9 / Fluorescein-5-isothiocyanate
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25. Marinuzzi G, Bellini V, Antimi M: [Anaplastic, insular, and medullary carcinoma of the thyroid]. Clin Ter; 2000 Nov-Dec;151(6):427-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Anaplastic, insular, and medullary carcinoma of the thyroid].
  • [Transliterated title] Il carcinoma anaplastico, insulare e midollare della tiroide.
  • Anaplastic carcinoma, insular carcinoma and medullary carcinoma (both familiar and sporadic forms) represent the 7-25% of all thyroid tumors.
  • Anaplastic carcinoma is one of most aggressive human tumors and the therapeutic options proposed have failed to improve the prognosis of these patients.
  • Insular carcinoma is a not well known thyroid neoplasia described for the first time in 1984 and showing intermediate biological behaviour between differentiated and anaplastic forms.
  • Medullary carcinoma arises from parafollicular"C" cells of the gland and then may be considered a neuroendocrine tumor.
  • Choice therapy is surgery, tiroxine is only substitutive, familiar screening is mandatory.
  • Chemotherapy (dacarbazine or cisplatin and doxorubicine), radiotherapy and recently octreotide anologues, may be useful for relapsing not operable forms.
  • [MeSH-major] Carcinoma, Medullary. Thyroid Neoplasms

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  • (PMID = 11211477.001).
  • [ISSN] 0009-9074
  • [Journal-full-title] La Clinica terapeutica
  • [ISO-abbreviation] Clin Ter
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 43
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26. Grozinsky-Glasberg S, Grossman AB, Korbonits M: The role of somatostatin analogues in the treatment of neuroendocrine tumours. Mol Cell Endocrinol; 2008 May 14;286(1-2):238-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of somatostatin analogues in the treatment of neuroendocrine tumours.
  • Neuroendocrine tumours belong to a heterogeneous family of neoplasms, originating in endocrine glands (such as the pituitary, parathyroid or the neuroendocrine adrenal glands), in endocrine islets (within the thyroid or pancreas) as well as in endocrine cells dispersed between exocrine cells throughout the digestive or respiratory tracts.
  • The clinical behaviour of neuroendocrine tumours is variable; they may be functioning or not functioning, ranging from well-differentiated slow growing neuroendocrine tumours to poorly differentiated neuroendocrine tumours, which are highly aggressive malignant tumours.
  • The development of somatostatin analogues as important diagnostic and treatment tools have revolutionised the clinical management of patients with neuroendocrine tumours.
  • However, although symptomatic relief and stabilisation of tumour growth for various periods of time are observed in many patients treated with somatostatin analogues, tumour regression is rare.
  • Development of new somatostatin analogues and new drug combination therapies should further improve the clinical management of these patients.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Neuroendocrine Tumors / drug therapy. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use
  • [MeSH-minor] Adrenal Gland Neoplasms / drug therapy. Carcinoma, Bronchogenic / drug therapy. Female. Humans. Ovarian Neoplasms / drug therapy. Pancreatic Neoplasms / drug therapy. Paraganglioma / drug therapy. Pheochromocytoma / drug therapy. Pituitary Neoplasms / drug therapy. Thyroid Neoplasms / drug therapy

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  • (PMID = 18037561.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 51110-01-1 / Somatostatin
  • [Number-of-references] 75
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27. Görges R, Kahaly G, Müller-Brand J, Mäcke H, Roser HW, Bockisch A: Radionuclide-labeled somatostatin analogues for diagnostic and therapeutic purposes in nonmedullary thyroid cancer. Thyroid; 2001 Jul;11(7):647-59
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radionuclide-labeled somatostatin analogues for diagnostic and therapeutic purposes in nonmedullary thyroid cancer.
  • Despite the fact that several recent studies report an expression of somatostatin receptors in nonmedullary thyroid cancer (non-MTC), there is still no consensus concerning the diagnostic and therapeutic usefulness of radionuclide-labeled somatostatin analogues in non-MTC.
  • We present the results of 50 scintigraphic studies with (111)In-Pentetreotide ((111)In-P) in 48 patients with metastasizing non-MTC (n = 9 papillary, n = 9 follicular, n = 29 Hurthle cell, n = 1 insular carcinoma).
  • Histopathology demonstrated that maximal uptake was observed in Hurthle cell carcinoma (95% positive examinations if thyroglobulin exceeds 10 ng/mL).
  • We also describe for the first time dosimetric and clinical data from the courses of 90Y-DOTATOC therapy in three patients with progressive, somatostatin-receptor-positive non-MTC (up to 9.3 GBq per 4 cycles).
  • We conclude that (111)In-P is a promising tool for whole-body diagnosis in nonradioiodine-accumulating non-MTC, especially in Hürthle cell cancer, and if 2-[18F]fluorodeoxyglucose-positron emission tomography (FDG-PET) is not available.
  • Although the number of patients treated with 90Y-DOTATOC is still limited, our applied treatment protocol appears to be ineffective in metastasizing non-MTC.
  • [MeSH-major] Octreotide / analogs & derivatives. Octreotide / therapeutic use. Radiopharmaceuticals / therapeutic use. Somatostatin / analogs & derivatives. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / radionuclide imaging. Yttrium Radioisotopes / therapeutic use

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  • (PMID = 11484893.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indium Radioisotopes; 0 / Radiopharmaceuticals; 0 / Yttrium Radioisotopes; 51110-01-1 / Somatostatin; G083B71P98 / pentetreotide; RWM8CCW8GP / Octreotide; U194AS08HZ / Edotreotide
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28. Dackiw AP, Ezzat S, Huang P, Liu W, Asa SL: Vitamin D3 administration induces nuclear p27 accumulation, restores differentiation, and reduces tumor burden in a mouse model of metastatic follicular thyroid cancer. Endocrinology; 2004 Dec;145(12):5840-6
Hazardous Substances Data Bank. THYROGLOBULIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vitamin D3 administration induces nuclear p27 accumulation, restores differentiation, and reduces tumor burden in a mouse model of metastatic follicular thyroid cancer.
  • We have previously demonstrated in vitro that 1alpha,25-dihydroxyvitamin D3 (calcitriol) treatment increases p27 expression and decreases cell proliferation in cultured thyroid carcinoma cell lines.
  • We hypothesized that in vivo treatment with calcitriol would have a beneficial effect on thyroid carcinoma growth and progression.
  • Five x 10(6) WRO (human thyroid follicular carcinoma derived) cells were implanted in the neck in 4- to 5-wk-old female SCID mice in an orthotopic xenograft model.
  • Animals (n = 15) were treated i.p. three times a week for 21 d with 0.75 microg/kg calcitriol or vehicle.
  • Mice were killed 21 d after tumor implantation, tumor volume was measured, and excised tumor tissue was examined by light microscopy and immunohistochemistry for p27 and thyroglobulin reactivity.
  • Average tumor volume in control mice after 21 d of vehicle treatment was 2002 +/- 207 mm3 compared with a mean tumor volume of 1241 +/- 115 mm3 in animals receiving calcitriol, reflecting a 38% reduction in tumor volume size (P < 0.003).
  • Tumors from vehicle-treated animals demonstrated morphological features of epithelial malignancies with characteristics of insular carcinoma and multiple metastases to the lungs.
  • This was associated with a marked accumulation of p27 immunoreactivity in the nuclear compartment.
  • These studies demonstrate that in vivo calcitriol administration can effectively restore p27 accumulation in thyroid carcinoma cells, an effect associated with appreciably enhanced cellular differentiation, reduction in tumor burden, and prevention of metastatic growth.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Cholecalciferol / pharmacology. Proliferating Cell Nuclear Antigen / metabolism. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Line, Tumor. Disease Models, Animal. Humans. Immunohistochemistry. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Mice. Thyroglobulin / metabolism. Xenograft Model Antitumor Assays


29. Massart C, Denais A, Gibassier J: Effect of all-trans retinoic acid and sodium butyrate in vitro and in vivo on thyroid carcinoma xenografts. Anticancer Drugs; 2006 Jun;17(5):559-63
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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 all-trans retinoic acid and sodium butyrate in vitro and in vivo on thyroid carcinoma xenografts.
  • In this work, we studied the effects of RA alone or combined with the HDAC inhibitor sodium butyrate (NaB) in a poorly differentiated thyroid carcinoma cell line (FTC-133) cultured in vitro or transplanted into nude mice.
  • Body weight, tumoral volume (TV), doubling time of the tumor, specific growth delay and inhibition of tumoral growth at day 35 were determined in each group.
  • [MeSH-major] Butyrates / pharmacology. Thyroid Neoplasms / drug therapy. Tretinoin / pharmacology
  • [MeSH-minor] Alkaline Phosphatase / metabolism. Animals. Body Weight / drug effects. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Drug Synergism. Female. Humans. Mice. Mice, Nude. Neoplasm Transplantation

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  • (PMID = 16702813.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Butyrates; 5688UTC01R / Tretinoin; EC 3.1.3.1 / Alkaline Phosphatase
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30. Bombardieri E, Seregni E, Villano C, Aliberti G, Mattavelli F: Recombinant human thyrotropin (rhTSH) in the follow-up and treatment of patients with thyroid cancer. Tumori; 2003 Sep-Oct;89(5):533-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recombinant human thyrotropin (rhTSH) in the follow-up and treatment of patients with thyroid cancer.
  • The follow-up of thyroid cancer is based on the detection of residual and recurrent thyroid carcinoma.
  • Tg serum levels and the uptake of 131I on a whole body scan (WBS) depend on TSH stimulation, which in thyroidectomized patients can be obtained either by withdrawal of thyroid hormone treatment (thyroxine) or by administration of exogenous TSH.
  • Even if the administration of rhTSH and withdrawal of thyroid hormone are not completely equivalent, the use of rhTSH has already entered the clinical routine (rhTSH Tg test and rhTSH WBS) because with rhTSH the morbidity and discomfort associated with the withdrawal of thyroid hormone can be avoided.
  • At a recent International Consensus Conference on the follow-up of differentiated thyroid carcinoma it was proposed to carry out only Tg measurement after rhTSH stimulation; moreover, it was stated that 131I whole body scan has to be discouraged in patients submitted to radical surgery and radioiodine ablation with no clinical evidence of residual tumor and with undetectable levels of Tg during hormonal suppression of TSH.
  • This is still a matter of debate, also because it is not valid for all risk groups and not all patients undergo the same clinical management (radical surgery or not, thyroid ablation with 131I or not).
  • However, the availability of rhTSH will definitely change the management of papillary and follicular thyroid carcinoma, also with regard to iodine treatment.
  • In fact, rhTSH can be used during radioiodine treatment to enhance the 131I uptake by the cancer cells in particular groups of patients.
  • 2) patients affected by tumors with marked biological aggressiveness and a low iodine uptake (variants of follicular carcinoma, insular carcinoma, tall and columnar cell variants of papillary thyroid carcinoma, Hürthle cell carcinoma);.
  • The potential efficiency of rhTSH in radiometabolic treatment is an important issue that has been studied in a limited number of patients, but is worthy of further investigations in large perspective.
  • A recent clinical prospective trial has been proposed by the Thyroid Cancer Study Group of the Istituto Nazionale Tumori and is now ongoing.
  • [MeSH-major] Thyroid Neoplasms / blood. Thyroid Neoplasms / drug therapy. Thyrotropin / blood. Thyrotropin / therapeutic use
  • [MeSH-minor] Humans. Recombinant Proteins / therapeutic use. Thyroglobulin / blood

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  • (PMID = 14870779.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; 9002-71-5 / Thyrotropin; 9010-34-8 / Thyroglobulin
  • [Number-of-references] 32
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31. Landriscina M, Modoni S, Fabiano A, Fersini A, Barone C, Ambrosi A, Cignarelli M: Cell differentiation and iodine-131 uptake in poorly differentiated thyroid tumour in response to nevirapine. Lancet Oncol; 2006 Oct;7(10):877-9
Hazardous Substances Data Bank. THYROGLOBULIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell differentiation and iodine-131 uptake in poorly differentiated thyroid tumour in response to nevirapine.
  • [MeSH-major] Carcinoma, Papillary / therapy. Cell Differentiation / drug effects. Nevirapine / therapeutic use. Thyroid Neoplasms / therapy
  • [MeSH-minor] Aged. Cells, Cultured. Female. Fluorescent Antibody Technique. Humans. Iodine Radioisotopes / pharmacokinetics. Iodine Radioisotopes / therapeutic use. Reverse Transcriptase Inhibitors / therapeutic use. Thyroglobulin / analysis. Thyroid Gland / cytology. Thyroid Gland / drug effects. Thyroid Gland / metabolism. Thyroidectomy. Tumor Cells, Cultured






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