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1. National Toxicology Program: NTP toxicology and carcinogenesis studies of decalin (CAS No. 91-17-8) in F344/N rats and B6C3F(1) mice and a toxicology study of decalin in male NBR rats (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2005 Jan;(513):1-316
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Decalin was nominated for study by the National Cancer Institute because of its chemical structure, its potential for consumer exposure, and a lack of adequate testing of the chemical.
  • Male NBR rats do not produce alpha2u-globulin; the NBR rats were included to study the relationship of alpha2u-globulin and renal lesion induction.
  • All rats survived to the end of the study, and mean body weights of exposed groups were similar to those of the chamber controls.
  • Renal toxicity studies were performed in male F344/N and NBR rats.
  • Exposure-related hyaline droplet accumulation, degeneration and regeneration of renal cortical tubules, and granular casts occurred in the kidney of exposed F344/N male rats.
  • All mice survived to the end of the study, and mean body weights of exposed groups were similar to those of the chamber control groups.
  • 3-MONTH STUDY IN RATS: Groups of 25 male and 20 female F344/N rats were exposed to 0, 25, 50, 100, 200, or 400 ppm decalin vapor 6 hours per day, 5 days per week for 2 (five male renal toxicity rats), 6 (10 male and 10 female clinical pathology rats), or 14 (10 core study rats) weeks.
  • All rats survived to the end of the study, and mean body weights of exposed groups were similar to those of the chamber control groups.
  • Urinalysis results indicated that decalin exposure caused increases in urine glucose and protein concentrations and enzyme activities that were consistent with the renal lesions observed microscopically.
  • Renal toxicity studies were performed on rats sacrificed at 2 and 6 weeks and at the end of the study.
  • In kidney tissue examined for cell proliferation, the numbers of PCNA-labeled cells and labeling indices were generally significantly greater than those of the chamber controls in exposed groups of rats at all three time points.
  • Incidences of renal tubule regeneration and granular casts in the medulla of the kidney in exposed male rats were increased, and the severities of hyaline droplets generally increased with increasing exposure concentration.
  • All mice survived to the end of the study, and mean body weights of exposed groups were similar to those of the chamber control groups.
  • Mean body weights of 400 ppm males were slightly less than those of the chamber controls during the second year of the study.
  • Incidences of renal tubule adenoma and adenoma or carcinoma (combined) and of benign or malignant pheochromocytoma (combined) of the adrenal medulla in 100 and 400 ppm males were significantly increased.
  • There was a significant association between nephropathy severity and adrenal pheochromocytoma incidence.
  • Mean body weights of exposed groups were generally similar to those of the chamber control groups throughout the study.
  • Increased incidences of hepatocellular neoplasms occurred in 25 and 400 ppm female mice, and the incidences of centrilobular hypertrophy, necrosis, syncytial alteration, and erythrophagocytosis of the liver in 400 ppm males were significantly increased.
  • CONCLUSIONS: Under the conditions of these studies, there was clear evidence of carcinogenic activity of decalin in male F344/N rats based on increased incidences of renal tubule neoplasms.
  • The increased incidences of benign or malignant pheochromocytoma (combined) of the adrenal medulla in male rats were also considered to be exposure related.
  • There was equivocal evidence of carcinogenic activity of decalin in female B6C3F(1) mice based on marginally increased incidences of hepatocellular and uterine neoplasms.
  • [MeSH-minor] Administration, Inhalation. Animal Feed / analysis. Animals. Atmosphere Exposure Chambers. Body Weight / drug effects. Female. Genitalia, Male / pathology. Kidney Diseases / chemically induced. Kidney Diseases / pathology. Male. Mice. Mice, Inbred Strains. Mutagens / toxicity. Organ Size / drug effects. Rats. Rats, Inbred F344. Reproduction / drug effects

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  • (PMID = 15891779.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mutagens; 0 / Naphthalenes; 88451Q4XYF / decalin
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2. Fassnacht M, Kreissl MC, Weismann D, Allolio B: New targets and therapeutic approaches for endocrine malignancies. Pharmacol Ther; 2009 Jul;123(1):117-41
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  • In endocrine malignancies (thyroid carcinoma, parathyroid carcinoma, adrenocortical carcinoma, malignant pheochromocytoma) surgery is currently the treatment of choice, in case of differentiated thyroid carcinomas followed by 131-I-radioiodine administration.
  • This approach is often successful in early disease; however, treatment options for advanced endocrine malignancies remain unsatisfactory and prognosis is poor.
  • Advances in the understanding of the molecular pathology of endocrine malignancies has recently led to identification of key events in endocrine oncogenesis (e.g. oncogenic RET mutations in medullary thyroid carcinoma or RET/PTC rearrangements in papillary thyroid carcinoma).
  • These new insights are increasingly matched by new compounds (e.g. tyrosine kinase inhibitors) targeting signaling pathways essential for tumor cell survival, proliferation and metastases.
  • First results of "targeted therapies" in medullary and differentiated thyroid carcinoma are impressive: phase II trials targeting RET or VEGF receptor kinases led to objective tumor response in up to 50% of patients.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Drug Design. Endocrine Gland Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 19374919.001).
  • [ISSN] 1879-016X
  • [Journal-full-title] Pharmacology & therapeutics
  • [ISO-abbreviation] Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Protein Kinase Inhibitors
  • [Number-of-references] 438
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3. Yao JC, Hoff PM: Molecular targeted therapy for neuroendocrine tumors. Hematol Oncol Clin North Am; 2007 Jun;21(3):575-81; x
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  • [Title] Molecular targeted therapy for neuroendocrine tumors.
  • Although endocrine tumors are often slow growing, most can be life threatening and are considered resistant to conventional cytotoxic chemotherapy.
  • The recent emergence of molecularly targeted therapy in oncology has brought renewed interest in the development of novel agents for this rare group of diseases.
  • Preliminary results from phase II studies have shown promising results for VEGF and mTOR inhibitors in carcinoid and islet cell carcinoma and RET inhibitors in medullary thyroid carcinoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neuroendocrine Tumors / drug therapy. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Humans. Lymphokines / antagonists & inhibitors. Platelet-Derived Growth Factor / antagonists & inhibitors. Protein Kinases / drug effects. Proto-Oncogene Proteins c-ret / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Structure-Activity Relationship. TOR Serine-Threonine Kinases

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  • (PMID = 17548041.001).
  • [ISSN] 0889-8588
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Lymphokines; 0 / PDGFD protein, human; 0 / Platelet-Derived Growth Factor; 0 / Protein Kinase Inhibitors; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 40
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4. Sala E, Mologni L, Cazzaniga S, Papinutto E, Gambacorti-Passerini C: A rapid method for the purification of wild-type and V804M mutant ret catalytic domain: A tool to study thyroid cancer. Int J Biol Macromol; 2006 Aug 15;39(1-3):60-5
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  • [Title] A rapid method for the purification of wild-type and V804M mutant ret catalytic domain: A tool to study thyroid cancer.
  • RET (rearranged during transfection) is a transmembrane tyrosine kinase and acts as co-receptor of glial-derived neurotrophic factor (GDNF) family neurothrofic factors in complex with GFRalpha family proteins; RET is important for development of enteric nervous system and renal organogenesis during embryonal life.
  • Alterations in Ret gene are related to several neoplasias: point mutations are identified in medullary thyroid carcinoma (MTC) and multiple endocrine neoplasias 2A and B (MEN2A and B), while translocations and chromosomal inversions cause papillary thyroid carcinoma (PTC).
  • We expressed recombinant RET kinase domain (rRET) containing the active site, the ATP binding pocket, and the activation loop with regulatory activity, with the Baculovirus expression system.
  • Moreover a biochemical characterization of the recombinant product was performed in order to verify its activity (by ELISA) and physical state (dynamic light scattering).
  • The catalytic domain of RET can be used also for X-ray diffraction to obtain information about the three-dimensional structure, necessary for a rational design of selective inhibitors: it represents an important tool to understand the molecular mechanisms causing thyroid cancer and to care it.
  • [MeSH-major] Amino Acid Substitution. Point Mutation. Proto-Oncogene Proteins c-ret / isolation & purification
  • [MeSH-minor] Animals. Cell Line. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Enzyme Inhibitors / therapeutic use. Humans. Piperidines / therapeutic use. Protein Structure, Tertiary / genetics. Pyrazoles / therapeutic use. Pyrimidines / therapeutic use. Quinazolines / therapeutic use. Recombinant Proteins / biosynthesis. Recombinant Proteins / genetics. Recombinant Proteins / isolation & purification. Spodoptera / cytology. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / genetics. Thyroid Neoplasms / metabolism

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  • (PMID = 16490247.001).
  • [ISSN] 0141-8130
  • [Journal-full-title] International journal of biological macromolecules
  • [ISO-abbreviation] Int. J. Biol. Macromol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-amino-5-(4-methylphenyl)-7-(tert-butyl)pyrazolo(3,4-d)pyrimidine; 0 / Enzyme Inhibitors; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Pyrazoles; 0 / Pyrimidines; 0 / Quinazolines; 0 / Recombinant Proteins; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human
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5. Opocher G, Schiavi F, Cicala MV, Patalano A, Mariniello B, Boaretto F, Zovato S, Pignataro V, Macino B, Negro I, Mantero F: Genetics of adrenal tumors. Minerva Endocrinol; 2009 Jun;34(2):107-21
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  • [Title] Genetics of adrenal tumors.
  • The impact of genetics and genomics on clinical medicine is becoming more and more important.
  • Endocrinology pioneered the development of molecular medicine, but also the study of adrenal tumors had a great impact in this field.
  • Particularly important was the detection of genetics of tumors derived from the adrenal medulla, as well as that of those derived from the sympathetic and parasympathetic paraganglia.
  • Less well understood is the genetics of adrenal cortex tumors, in particular adrenocortical carcinoma, a rare and particularly aggressive disease.
  • There are only a few examples of hereditary transmission of adrenocortical carcinoma, but the analysis of low penetrance genes by genome wide association study may enable us to discover new genetic mechanisms responsible for adrenocortical-derived tumors.
  • [MeSH-major] Adrenal Gland Neoplasms / genetics. Biomarkers, Tumor / genetics. Mutation. Pheochromocytoma / genetics
  • [MeSH-minor] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Genetic Predisposition to Disease. Genomics. Humans. Neoplasm Proteins / genetics. Paraganglioma / genetics

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  • (PMID = 19471236.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Number-of-references] 81
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6. Castellani MR, Seregni E, Maccauro M, Chiesa C, Aliberti G, Orunesu E, Bombardieri E: MIBG for diagnosis and therapy of medullary thyroid carcinoma: is there still a role? Q J Nucl Med Mol Imaging; 2008 Dec;52(4):430-40
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  • [Title] MIBG for diagnosis and therapy of medullary thyroid carcinoma: is there still a role?
  • Medullary thyroid carcinoma (MTC) is a relatively rare neuroendocrine tumour originating from the parafollicular C cells and releases calcitonin (hCt), carcinoembryonic antigen (CEA) and occasionally other substances.
  • Prognosis of MTC is largely related to tumour extension at disease onset.
  • After surgery, serum hCt remains the most sensitive test for occult disease.
  • Diagnostic imaging work-up includes ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), bone scintigraphy, as the more frequent sites of recurrence or metastases are cervical and mediastinal lymph nodes, lungs, liver and bone.
  • Nuclear medicine procedures include (111)In-labelled somatostatin analogs, radioiodinated metaiodobenzylguanidine (MIBG), and several PET radiopharmaceuticals.
  • Since 1987, 1 027 diagnostic MIBG scans were performed in the Department Department of Diagnostic Imaging and Therapy of the Istituto Nazionale Tumori IRCCS Foundation (Milan, Italy), 85 of which for MTC, with a sensitivity of 38.7% in patients with evidence of disease and 30.7 % if all patients were considered.
  • Patients with liver or bone involvement responded to therapy and showed long-term partial remission of disease, others showed stability of disease, which was apparently unrelated to therapy.
  • [MeSH-major] 3-Iodobenzylguanidine / therapeutic use. Carcinoma, Medullary / diagnosis. Carcinoma, Medullary / radiotherapy. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / radiotherapy
  • [MeSH-minor] Humans. Neoplasm Metastasis / therapy. Neoplasm, Residual / diagnosis. Recurrence

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  • (PMID = 19088696.001).
  • [ISSN] 1824-4785
  • [Journal-full-title] The quarterly journal of nuclear medicine and molecular imaging : official publication of the Italian Association of Nuclear Medicine (AIMN) [and] the International Association of Radiopharmacology (IAR), [and] Section of the Society of Radiopharmaceutical Chemistry and Biology
  • [ISO-abbreviation] Q J Nucl Med Mol Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 35MRW7B4AD / 3-Iodobenzylguanidine
  • [Number-of-references] 69
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7. Milano A, Chiofalo MG, Basile M, Salzano de Luna A, Pezzullo L, Caponigro F: New molecular targeted therapies in thyroid cancer. Anticancer Drugs; 2006 Sep;17(8):869-79
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Carcinoma of the thyroid gland is the most common malignancy of the endocrine system.
  • Differentiated tumors are often curable with surgical resection and radioactive iodine.
  • Both anaplastic and medullary thyroid carcinomas exhibit aggressive behavior and are usually resistant to current therapeutic modalities.
  • Thyroid carcinoma represents a fascinating model and a particularly promising paradigm for targeted therapy because some of the key oncogenic events are activating mutations of genes coding for tyrosine kinases, and these occur early in cancer development.
  • Mutations in the RET proto-oncogene have been identified as causative for papillary carcinoma and familial medullary thyroid carcinoma, making it an attractive target for selective inhibition in these subtypes.
  • ZD 6474 has shown promising activity in preclinical models against RET kinase, and its contemporary inhibition of vascular endothelial growth factor and epidermal growth factor pathways renders it a very attractive drug for clinical trials in thyroid cancer.
  • Activating point mutation of B-RAF can occur early in the development of papillary carcinoma.
  • Moreover, papillary carcinomas with these mutations have more aggressive properties and are diagnosed more often at an advanced stage.
  • Clinical evaluation of B-RAF-targeting drugs is undergoing and trials in thyroid cancer are planned.
  • Agents that restore radioiodine uptake, such as histone deacetylase inhibitors and retinoids, represent another exciting field in new drug development in thyroid cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma / drug therapy. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Cell Membrane / drug effects. Cell Membrane / metabolism. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cytoplasm / drug effects. Cytoplasm / metabolism. Humans. Models, Biological. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-ret / genetics. Proto-Oncogene Proteins c-ret / metabolism. Receptor Protein-Tyrosine Kinases / metabolism


8. Gerschpacher M, Göbl C, Anderwald C, Gessl A, Krebs M: Thyrotropin serum concentrations in patients with papillary thyroid microcancers. Thyroid; 2010 Apr;20(4):389-92
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  • Thus, the objective of this study was to compare preoperative serum TSH concentrations in patients with papillary thyroid microcarcinoma (PTMC) and individuals in whom the presence of even small differentiated thyroid cancers was excluded by thorough histological examination of the thyroid after total thyroidectomy because of medullary thyroid carcinoma or c-cell hyperplasia.
  • Thirty-three patients with PTMC who had undergone a hemi- or total thyroidectomy and 54 subjects with medullary thyroid carcinoma or c-cell hyperplasia in whom a total thyroidectomy had been performed between 1994 and 2008 were included.
  • Exclusion criteria were the intake of medication that might affect thyroid function and previous thyroid cancer or thyroid surgery.
  • CONCLUSIONS: TSH is not elevated in subjects with PTMCs, indicating that it is not likely involved in the de novo oncogenesis of these small cancers.
  • [MeSH-major] Carcinoma, Papillary / pathology. Thyroid Neoplasms / pathology. Thyrotropin / blood
  • [MeSH-minor] Adult. Carcinoma, Medullary / pathology. Carcinoma, Medullary / surgery. Cross-Sectional Studies. Female. Humans. Male. Middle Aged. Retrospective Studies. Thyroid Nodule / pathology. Thyroidectomy

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  • (PMID = 20210672.001).
  • [ISSN] 1557-9077
  • [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] 9002-71-5 / Thyrotropin
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9. Iagaru A, Masamed R, Singer PA, Conti PS: Detection of occult medullary thyroid cancer recurrence with 2-deoxy-2-[F-18]fluoro-D-glucose-PET and PET/CT. Mol Imaging Biol; 2007 Mar-Apr;9(2):72-7
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  • [Title] Detection of occult medullary thyroid cancer recurrence with 2-deoxy-2-[F-18]fluoro-D-glucose-PET and PET/CT.
  • PURPOSE: 2-deoxy-2-[F-18]fluoro-D-glucose (FDG)-positron emission tomography (PET) has an established role in restaging of various cancers, including papillary and undifferentiated thyroid carcinoma.
  • However, controversies exist regarding its ability to reliably assess recurrent medullary thyroid cancer (MTC).
  • METHODS: This is a retrospective study (Apr 1, 1997-Mar 31, 2004) of 13 patients with histologic diagnosis of MTC, who had PET examinations.
  • RESULTS: Recurrent/metastatic disease was identified by PET in seven (54%) of the 13 patients.
  • The sensitivity and specificity of FDG-PET for disease detection in this cohort were 85.7% (95% CI: 48.7-97.4) and 83.3% (95% CI: 43.6-96.9), respectively.
  • CONCLUSION: Our findings suggest a significant role for FDG-PET in patients with suspected MTC recurrence, with sensitivity of 85.7% and specificity of 83.3% for disease detection.
  • [MeSH-major] Brain Stem Neoplasms / diagnosis. Fluorodeoxyglucose F18. Neoplasm Recurrence, Local / diagnosis. Positron-Emission Tomography / methods. Thyroid Neoplasms / diagnosis

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  • (PMID = 17186139.001).
  • [ISSN] 1536-1632
  • [Journal-full-title] Molecular imaging and biology : MIB : the official publication of the Academy of Molecular Imaging
  • [ISO-abbreviation] Mol Imaging Biol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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10. Qari FA: Pattern of thyroid malignancy at a University Hospital in Western Saudi Arabia. Saudi Med J; 2004 Jul;25(7):866-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The aim is to study the incidence of thyroid cancer in surgically treated nodular thyroid disease, clinicopathological characteristics and treatment results.
  • Forty-five (37.5%) patients had histopathology confirmed diagnosis of thyroid cancer.
  • Eighty-two point two percent cases of papillary carcinoma, 4.4% follicular type and 6.7% anaplastic and medullary carcinoma of thyroid.
  • Ninety-seven patients with papillary carcinoma received ablative dose of radioiodine with average dose of 100-200 mCi.
  • One female patient with follicular carcinoma of thyroid with bone, lung, and brain metastases received 4 doses of radioiodine with total dose of 800 mCi.
  • Mortality rate was (2.2%), one patient died of complication of invasive anaplastic carcinoma with invasion of the trachea.
  • We recommend that thyroid cancer patients should be treated by a team of endocrinologist, pathologist, experience thyroid surgeon, nuclear medicine and external radiotherapy physician to achieve an optimum care and good prognosis.
  • [MeSH-major] Thyroid Neoplasms / epidemiology
  • [MeSH-minor] Adult. Combined Modality Therapy. Cross-Sectional Studies. Female. Follow-Up Studies. Hospitals, University / statistics & numerical data. Humans. Iodine Radioisotopes / therapeutic use. Male. Middle Aged. Neoplasm Invasiveness / pathology. Retrospective Studies. Saudi Arabia / epidemiology. Thyroid Gland / pathology. Thyroidectomy

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  • (PMID = 15235690.001).
  • [ISSN] 0379-5284
  • [Journal-full-title] Saudi medical journal
  • [ISO-abbreviation] Saudi Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Iodine Radioisotopes
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11. Higgins MJ, Forastiere A, Marur S: New directions in the systemic treatment of metastatic thyroid cancer. Oncology (Williston Park); 2009 Aug;23(9):768-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In recent years, however, huge advances have been made in understanding the molecular pathways and cellular pathogenesis of this disease.
  • This knowledge has in turn led to the development of a range of targeted therapies, some specific to thyroid cancer genetic alterations such as the RET/PTC translocation, and others that exploit general malignant properties such as angiogenesis.
  • This review highlights novel targeted agents for the treatment of differentiated and medullary thyroid cancers being studied at this time, and the results of recently published trials.
  • We propose that such patients should be managed, whenever possible, within a clinical trial, in order to access the most promising new drugs for thyroid cancer.
  • [MeSH-major] Carcinoma, Medullary / therapy. Thyroid Neoplasms / therapy

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  • [CommentIn] Oncology (Williston Park). 2009 Aug;23(9):775-6 [19777763.001]
  • [CommentIn] Oncology (Williston Park). 2009 Aug;23(9):778, 781 [19777764.001]
  • (PMID = 19777762.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 76
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12. Kunnimalaiyaan M, Ndiaye M, Chen H: Apoptosis-mediated medullary thyroid cancer growth suppression by the PI3K inhibitor LY294002. Surgery; 2006 Dec;140(6):1009-14; discussion 1014-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Apoptosis-mediated medullary thyroid cancer growth suppression by the PI3K inhibitor LY294002.
  • BACKGROUND: Medullary thyroid cancer (MTC) cells exhibit frequent activation of the PI3K pathway as evidenced by the presence of hyperactivation of Akt kinases and overexpression of neuroendocrine (NE) markers.
  • We hypothesized that the inhibition of the PI3K pathway in MTC may lead to a reduction in cell growth and NE tumor marker production.
  • Further, TT cells were treated with nontoxic concentrations of LY294002 for 2 days, and Western blot analyses were performed for phospho-Akt, total Akt, and the NE tumor markers CgA and human achaete-scute homolog1 (ASCL1).
  • Importantly, NE marker production was also reduced.
  • Mechanistically, we show that cell growth inhibition by PI3K inactivation is mediated by apoptosis attributable to an increase in the levels of cleaved poly(ADP-ribose) polymerase and caspase-3.
  • CONCLUSIONS: MTC cell growth and NE marker production appear to depend on activation of the PI3K-signaling cascade.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma, Medullary / pathology. Cell Proliferation / drug effects. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. Morpholines / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Thyroid Neoplasms / pathology
  • [MeSH-minor] Basic Helix-Loop-Helix Transcription Factors / metabolism. Caspase 3 / metabolism. Cell Line, Tumor. Chromogranin A / metabolism. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic / drug effects. Humans. Oncogene Protein v-akt / genetics. Oncogene Protein v-akt / metabolism. Phosphorylation / drug effects. Poly(ADP-ribose) Polymerases / metabolism. Signal Transduction / drug effects. Signal Transduction / genetics

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  • (PMID = 17188151.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R21-DK064735; United States / NIDDK NIH HHS / DK / R21-DK066169
  • [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 / ASCL1 protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Chromogranin A; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Oncogene Protein v-akt; EC 3.4.22.- / Caspase 3
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13. Vitale G, Caraglia M, Ciccarelli A, Lupoli G, Abbruzzese A, Tagliaferri P, Lupoli G: Current approaches and perspectives in the therapy of medullary thyroid carcinoma. Cancer; 2001 May 1;91(9):1797-808
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current approaches and perspectives in the therapy of medullary thyroid carcinoma.
  • BACKGROUND: Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor derived from parafollicular cells.
  • METHODS: We describe the current approaches of MTC treatment (surgery, chemotherapy, radiation therapy, and biologic therapy).
  • Recently, it has been found that somatostatin analogs and type I interferon are able to control the neuroendocrine symptoms induced by advanced MTC and that they provide clinical benefit by improving the lifestyle of these patients.
  • CONCLUSION: Although these agents are poorly active in inducing a shrinkage in tumor mass, the combined use of different biologic agents and cytotoxic drugs needs to be explored in advanced MTC.
  • [MeSH-major] Carcinoma, Medullary / therapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. DNA, Neoplasm / analysis. Drug Therapy / trends. Genetic Counseling. Humans. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

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  • [Copyright] Copyright 2001 American Cancer Society.
  • (PMID = 11335906.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 51110-01-1 / Somatostatin
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14. Stoll L, Mudali S, Ali SZ: Merkel cell carcinoma metastatic to the thyroid gland: Aspiration findings and differential diagnosis. Diagn Cytopathol; 2010 Oct;38(10):754-7
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  • [Title] Merkel cell carcinoma metastatic to the thyroid gland: Aspiration findings and differential diagnosis.
  • Clinically diagnosed metastasis to the thyroid gland is exceptionally rare and may present diagnostic issues on fine needle aspiration.
  • Herein, we report a case of metastatic Merkel cell carcinoma to the thyroid presenting as a 2.1-cm solid nodule in a 50-year-old male with a previous history of Merkel cell carcinoma of the upper extremity.
  • The differential diagnosis centered on the "small round blue cell" tumor group such as medullary thyroid carcinoma and non-Hodgkin lymphoma.
  • However, in light of our patient's previous history, the FNA findings were most consistent with a metastasis of Merkel cell carcinoma.
  • In patients with a known history of a primary neoplasm, the differential diagnosis of a thyroid nodule should always include potential metastasis.
  • [MeSH-major] Carcinoma, Merkel Cell / secondary. Skin Neoplasms / pathology. Thyroid Neoplasms / secondary
  • [MeSH-minor] 6-Mercaptopurine / therapeutic use. Biopsy, Fine-Needle. Carcinoma, Small Cell / pathology. Crohn Disease / complications. Crohn Disease / drug therapy. Diagnosis, Differential. Fibrosis / complications. Humans. Immunosuppressive Agents / therapeutic use. Male. Middle Aged

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  • [Copyright] © 2010 Wiley-Liss, Inc.
  • (PMID = 20082438.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; E7WED276I5 / 6-Mercaptopurine
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15. Gotthardt M, Battmann A, Höffken H, Schurrat T, Pollum H, Beuter D, Gratz S, Béhé M, Bauhofer A, Klose KJ, Behr TM: 18F-FDG PET, somatostatin receptor scintigraphy, and CT in metastatic medullary thyroid carcinoma: a clinical study and an analysis of the literature. Nucl Med Commun; 2004 May;25(5):439-43
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  • [Title] 18F-FDG PET, somatostatin receptor scintigraphy, and CT in metastatic medullary thyroid carcinoma: a clinical study and an analysis of the literature.
  • AIM: To determine the clinical potential of 2-[F]fluoro-2-deoxy-D-glucose positron emission tomography (F-FDG PET) in patients with medullary thyroid carcinoma (MTC), we compared it to computed tomography (CT), and somatostatin receptor scintigraphy (SRS).
  • PATIENTS AND METHODS: Blinded evaluation of PET, CT and SRS images obtained from 26 patients with histologically proven metastatic MTC was done by nuclear medicine and radiology specialists.
  • Sites of tumour involvement were classified as "sure" or "suspicious".
  • RESULTS: Dependent on the type of data analysis performed, PET was able to demonstrate 56.8%/80.6% of the tumour sites, CT showed 64.5%/79.6%, and SRS showed 47.5%/69.9% of the tumour sites.
  • Our data are in agreement with publications that consider CT superior to PET in the diagnosis of metastatic MTC while other studies show superiority of PET.
  • However, a combination of CT and PET seems to be the most appropriate non-invasive diagnostic approach in patients with MTC.
  • [MeSH-major] Carcinoma, Medullary / radiography. Carcinoma, Medullary / radionuclide imaging. Fluorodeoxyglucose F18. Receptors, Somatostatin / metabolism. Thyroid Neoplasms / radiography. Thyroid Neoplasms / radionuclide imaging

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  • (PMID = 15100501.001).
  • [ISSN] 0143-3636
  • [Journal-full-title] Nuclear medicine communications
  • [ISO-abbreviation] Nucl Med Commun
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Controlled Clinical Trial; Journal Article; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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16. Barbosa SL, Rodien P, Leboulleux S, Niccoli-Sire P, Kraimps JL, Caron P, Archambeaud-Mouveroux F, Conte-Devolx B, Rohmer V, Groupe d'Etude des Tumeurs Endocrines: Ectopic adrenocorticotropic hormone-syndrome in medullary carcinoma of the thyroid: a retrospective analysis and review of the literature. Thyroid; 2005 Jun;15(6):618-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic adrenocorticotropic hormone-syndrome in medullary carcinoma of the thyroid: a retrospective analysis and review of the literature.
  • Cushing's syndrome (CS) in medullary thyroid carcinoma (MTC) is rare.
  • It revealed MTC in 3 cases and followed diagnosis by an average of 34.5 months in the others.
  • Metastases were often present at diagnosis.
  • Diagnosis of ectopic CS was established according to clinical and biologic features, and absence of corticotropic adenoma as well as parallel evolution between tumor and CS.
  • Therapy was medical and surgical: anticortisolic drugs alone or in association with somatostatin analogue, somatostatin analogue alone, and bilateral adrenalectomy.
  • The prognosis is poor because of frequency of metastasis at diagnosis.
  • [MeSH-major] Adrenocorticotropic Hormone / metabolism. Carcinoma, Medullary / pathology. Paraneoplastic Endocrine Syndromes / pathology. Thyroid Neoplasms / pathology

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  • (PMID = 16029131.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 26
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17. 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.
  • 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.
  • A tissue microarray was constructed from these anaplastic thyroid tumors and immunohistochemistry was utilized to evaluate expression of 31 molecular markers.
  • The markers evaluated were: epidermal growth factor receptor (EGFR), HER2, HER3, HER4, ER, PR, uPA-R, clusterin, E-cadherin, beta-catenin, AMF-R, c-kit, VEGF, ILK, aurora A, aurora B, aurora C, RET, CA-IX, IGF1-R, p53, MDM2, p21, Bcl-2, cyclin D1, cyclin E, p27, calcitonin, MIB-1, TTF-1, and thyroglobulin.
  • RESULTS: A single tumor with strong calcitonin expression was identified as a poorly differentiated medullary carcinoma and excluded from the study cohort.
  • 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


18. Zhang R, DeGroot LJ: Gene therapy of established medullary thyroid carcinoma with herpes simplex viral thymidine kinase in a rat tumor model: relationship of bystander effect and antitumor efficacy. Thyroid; 2000 Apr;10(4):313-9
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  • [Title] Gene therapy of established medullary thyroid carcinoma with herpes simplex viral thymidine kinase in a rat tumor model: relationship of bystander effect and antitumor efficacy.
  • Bystander effect (BSE) refers to killing of cells adjacent to a cell engineered to express a killing gene segment.
  • We evaluated the BSE of adenovirus expressing herpes simplex thymidine kinase (AdCMVtk) in rat medullary thyroid carcinomas (rMTC) and three rat thyroid epithelial cancer cell lines using an in vitro BSE assay.
  • This indicates that there is little BSE in this cell line.
  • One rat thyroid epithelial cancer cell line (RTC-R2) has a high BSE, with BSE index (BSEi) of 7.
  • BSE was also evaluated during in vivo tumor growth by subcutaneous injection of mixtures of AdCMVtk infected and uninfected cells.
  • Ganciclovir (GCV) treatment of tumors developing from a 1:1 mixture of infected to uninfected rMTC cells failed to inhibit their growth.
  • In contrast, GCV treatment of a 2:8 mixture of infected to uninfected RTC-R2 cells completely inhibit tumor development, indicating a high BSE.
  • BSE is related to in vivo antitumor efficacy when replication-defective adenovirus AdCMVtk is directly injected into rMTC tumors.
  • After treatment with 100 mg/kg per day of GCV, a growth-retardation effect was observed in small tumors (<100 mm3), but there was little antitumor activity in large tumors (>100 mm3).
  • Not all kinds of tumors are suitable for thymidine kinase (TK)/GCV gene therapy because some lack BSE.
  • It will be appropriate to test the BSE in human tumor cells before performing clinical trials with current adenoviral vectors expressing TK.
  • [MeSH-major] Carcinoma, Medullary / therapy. Genetic Therapy. Simplexvirus / enzymology. Simplexvirus / genetics. Thymidine Kinase / genetics. Thyroid Neoplasms / therapy
  • [MeSH-minor] Adenoviridae / genetics. Animals. Cell Division / drug effects. Cell Line, Transformed. Ganciclovir / therapeutic use. Genetic Vectors. Humans. Injections, Intralesional. Rats. Rats, Wistar. Transduction, Genetic. Tumor Cells, Cultured

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  • (PMID = 10807059.001).
  • [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] EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
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19. Fagin JA, Tuttle RM, Pfister DG: Harvesting the low-hanging fruit: kinase inhibitors for therapy of advanced medullary and nonmedullary thyroid cancer. J Clin Endocrinol Metab; 2010 Jun;95(6):2621-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Harvesting the low-hanging fruit: kinase inhibitors for therapy of advanced medullary and nonmedullary thyroid cancer.

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  • (PMID = 20525911.001).
  • [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 / R01 CA050706; United States / NCI NIH HHS / CA / R01 CA072597; United States / NCI NIH HHS / CA / CA50706; United States / NCI NIH HHS / CA / CA72597
  • [Publication-type] Comment; Editorial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Biomarkers, Tumor; 0 / Indoles; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / Pyrroles; 0 / sunitinib; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib
  • [Other-IDs] NLM/ PMC2902070
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20. Fadda GM, Santeufemia DA, Rocca PC, Costantino S, Sanna G, Sarobba MG, Putzu C, Rocca MC, Pinna MA, Farris A: Small cell lung cancer in a young patient with osteopetrosis. Tumori; 2006 Nov-Dec;92(6):563-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small cell lung cancer in a young patient with osteopetrosis.
  • BACKGROUND: Osteopetrosis or Albers-Schönberg's disease is a heterogeneous group of rare hereditary troubles of the bone characterized by bone sclerosis due to an alteration of the bone reabsorption mediated by osteoclasts.
  • The defect in the osteoclastic activity is responsible for complete or partial medullary cavities occlusion, with consequent reduced hemopoiesis, and for the excessive fragility of the affected bone segments.
  • CASE REPORT: We reported the case of a young man of 31 years affected by osteopetrosis in which a small cell lung cancer developed.
  • RESULTS: Small cell lung cancer is a particularly rare neoplasm in the young, and even though it is highly sensitive to chemotherapeutic treatment its prognosis remains poor.
  • The greatest clinical problem connected with chemotherapeutic treatment of patients affected by osteopetrosis is the variability of the reduction of their bone marrow reserve, which could expose them to an excessive hematological toxicity caused by the therapy.
  • CONCLUSIONS: The adoption of suitable prophylactic measures, such as the use of growth factors and drugs selected in relation to their toxicity or given in reduced doses, should be appropriately considered in these subjects.
  • [MeSH-major] Carcinoma, Small Cell / diagnosis. Lung Neoplasms / diagnosis. Osteopetrosis / complications

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  • (PMID = 17260504.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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21. Guerrieri M, Filipponi S, Arnaldi G, Giovagnetti M, Lezoche E, Mantero F, Taccaliti A: Unusual clinical manifestation of pheochromocytoma in a MEN2A patient. J Endocrinol Invest; 2002 Jan;25(1):53-7
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  • A case of unusual clinical manifestation of pheochromocytoma in a type 2A multiple endocrine neoplasia (MEN2A) patient is presented.
  • Past medical history included a total thyroidectomy for medullary carcinoma in 1985, and left adrenalectomy for pheochromocytoma in 1994.
  • Magnetic resonance imaging (MRI) and meta-iodobenzylguanidine (MIBG) scintiscan confirmed the presence of bilateral adrenal masses.
  • Histology was consistent with adrenal pheochromocytomas.
  • After surgical approach, psychiatric findings disappeared and did not recur at follow-up in spite of no medication for two years.
  • Differential diagnosis among typical features of neuropsychiatric disorders and pheochromocytoma must be considered.
  • [MeSH-major] Adrenal Gland Neoplasms / complications. Adrenal Gland Neoplasms / psychology. Anxiety / etiology. Depression / etiology. Multiple Endocrine Neoplasia Type 2a / complications. Pheochromocytoma / complications. Pheochromocytoma / psychology


22. Nocera M, Baudin E, Pellegriti G, Cailleux AF, Mechelany-Corone C, Schlumberger M: Treatment of advanced medullary thyroid cancer with an alternating combination of doxorubicin-streptozocin and 5 FU-dacarbazine. Groupe d'Etude des Tumeurs à Calcitonine (GETC). Br J Cancer; 2000 Sep;83(6):715-8
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  • [Title] Treatment of advanced medullary thyroid cancer with an alternating combination of doxorubicin-streptozocin and 5 FU-dacarbazine. Groupe d'Etude des Tumeurs à Calcitonine (GETC).
  • Combinations of doxorubicin and streptozocin and 5-FU and dacarbazine were given alternately to 20 patients with metastatic medullary thyroid carcinoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Medullary / drug therapy. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Dacarbazine / administration & dosage. Doxorubicin / administration & dosage. Drug Administration Schedule. Female. Fluorouracil / administration & dosage. Humans. Male. Middle Aged. Streptozocin / administration & dosage. Treatment Outcome

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  • [Copyright] Copyright 2000 Cancer Research Campaign.
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  • (PMID = 10952773.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] SCOTLAND
  • [Chemical-registry-number] 5W494URQ81 / Streptozocin; 7GR28W0FJI / Dacarbazine; 80168379AG / Doxorubicin; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2363532
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23. Rinner B, Li ZX, Haas H, Siegl V, Sturm S, Stuppner H, Pfragner R: Antiproliferative and pro-apoptotic effects of Uncaria tomentosa in human medullary thyroid carcinoma cells. Anticancer Res; 2009 Nov;29(11):4519-28
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  • [Title] Antiproliferative and pro-apoptotic effects of Uncaria tomentosa in human medullary thyroid carcinoma cells.
  • Medullary thyroid carcinoma (MTC), a rare calcitonin-producing tumor, is derived from parafollicular C-cells of the thyroid and is characterized by constitutive Bcl-2 overexpression.
  • The tumor is relatively insensitive to radiation therapy as well as conventional chemotherapy.
  • ) DC, commonly known as uña de gato or cat's claw were investigated.
  • Cell growth of MTC cells as well as enzymatic activity of mitochondrial dehydrogenase was markedly inhibited after treatment with different fractions of the plant.
  • In particular, the alkaloids isopterpodine and pteropodine of U. tomentosa exhibited a significant pro-apoptotic effect on MTC cells, whereas the alkaloid-poor fraction inhibited cell proliferation but did not show any pro-apoptotic effects.
  • These promising results indicate the growth-restraining and apoptotic potential of plant extracts against neuroendocrine tumors, which may add to existing therapies for cancer.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Carcinoma, Medullary / drug therapy. Cat's Claw / chemistry. Plant Extracts / pharmacology. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Caspase 3 / metabolism. Caspase 7 / metabolism. Cell Growth Processes / drug effects. Cell Line, Tumor. Humans. Indoles / chemistry. Staining and Labeling / methods

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  • (PMID = 20032400.001).
  • [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, Phytogenic; 0 / Indoles; 0 / Plant Extracts; 47165-04-8 / DAPI; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7
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24. Pestourie C, Thézé B, Kuhnast B, Le Helleix S, Gombert K, Dollé F, Tavitian B, Ducongé F: PET imaging of medullary thyroid carcinoma in MEN2A transgenic mice using 6-[(18)F]F-L-DOPA. Eur J Nucl Med Mol Imaging; 2010 Jan;37(1):58-66
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  • [Title] PET imaging of medullary thyroid carcinoma in MEN2A transgenic mice using 6-[(18)F]F-L-DOPA.
  • In this study, we investigated the use of 6-[(18)F]F-L-DOPA to detect and to monitor the progression of medullary thyroid carcinoma (MTC) in a genetically engineered mouse model of multiple endocrine neoplasia type 2A (MEN2A).
  • The kinetics of 6-[(18)F]F-L-DOPA, standardized uptake values (SUV) at 60 min and tumour volumes were recorded.
  • [MeSH-major] Carcinoma, Medullary / diagnostic imaging. Dihydroxyphenylalanine / analogs & derivatives. Multiple Endocrine Neoplasia Type 2a / diagnostic imaging. Positron-Emission Tomography / methods. Thyroid Neoplasms / diagnostic imaging
  • [MeSH-minor] Animals. Mice. Mice, Transgenic. Radiopharmaceuticals. Reproducibility of Results. Sensitivity and Specificity

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  • [CommentIn] Eur J Nucl Med Mol Imaging. 2010 Jan;37(1):46-8 [19690853.001]
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  • (PMID = 19655139.001).
  • [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] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 2C598205QX / fluorodopa F 18; 63-84-3 / Dihydroxyphenylalanine
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25. Michels G, Matthes J, Handrock R, Kuchinke U, Groner F, Cribbs LL, Pereverzev A, Schneider T, Perez-Reyes E, Herzig S: Single-channel pharmacology of mibefradil in human native T-type and recombinant Ca(v)3.2 calcium channels. Mol Pharmacol; 2002 Mar;61(3):682-94
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  • [Title] Single-channel pharmacology of mibefradil in human native T-type and recombinant Ca(v)3.2 calcium channels.
  • To study the molecular pharmacology of low-voltage-activated calcium channels in biophysical detail, human medullary thyroid carcinoma (hMTC) cells were investigated using the single-channel technique.
  • These cells had been reported to express T-type whole-cell currents and a Ca(v)3.2 (or alpha 1H) channel subunit.
  • Type II channels had biophysical properties (activation, inactivation, conductance) typical for high-voltage-activated calcium channels.
  • They were markedly stimulated by 1 microM (S)-Bay K 8644, allowing to identify them as L-type channels.
  • The channel termed type I is a low-voltage-activated, small-conductance (7.2 pS) channel that inactivates rapidly and is not modulated by (S)-Bay K 8644.
  • Type I channels are therefore classified as T-type channels.
  • Single recombinant low-voltage-activated T-type calcium channels were studied in comparison, using human embryonic kidney 293 cells overexpressing the pore-forming Ca(v)3.2 subunit.
  • In conclusion, the pharmacologic phenotype of these native human T-type channels--as probed by mibefradil--is similar to recombinant human Ca(v)3.2.
  • [MeSH-major] Calcium Channel Blockers / pharmacology. Calcium Channels, T-Type / metabolism. Mibefradil / pharmacology
  • [MeSH-minor] Calcium Channels, L-Type / drug effects. Calcium Channels, L-Type / metabolism. Cells, Cultured. Electrophysiology. Humans. Recombinant Proteins / drug effects. Recombinant Proteins / metabolism

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  • (PMID = 11854450.001).
  • [ISSN] 0026-895X
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Calcium Channels, L-Type; 0 / Calcium Channels, T-Type; 0 / Recombinant Proteins; 27B90X776A / Mibefradil
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26. Bongarzone I, Carniti C, Perego C, Mondellini P, Pierotti MA: RETMEN2A and RETMEN2B oncoproteins are targets of PP1 inhibitor. Tumori; 2003 Sep-Oct;89(5):550-2
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  • Medullary thyroid carcinoma (MTC) responds very poorly to chemotherapy.
  • The accumulation of evidence from laboratory studies strongly suggests that PP1 inhibitor is a cytostatic agent for cells expressing RET oncoproteins.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Medullary / drug therapy. Multiple Endocrine Neoplasia Type 2a / metabolism. Multiple Endocrine Neoplasia Type 2b / metabolism. Oncogene Proteins / drug effects. Oncogene Proteins / metabolism. Pyrazoles / pharmacology. Pyrimidines / pharmacology. Receptor Protein-Tyrosine Kinases / drug effects. Receptor Protein-Tyrosine Kinases / metabolism. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Humans. Phosphorylation / drug effects. Proto-Oncogene Proteins c-ret

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  • (PMID = 14870784.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-amino-5-(4-methylphenyl)-7-(tert-butyl)pyrazolo(3,4-d)pyrimidine; 0 / Antineoplastic Agents; 0 / Oncogene Proteins; 0 / Pyrazoles; 0 / Pyrimidines; 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
  • [Number-of-references] 7
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27. Zatelli MC, Molè D, Tagliati F, Minoia M, Ambrosio MR, degli Uberti E: Cyclo-oxygenase 2 modulates chemoresistance in breast cancer cells involving NF-kappaB. Cell Oncol; 2009;31(6):457-65
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  • BACKGROUND: Breast cancer cells can develop chemoresistance after prolonged exposure to cytotoxic drugs due to expression of the multi drug resistance (MDR) 1 gene.
  • Type 2 cyclo-oxygenase (COX-2) inhibitors reverse the chemoresistance phenotype of a medullary thyroid carcinoma cell line, TT, and of a breast cancer cell line, MCF7, by inhibiting MDR1 expression and P-gp function.
  • [MeSH-major] Cell Proliferation / drug effects. Cyclooxygenase 2 / metabolism. Drug Resistance, Neoplasm. NF-kappa B / metabolism
  • [MeSH-minor] Antibiotics, Antineoplastic / pharmacology. Blotting, Western. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Line, Tumor. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cyclooxygenase 2 Inhibitors / pharmacology. Doxorubicin / pharmacology. Female. Humans. Luciferases / genetics. Luciferases / metabolism. Microscopy, Fluorescence. Nitrobenzenes. P-Glycoprotein / metabolism. Prostaglandin H2 / pharmacology. Protein Transport / drug effects. Sulfonamides. Transfection

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  • (PMID = 19940361.001).
  • [ISSN] 1875-8606
  • [Journal-full-title] Cellular oncology : the official journal of the International Society for Cellular Oncology
  • [ISO-abbreviation] Cell. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Cyclooxygenase 2 Inhibitors; 0 / NF-kappa B; 0 / Nitrobenzenes; 0 / P-Glycoprotein; 0 / Sulfonamides; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; 42935-17-1 / Prostaglandin H2; 80168379AG / Doxorubicin; EC 1.13.12.- / Luciferases; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
  • [Other-IDs] NLM/ PMC4619115
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28. Lewiński A, Wojciechowska K: Genetic background of carcinogenesis in the thyroid gland. Neuro Endocrinol Lett; 2007 Apr;28(2):77-105
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  • [Title] Genetic background of carcinogenesis in the thyroid gland.
  • The process of carcinogenesis is permanently one of the most interesting and significant issues for researchers in different fields of medicine.
  • Therefore, we attempted to bring closer the problem of neoplastic transformation in the thyroid gland.
  • We have presented results of the most recent studies referred to molecular biology of thyroid neoplasms.
  • We have demonstrated not only the genetic background of cancers, derived from the thyroid follicular cell, but also genetic aspects related to medullary thyroid carcinoma and some benign thyroid lesions.
  • Additionally, we discuss overexpression of cyclin D1 gene in benign and malignant thyroid lesions.
  • [MeSH-major] Carcinoma / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 3. GTP-Binding Proteins / genetics. Genes, Suppressor. Genetic Predisposition to Disease. Humans. Models, Biological. Proto-Oncogene Proteins / genetics. Receptors, Thyrotropin / genetics. Thyroid Gland / pathology


29. Körber C, Geling M, Werner E, Mörtl M, Mäder U, Reiners C, Farahati J: [Incidence of familial non-medullary thyroid carcinoma in the patient register of the Clinic and Polyclinic of Nuclear Medicine, University of Würzburg]. Nuklearmedizin; 2000;39(1):27-32
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  • [Title] [Incidence of familial non-medullary thyroid carcinoma in the patient register of the Clinic and Polyclinic of Nuclear Medicine, University of Würzburg].
  • AIM: In this study the incidence rate of familial non-medullary thyroid carcinoma was investigated in the first and second grade relatives of patients registered at the Clinic and Polyclinic for Nuclear Medicine, University of Würzburg.
  • PATIENTS AND METHODS: In this study 596 patients with differentiated thyroid carcinoma were enclosed, who were treated between 01.01.81 and 31.12.95.
  • These data were compared to a literature analysis for familial non-medullary thyroid carcinoma.
  • All these patients suffered from papillary thyroid carcinoma.
  • According to the prognostic factors (tumor state, lymph node involvement, metastatic disease) no differences could be evaluated in the different groups (sporadic versus familial non-medullary thyroid disease).
  • CONCLUSION: A familial occurrence of differentiated thyroid carcinomas is not frequently observed, but should be considered due to further genetic diseases.
  • [MeSH-major] Thyroid Neoplasms / epidemiology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / blood. Family. Female. Germany / epidemiology. Hospitals, University / statistics & numerical data. Humans. Incidence. Male. Middle Aged. Nuclear Medicine. Pedigree. Thyroglobulin / blood

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  • (PMID = 10726254.001).
  • [ISSN] 0029-5566
  • [Journal-full-title] Nuklearmedizin. Nuclear medicine
  • [ISO-abbreviation] Nuklearmedizin
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9010-34-8 / Thyroglobulin
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30. Yalcin M, Dyskin E, Lansing L, Bharali DJ, Mousa SS, Bridoux A, Hercbergs AH, Lin HY, Davis FB, Glinsky GV, Glinskii A, Ma J, Davis PJ, Mousa SA: Tetraiodothyroacetic acid (tetrac) and nanoparticulate tetrac arrest growth of medullary carcinoma of the thyroid. J Clin Endocrinol Metab; 2010 Apr;95(4):1972-80
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  • [Title] Tetraiodothyroacetic acid (tetrac) and nanoparticulate tetrac arrest growth of medullary carcinoma of the thyroid.
  • CONTEXT: Tetraiodothyroacetic acid (tetrac) blocks angiogenic and tumor cell proliferation actions of thyroid hormone initiated at the cell surface hormone receptor on integrin alphavbeta3.
  • OBJECTIVE: We tested antiangiogenic and antiproliferative efficacy of tetrac and tetrac nanoparticles (tetrac NP) against human medullary thyroid carcinoma (h-MTC) implants in the chick chorioallantoic membrane (CAM) and h-MTC xenografts in the nude mouse.
  • DESIGN: h-MTC cells were implanted in the CAM model (n = 8 per group); effects of tetrac and tetrac NP at 1 microg/CAM were determined on tumor angiogenesis and tumor growth after 8 d. h-MTC cells were also implanted sc in nude mice (n = 6 animals per group), and actions on established tumor growth of unmodified tetrac and tetrac NP ip were determined.
  • RESULTS: In the CAM, tetrac and tetrac NP inhibited tumor growth and tumor-associated angiogenesis.
  • In the nude mouse xenograft model, established 450-500 mm(3) h-MTC tumors were reduced in size over 21 d by both tetrac formulations to less than the initial cell mass (100 mm(3)).
  • Tumor tissue hemoglobin content of xenografts decreased by 66% over the course of administration of each drug.
  • RNA microarray and quantitative real-time PCR of tumor cell mRNAs revealed that both tetrac formulations significantly induced antiangiogenic thrombospondin 1 and apoptosis activator gene expression.
  • CONCLUSIONS: Acting via a cell surface receptor, tetrac and tetrac NP inhibit growth of h-MTC cells and associated angiogenesis in CAM and mouse xenograft models.
  • [MeSH-major] Antineoplastic Agents. Carcinoma, Medullary / drug therapy. Thyroid Neoplasms / drug therapy. Thyroxine / analogs & derivatives
  • [MeSH-minor] Animals. Body Weight / drug effects. Cells, Cultured. Chick Embryo. Chorioallantoic Membrane / pathology. Excipients. Female. Hemoglobins / metabolism. Humans. Lactic Acid. Mice. Mice, Nude. Nanoparticles. Neovascularization, Pathologic / pathology. Neovascularization, Pathologic / prevention & control. Oligonucleotide Array Sequence Analysis. Polyglycolic Acid. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Xenograft Model Antitumor Assays

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  • (PMID = 20133461.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Excipients; 0 / Hemoglobins; 0 / RNA, Neoplasm; 0 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid; PA7UX1FFYQ / tetraiodothyroacetic acid; Q51BO43MG4 / Thyroxine
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31. Ning L, Greenblatt DY, Kunnimalaiyaan M, Chen H: Suberoyl bis-hydroxamic acid activates Notch-1 signaling and induces apoptosis in medullary thyroid carcinoma cells. Oncologist; 2008 Feb;13(2):98-104
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  • [Title] Suberoyl bis-hydroxamic acid activates Notch-1 signaling and induces apoptosis in medullary thyroid carcinoma cells.
  • Medullary thyroid carcinoma (MTC) is a neuroendocrine (NE) malignancy that frequently metastasizes and has limited treatments.
  • Furthermore, with Notch-1 activation there was a concomitant decrease in achaete-scute complex-like 1 (ASCL-1), a downstream target of Notch-1 signaling, as well as the NE tumor marker chromogranin A (CgA).
  • Importantly, SBHA treatment resulted in a dose-dependent decrease in cell viability.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Carcinoma, Medullary / drug therapy. Hydroxamic Acids / pharmacology. Receptor, Notch1 / metabolism. Signal Transduction / drug effects. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Blotting, Western. Caspase 3 / metabolism. Cell Proliferation / drug effects. Chromogranin A / metabolism. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. Poly(ADP-ribose) Polymerases / drug effects. Tumor Cells, Cultured

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  • (PMID = 18305053.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA109053; United States / NIDDK NIH HHS / DK / DK064735; United States / NIDDK NIH HHS / DK / DK066169
  • [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 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Hydroxamic Acids; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / suberoyl bis-hydroxamic acid; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3
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32. Gollini P, Cataldi A, Fava C: [MEN 1 and 2: the role of diagnostic imaging]. Radiol Med; 2004 Jan-Feb;107(1-2):78-87
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  • [Title] [MEN 1 and 2: the role of diagnostic imaging].
  • PURPOSE: To report the results of a retrospective study on the use of the different imaging methods in the diagnosis of type 1 and type 2 multiple endocrine neoplasias, and to provide an overall evaluation of the diagnostic yield of the various examinations performed correlating the results with the surgical findings.
  • In the patients with MEN1 the examinations revealed 4 parathyroid hyperplasias, 4 gastro-pancreatic endocrine-secreting lesions, one hypophyseal adenoma, one bronchial carcinoid and two bilateral adrenal hyperplasias.
  • In the patients with MEN2 the examinations revealed 6 medullary thyroid carcinomas (MTC), 4 pheochromocytomas and 3 parathyroid hyperplasias.
  • In only one patient with MEN1 did the chest X-ray detect a bronchial carcinoma, confirmed by CT.
  • CT also enabled identification of a single hypophyseal adenoma.
  • DISCUSSION AND CONCLUSIONS: Given the rarity of this condition we believe that the only statistically important finding in our series concerns the sensitivity of the imaging examinations performed in that, with adequate clinical and laboratory data, the possible problem of false positive results is exceptional.
  • The role of diagnostic imaging in the management of patients with MEN1 and 2 is twofold: identification of the target organs of lesions suspected on the basis of clinical and laboratory findings to enable adequate medical and/or surgical treatment; staging of malignant lesions to enable correct surgical planning.
  • In particular, our study once again highlights the diagnostic efficacy of CT for the diagnosis of pheochromocytomas and of the combination of biopsy plus ultrasound and ultrasound plus scintigraphy for the diagnosis of MTC in MEN 2.
  • As for MEN1 spiral CT was found to have good sensitivity (66%) in localising endocrine neoplasias of the gastrointestinal tract; endoscopic ultrasound on the other hand revealed good diagnostic efficacy, showing constantly positive findings.
  • Finally, in both pathologies we believe that the assessment of parathyroid conditions to be mainly a matter for nuclear medicine.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Carcinoma, Medullary / diagnosis. Gastrinoma / diagnosis. Multiple Endocrine Neoplasia Type 1 / diagnosis. Multiple Endocrine Neoplasia Type 2a / diagnosis. Pancreatic Neoplasms / diagnosis. Pheochromocytoma / diagnosis. Pituitary Neoplasms / diagnosis. Thyroid Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Biopsy. Bronchial Neoplasms / diagnosis. Bronchial Neoplasms / radiography. Bronchial Neoplasms / radionuclide imaging. Bronchial Neoplasms / ultrasonography. Carcinoid Tumor / diagnosis. Carcinoid Tumor / radiography. Carcinoid Tumor / radionuclide imaging. Carcinoid Tumor / ultrasonography. Endosonography. Female. Humans. Male. Middle Aged. Retrospective Studies. Sensitivity and Specificity. Thyroid Gland / pathology. Tomography, Spiral Computed. Tomography, X-Ray Computed


33. Yamaguchi H, Sasaki K, Satomi Y, Shimbara T, Kageyama H, Mondal MS, Toshinai K, Date Y, González LJ, Shioda S, Takao T, Nakazato M, Minamino N: Peptidomic identification and biological validation of neuroendocrine regulatory peptide-1 and -2. J Biol Chem; 2007 Sep 7;282(36):26354-60
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  • [Title] Peptidomic identification and biological validation of neuroendocrine regulatory peptide-1 and -2.
  • We analyzed peptides secreted from human medullary thyroid carcinoma TT cells that produce amidated peptides, and we identified two novel amidated peptides, designated neuroendocrine regulatory peptide (NERP)-1 and NERP-2.
  • NERPs are derived from distinct regions of the neurosecretory protein that was originally identified as a product of a nerve growth factor-responsive gene in PC12 cells.
  • These findings suggest that NERPs are novel modulators in body fluid homeostasis.
  • [MeSH-major] Brain Chemistry / drug effects. Nerve Tissue Proteins / pharmacology. Peptides / pharmacology. Protein Processing, Post-Translational. Water-Electrolyte Balance / drug effects
  • [MeSH-minor] Angiotensin II / pharmacology. Animals. Antibodies / pharmacology. Dose-Response Relationship, Drug. Humans. Male. Oxytocin / metabolism. PC12 Cells. Paraventricular Hypothalamic Nucleus / chemistry. Paraventricular Hypothalamic Nucleus / metabolism. Rats. Rats, Wistar. Saline Solution, Hypertonic. Supraoptic Nucleus / chemistry. Supraoptic Nucleus / metabolism. Vasoconstrictor Agents / pharmacology. Vasopressins / metabolism. Water / metabolism

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  • (PMID = 17609209.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Nerve Tissue Proteins; 0 / Peptides; 0 / Saline Solution, Hypertonic; 0 / Vasoconstrictor Agents; 0 / neuroendocrine regulatory peptide-1, human; 0 / neuroendocrine regulatory peptide-1, rat; 0 / neuroendocrine regulatory peptide-2, human; 0 / neuroendocrine regulatory peptide-2, rat; 059QF0KO0R / Water; 11000-17-2 / Vasopressins; 11128-99-7 / Angiotensin II; 50-56-6 / Oxytocin
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34. Basu S, Nair N: Novel diagnostic and therapeutic approaches in medullary carcinoma of thyroid: emerging role of nuclear medicine in its management. J Assoc Physicians India; 2002 May;50(5):702-6
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  • [Title] Novel diagnostic and therapeutic approaches in medullary carcinoma of thyroid: emerging role of nuclear medicine in its management.
  • [MeSH-major] Carcinoma, Medullary / radionuclide imaging. Thyroid Neoplasms / radionuclide imaging
  • [MeSH-minor] Humans. Nuclear Medicine. Sensitivity and Specificity

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  • (PMID = 12186130.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Number-of-references] 10
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35. Kraeber-Bodéré F, Saï-Maurel C, Campion L, Faivre-Chauvet A, Mirallié E, Chérel M, Supiot S, Barbet J, Chatal JF, Thédrez P: Enhanced antitumor activity of combined pretargeted radioimmunotherapy and paclitaxel in medullary thyroid cancer xenograft. Mol Cancer Ther; 2002 Feb;1(4):267-74
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  • [Title] Enhanced antitumor activity of combined pretargeted radioimmunotherapy and paclitaxel in medullary thyroid cancer xenograft.
  • A significant antitumor effect associated with moderate toxicity was obtained previously with anticarcinoembryonic antigen x antidiethylene-triaminepentaacetic acid (DTPA)-indium F6-734 bispecific antibody and iodine-131-labeled DTPA-indium bivalent hapten in an animal model of medullary thyroid cancer (MTC).
  • The purpose of this study was to determine whether the cytotoxic agents doxorubicin and paclitaxel, also known as radiosensitizers, improve efficacy of pretargeted radioimmunotherapy (RIT) in experimental MTC.
  • Animal weight, hematotoxicity, tumor volume, and serum calcitonin were monitored for 5 months.
  • Tumor growth inhibition induced by drugs alone, RIT alone, or combined therapy was characterized by measuring relative tumor volume 20, 40, and 60 days after treatment to detect additivity or synergism.
  • Mean tumor volume doubling time (MTVDT) was 13 +/- 4 days in the control group, 15 +/- 8 days in the group treated with the MTD of doxorubicin, and 32 +/- 13 days in the group treated with the MTD of paclitaxel.
  • MTVDT was not significantly different from this value after RIT plus doxorubicin, 60 +/- 16 days (65 and 100% of the respective single-agent MTDs).
  • Combination of RIT with paclitaxel (65 and 100% of the respective single-agent MTDs) prolonged the suppression of tumor growth.
  • The change in serum calcitonin levels paralleled those in tumor volume.
  • [MeSH-major] Carcinoma, Medullary / therapy. Paclitaxel / therapeutic use. Pentetic Acid / analogs & derivatives. Radiation-Sensitizing Agents / therapeutic use. Radioimmunotherapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Animals. Antibodies, Bispecific. Carcinoembryonic Antigen / immunology. Combined Modality Therapy. Doxorubicin / therapeutic use. Humans. Immunoglobulin G / therapeutic use. Iodine Radioisotopes / therapeutic use. Mice. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 12467222.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Carcinoembryonic Antigen; 0 / DTPA-IgG complex; 0 / Immunoglobulin G; 0 / Iodine Radioisotopes; 0 / Radiation-Sensitizing Agents; 7A314HQM0I / Pentetic Acid; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel
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36. Faivre S, Chièze S, Delbaldo C, Ady-Vago N, Guzman C, Lopez-Lazaro L, Lozahic S, Jimeno J, Pico F, Armand JP, Martin JA, Raymond E: Phase I and pharmacokinetic study of aplidine, a new marine cyclodepsipeptide in patients with advanced malignancies. J Clin Oncol; 2005 Nov 1;23(31):7871-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Minor responses and prolonged tumor stabilizations were observed in patients with medullary thyroid carcinoma.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Depsipeptides / pharmacokinetics. Neoplasm Metastasis / drug therapy. Neoplasms / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Carnitine / therapeutic use. Dose-Response Relationship, Drug. Drug Therapy, Combination. Female. Humans. Infusions, Intravenous. Male. Maximum Tolerated Dose. Metabolic Clearance Rate. Middle Aged. Vitamin B Complex / therapeutic use

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  • [CommentIn] J Clin Oncol. 2005 Nov 1;23(31):7780-2 [16204006.001]
  • (PMID = 16172454.001).
  • [ISSN] 0732-183X
  • [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] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Depsipeptides; 12001-76-2 / Vitamin B Complex; S7UI8SM58A / Carnitine; Y76ID234HW / aplidine
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37. Rufini V, Castaldi P, Treglia G, Perotti G, Gross MD, Al-Nahhas A, Rubello D: Nuclear medicine procedures in the diagnosis and therapy of medullary thyroid carcinoma. Biomed Pharmacother; 2008 Mar;62(3):139-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear medicine procedures in the diagnosis and therapy of medullary thyroid carcinoma.
  • Medullary thyroid carcinoma (MTC) is a rare neuroendocrine tumor originating in the parafollicular cells (C cells) of the thyroid and secretes both calcitonin and carcino-embryonic antigen (CEA).
  • Sporadic MTC usually presents as a solitary thyroid nodule; the diagnosis can be made preoperatively by fine-needle aspiration or by calcitonin assay, though it is usually established at the time of surgery.
  • In the diagnostic assessment of MTC, nuclear medicine imaging provides its contribution mainly in the post-operative work-up to detect residual/recurrent tumor.
  • [MeSH-major] Carcinoma, Medullary / radionuclide imaging. Carcinoma, Medullary / radiotherapy. Nuclear Medicine. Radiopharmaceuticals / therapeutic use. Thyroid Neoplasms / radionuclide imaging. Thyroid Neoplasms / radiotherapy
  • [MeSH-minor] 3-Iodobenzylguanidine. Animals. Carcinoembryonic Antigen / immunology. Humans. Iodine Radioisotopes. Positron-Emission Tomography. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Tomography, Emission-Computed, Single-Photon

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  • (PMID = 17892924.001).
  • [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 / Carcinoembryonic Antigen; 0 / Iodine Radioisotopes; 0 / Radiopharmaceuticals; 35MRW7B4AD / 3-Iodobenzylguanidine; 51110-01-1 / Somatostatin
  • [Number-of-references] 90
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38. National Toxicology Program: Toxicology and carcinogenesis studies of methyl isobutyl ketone (Cas No. 108-10-1) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2007 Feb;(538):1-236
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  • Methyl isobutyl ketone is used as a denaturant for rubbing alcohol; as a solvent for paints, varnishes, nitrocellulose, lacquers, and protective coatings; in industrial extraction processes; in dry-cleaning preparations; and in the synthesis of methyl isobutyl carbinol.
  • The mean body weights of the 900 and 1,800 ppm males were less than those of the chamber controls after weeks 97 and 89, respectively.
  • In the standard evaluation of the kidney, there were slightly increased incidences of renal tubule adenoma and renal tubule adenoma or carcinoma (combined) in males exposed to 900 or 1,800 ppm, and renal tubule carcinoma in males exposed to 1,800 ppm.
  • The incidences of renal tubule hyperplasia were also significantly increased in the 450 and 1,800 ppm males, and the severities were greater than in the chamber controls.
  • The incidences of transitional epithelial hyperplasia of the renal pelvis in males exposed to 900 or 1,800 ppm and mineralization of the renal papilla in all groups of exposed males were significantly increased.
  • In addition, two female rats exposed to 1,800 ppm had renal mesenchymal tumors.
  • In the extended evaluation of the kidney, renal tubule adenomas and renal tubule hyperplasia occurred in all groups of exposed male rats.
  • In the combined single and step section analysis, the incidences of renal tubule adenoma and renal tubule adenoma or carcinoma (combined) were significantly increased in males exposed to 1,800 ppm.
  • The incidences of renal tubule hyperplasia were also significantly increased in all exposed groups of males.
  • There was a positive trend in the incidences of mononuclear cell leukemia in males, and the incidence in the 1,800 ppm group was significantly increased.
  • The incidence of adrenal medulla hyperplasia in the 1,800 ppm males was significantly increased.
  • The mean body weights of females exposed to 1,800 ppm were less than those of the chamber controls after week 17.
  • The incidences of hepatocellular adenoma and hepatocellular adenoma or carcinoma (combined) were significantly increased in males and females exposed to 1,800 ppm.
  • CONCLUSIONS: Under the conditions of these 2-year studies, there was some evidence of carcinogenic activity of methyl isobutyl ketone in male F344/N rats based on increased incidences of renal tubule neoplasms.
  • Increased incidences of mononuclear cell leukemia in 1,800 ppm male F344/N rats may have been related to methyl isobutyl ketone exposure.
  • There was equivocal evidence of carcinogenic activity of methyl isobutyl ketone in female F344/N rats based on the occurrence of renal mesenchymal tumors in the 1,800 ppm group.
  • There was some evidence of carcinogenic activity of methyl isobutyl ketone in male and female B6C3F1 mice based on increased incidences of liver neoplasms.
  • [MeSH-major] Carcinogens / toxicity. Environmental Pollutants / toxicity. Methyl n-Butyl Ketone / toxicity. Neoplasms, Experimental / etiology. Solvents / toxicity. Toxicity Tests
  • [MeSH-minor] Administration, Oral. Adrenal Glands / drug effects. Animals. Body Weight / drug effects. Female. Kidney / drug effects. Kidney / pathology. Kidney Neoplasms / chemically induced. Kidney Neoplasms / pathology. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / pathology. Liver / drug effects. Liver / pathology. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Lung Neoplasms / chemically induced. Lung Neoplasms / pathology. Male. Mice. Mice, Inbred Strains. Occupational Exposure. Rats. Rats, Inbred F344. Water Supply

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  • (PMID = 17557116.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Environmental Pollutants; 0 / Solvents; 6QDY60NH6N / Methyl n-Butyl Ketone; U5T7B88CNP / methyl isobutyl ketone
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39. Pinchot SN, Kunnimalaiyaan M, Sippel RS, Chen H: Medullary thyroid carcinoma: targeted therapies and future directions. J Oncol; 2009;2009:183031
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  • [Title] Medullary thyroid carcinoma: targeted therapies and future directions.
  • Medullary thyroid cancer (MTC) is a rare neuroendocrine neoplasm that accounts for approximately 5% of all thyroid malignancies.
  • Therefore, there is a great need to develop novel therapeutic strategies to affect symptom control and reduce tumor burden in patients with widely disseminated disease.
  • Here, we review several pathways which have been shown to be vital in MTC tumorigenesis and focus on the pathways of interest for which targeted drug therapies are currently being developed.

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  • (PMID = 20069043.001).
  • [ISSN] 1687-8469
  • [Journal-full-title] Journal of oncology
  • [ISO-abbreviation] J Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2798103
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40. Yu S, Peng HD, Ju DW, Wei PK, Xu L, Lao LX, Li J: Mechanisms of treatment of cancer pain with a topical Chinese herbal formula in rats. Chin Med J (Engl); 2009 Sep 5;122(17):2027-31
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  • BACKGROUND: Pain has a substantial impact on patients' activities and overall quality of life, but current conventional drugs have debilitating side effects, including gastrointestinal disorders.
  • METHODS: The rat model of bone cancer pain was established by inoculating Walker-256 rat carcinoma cells directly into the right tibial medullary cavity of Wistar rats.
  • (1) sham bone cancer control (sham group): vehicle (PBS) inoculation without carcinoma cells plus topical administration of blank gel;.
  • (2) Sham treatment control (vehicle group): Walker-256 cell inoculation plus topical administration of blank gel;.
  • (3) XTTL gel treatment (treatment group): Walker-256 cell inoculation plus topical administration of XTTL gel.
  • Outcomes were assessed 21 days after inoculation by mechanical allodynia, histological staining, and by measuring concentrations of type I collagen carboxy-terminal telopeptide (ICTP) and bone-specific alkaline phosphatase (BAP) in serum.
  • RESULTS: Fourteen days after cancer cell incubation, significant mechanical allodynia in the ipsilateral hind paw and tumor growth in proximal end of the tibia were observed in the vehicle and treatment groups but not in the sham group.
  • [MeSH-major] Bone Neoplasms / complications. Drugs, Chinese Herbal / therapeutic use. Pain / drug therapy. Pain / etiology
  • [MeSH-minor] Alkaline Phosphatase / metabolism. Animals. Body Weight. Cell Line, Tumor. Collagen Type I. Female. Peptide Fragments / blood. Peptides. Procollagen / blood. Random Allocation. Rats. Rats, Wistar

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  • (PMID = 19781391.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / Drugs, Chinese Herbal; 0 / Peptide Fragments; 0 / Peptides; 0 / Procollagen; 0 / collagen type I trimeric cross-linked peptide; EC 3.1.3.1 / Alkaline Phosphatase
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41. Herrmann BL, Schmid KW, Goerges R, Kemen M, Mann K: Calcitonin screening and pentagastrin testing: predictive value for the diagnosis of medullary carcinoma in nodular thyroid disease. Eur J Endocrinol; 2010 Jun;162(6):1141-5
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  • [Title] Calcitonin screening and pentagastrin testing: predictive value for the diagnosis of medullary carcinoma in nodular thyroid disease.
  • CONTEXT: Serum calcitonin (hCT) measurement may be useful for detecting medullary thyroid carcinoma (MTC), but the routine use of hCT after pentagastrin stimulation to screen patients with nodular thyroid disease remains controversial.
  • PATIENTS: A total of 1007 patients (567 females and 440 males) with nodular thyroid disease and a mean age of 55+/-14 (mean+/-S.D.) years were included in the study.
  • All patients did not have impaired renal function, bacterial infection, alcohol and drug abuse, pseudohypoparathyroidism, or proton-pump inhibitor therapy.
  • Individuals referred with known elevation of hCT, Graves' disease, or autoimmune thyroid disease were not considered or included in this investigation.
  • One patient had a basal hCT level of 4400 pg/ml with a histological confirmation of a MTC.
  • Of 17 patients with hCT>10 pg/ml, 2 had MTC, and of 17 patients, 3 had C-cell hyperplasia.
  • CONCLUSIONS: Basal hCT measurement together with pentagastrin-stimulated hCT measurement in cases of basal hCT>10 pg/ml detects MTC in 0.20% of patients with nodular thyroid disease.

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  • (PMID = 20332126.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9007-12-9 / Calcitonin; EF0NX91490 / Pentagastrin
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42. Brauckhoff M, Lorenz K, Ukkat J, Brauckhoff K, Gimm O, Dralle H: Medullary thyroid carcinoma. Scand J Surg; 2004;93(4):249-60
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  • [Title] Medullary thyroid carcinoma.
  • Medullary thyroid carcinoma (MTC) is subdivided into sporadic (75 %) and hereditary (25 %) forms.
  • In patients with sporadic MTC, routine calcitonin (CT) measurement in nodular goiter patients has been shown to reduce the frequency of advanced tumor stages.
  • New chemotherapeutic agents (tyrosine kinase inhibitors), therapeutic nuclids (90Yttrium-labeled octreotide), and chemoembolization of liver metastases are currently the most promising therapeutical concepts in patients with distant metastases.
  • [MeSH-major] Calcitonin / analysis. Carcinoma, Medullary / therapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Lymph Nodes / pathology. Prognosis. Survival Analysis. Thyroid Gland / pathology. Thyroid Gland / surgery. Thyroidectomy. Treatment Outcome

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  • (PMID = 15658665.001).
  • [ISSN] 1457-4969
  • [Journal-full-title] Scandinavian journal of surgery : SJS : official organ for the Finnish Surgical Society and the Scandinavian Surgical Society
  • [ISO-abbreviation] Scand J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 9007-12-9 / Calcitonin
  • [Number-of-references] 107
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43. Skinner MA, Safford SD, Freemerman AJ: RET tyrosine kinase and medullary thyroid cells are unaffected by clinical doses of STI571. Anticancer Res; 2003 Sep-Oct;23(5A):3601-6
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  • [Title] RET tyrosine kinase and medullary thyroid cells are unaffected by clinical doses of STI571.
  • BACKGROUND: Activating mutations in the RET receptor tyrosine kinase are responsible for the development of medullary thyroid cancer (MTC) in persons with Multiple Endocrine Neoplasia type 2.
  • We hypothesized that STI571 (Gleevec) would inhibit RET kinase and be a useful agent in the treatment of MTC.
  • MATERIALS AND METHODS: We determined the IC50 of STI571 for RET using an in vitro kinase assay and also examined the effects of STI571 on cellular proliferation and viability in TT cells, a human MTC cell line.
  • Additionally, TT cells incubated with 10 microM STI571 for up to 8 days showed no apparent reduction in cell proliferation or viability.
  • CONCLUSION: The concentrations of STI571 required to significantly inhibit RET and to inhibit TT cell proliferation are not clinically achievable.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Medullary / drug therapy. Enzyme Inhibitors / pharmacology. Piperazines / pharmacology. Proto-Oncogene Proteins / antagonists & inhibitors. Pyrimidines / pharmacology. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Benzamides. Cell Death / drug effects. Cell Division / drug effects. Cell Line, Tumor. Humans. Imatinib Mesylate. Inhibitory Concentration 50. Phosphorylation / drug effects. Proto-Oncogene Proteins c-ret

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  • (PMID = 14666655.001).
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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44. Roman S, Mehta P, Sosa JA: Medullary thyroid cancer: early detection and novel treatments. Curr Opin Oncol; 2009 Jan;21(1):5-10
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  • [Title] Medullary thyroid cancer: early detection and novel treatments.
  • PURPOSE OF REVIEW: Medullary thyroid cancer (MTC) is derived from the parafollicular cells of the thyroid.
  • We review the most recent studies on the molecular biology, calcitonin screening, diagnosis, imaging, and treatment of MTC.
  • For metastatic or recurrent disease, neck ultrasound, chest computed tomography scan, liver MRI, bone scintigraphy, and axial skeleton MRI have been proven superior to 18F-FDG PET/computed tomography.
  • For patients with nonoperable metastatic disease, novel chemotherapeutic agents, such as vandetanib, targeting rearranged during transfection, vascular endothelial growth factor receptor and epidermal growth factor receptor, are showing promise.
  • Such agents are currently in phase II trials.
  • SUMMARY: There have been several recent advances in the diagnosis, molecular biology, imaging, and treatment options of MTC.
  • By potentially downstaging of disease, and treating metastatic disease more effectively, overall survival and outcomes of patients may improve.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Medullary / diagnosis. Carcinoma, Medullary / drug therapy. Fluorodeoxyglucose F18. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / drug therapy


45. Ning L, Jaskula-Sztul R, Kunnimalaiyaan M, Chen H: Suberoyl bishydroxamic acid activates notch1 signaling and suppresses tumor progression in an animal model of medullary thyroid carcinoma. Ann Surg Oncol; 2008 Sep;15(9):2600-5
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  • [Title] Suberoyl bishydroxamic acid activates notch1 signaling and suppresses tumor progression in an animal model of medullary thyroid carcinoma.
  • BACKGROUND: Medullary thyroid carcinoma (MTC) is a neuroendocrine malignancy that frequently metastasizes and has few treatments.
  • Tumors were measured every 4 days and collected at 12 days for Western blot analysis.
  • RESULTS: Treatment with SBHA resulted in an average 55% inhibition of tumor growth in the treatment group (P < .05).
  • Analysis of SBHA-treated MTC tumors revealed a marked increase in the active form of Notch1 (NICD) with a concomitant decrease in achaete-scute complex-like 1 (ASCL1), a downstream target of Notch1 signaling, as well as the neuroendocrine tumor marker chromogranin A.
  • Importantly, SBHA treatment resulted in an increase in protein levels of p21(CIP1/WAF1), p27(KIP1), cleaved caspase-9, cleaved caspase-3, and cleaved poly ADP-ribose polymerase and concomitant with a decrease in cyclin D1 and cyclin B1, indicating that the growth inhibition was due to both cell cycle arrest and apoptosis.
  • Moreover, SBHA downregulated cell survival proteins Bcl-2 and Bcl-X(L), but upregulated apoptotic proteins Bax, Bad, and Bmf.

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  • (PMID = 18563491.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA117117-01A2; United States / NCI NIH HHS / CA / CA109053-03; United States / NCI NIH HHS / CA / R21 CA117117-02; United States / NCI NIH HHS / CA / R01 CA109053-03; United States / NCI NIH HHS / CA / R01 CA109053-01A2; United States / NCI NIH HHS / CA / R01 CA109053; United States / NCI NIH HHS / CA / CA117117-02; United States / NCI NIH HHS / CA / R21 CA117117-01A2; United States / NCI NIH HHS / CA / CA109053-01A2; United States / NCI NIH HHS / CA / CA109053-02; United States / NCI NIH HHS / CA / R21CA117117; United States / NCI NIH HHS / CA / R21 CA117117; United States / NCI NIH HHS / CA / R01 CA109053-02
  • [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 / Ascl1 protein, mouse; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Cdkn1a protein, mouse; 0 / Chromogranin A; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Hydroxamic Acids; 0 / Receptor, Notch1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 58IFB293JI / vorinostat; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ NIHMS127896; NLM/ PMC2737668
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46. Cassoni P, Muccioli G, Marrocco T, Volante M, Allia E, Ghigo E, Deghenghi R, Papotti M: Cortistatin-14 inhibits cell proliferation of human thyroid carcinoma cell lines of both follicular and parafollicular origin. J Endocrinol Invest; 2002 Apr;25(4):362-8
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  • [Title] Cortistatin-14 inhibits cell proliferation of human thyroid carcinoma cell lines of both follicular and parafollicular origin.
  • The effect of CST-14 on cell proliferation was studied in 3 different human thyroid carcinoma cell lines of follicular origin (N-PAP, WRO, ARO) and in one thyroid medullary carcinoma cell line (TT).
  • CST-14 1 pM determined a significant inhibition of cell proliferation in TT, N-PAP and WRO cells and this effect was dose-dependent and more pronounced than that displayed by SRIH-14 (Ala-Gly-c[Cys-Lys-Asn-Phe-Phe-Trp-Lys-Thr-Phe-Thr-Ser-Cys]-OH) treatment.
  • To a minor extent, CST-14, but not SRIH-14, also temporary inhibited ARO cell proliferation.
  • By immunofluorescence, sst2, sst3 and sst5 have been demonstrated in TT cells, whereas types 3 and 5 only were expressed in N-PAP and WRO cells, and no sst subtype was found in ARO cells.
  • The presence of both GHS-Rla and lb mRNA has been studied and demonstrated in the TT medullary carcinoma cell line, whereas follicular derived cell lines were already known to express GHS binding sites.
  • Addition of EP-80874 (D-Mrp-c[D-Cyspyridilalanyl3-D-Trp-Lys-Val-Cys]-Mrp-NH2), a synthetic peptide that binds to SRIH and GHS-R, completely abolished the antiproliferative effects of CST-14 or SRIH-14 on sst/GHS-R positive thyroid carcinoma cell lines (WRO, N-PAP and TT).
  • [MeSH-major] Adenocarcinoma, Follicular / pathology. Carcinoma, Medullary / pathology. Neuropeptides / pharmacology. Peptides, Cyclic / pharmacology. Receptors, G-Protein-Coupled. Thyroid Neoplasms / pathology
  • [MeSH-minor] Cell Division / drug effects. Fluorescent Antibody Technique. Hormones / pharmacology. Humans. Receptors, Cell Surface / metabolism. Receptors, Ghrelin. Receptors, Somatostatin / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Somatostatin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 12030609.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Hormones; 0 / Neuropeptides; 0 / Peptides, Cyclic; 0 / Receptors, Cell Surface; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin; 0 / Receptors, Somatostatin; 0 / cortistatin 14; 51110-01-1 / Somatostatin
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47. Jurvansuu JM, Goldman A: Recent inventions on receptor tyrosine kinase RET modulation. Recent Pat Biotechnol; 2008;2(1):47-54
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  • Rearranged during transfection, RET, is a receptor tyrosine kinase expressed in neural crest derived cell lineages.
  • RET is activated by dimerisation facilitated by its binding to the heterodimeric complex formed by Glial cell-derived neurotrophic factor (GDNF) -family ligand (GFL) and GNDF-family receptor (GFR).
  • RET kinase mediated signaling can lead to survival, cell growth, differentiation, and migration.
  • Pharmaceutically RET is of interest due to its involvement in several disease conditions.
  • Oncogenic RET activation by mutations or rearragements predisposes to cancers like multiple endocrine neoplasia type 2 (A and B) and medullary thyroid carcinoma.
  • Loss-of-function mutations in RET are a strong susceptibility factor for Hirschsprung disease, which is characterized by lack of ganglion cells in gastrointestinal tract.
  • Therefore, the neuroprotective capacity of RET activation to override the apoptotic program in neurodegenerative diseases, like in dying midbrain dopaminergic neurons in Parkinson's disease, is of great interest.
  • [MeSH-major] Drug Design. Drug Industry / legislation & jurisprudence. Drug Industry / trends. Patents as Topic. Protein Kinase Inhibitors / chemistry. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-ret / antagonists & inhibitors

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  • (PMID = 19075852.001).
  • [ISSN] 2212-4012
  • [Journal-full-title] Recent patents on biotechnology
  • [ISO-abbreviation] Recent Pat Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human
  • [Number-of-references] 68
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48. Sexton PM, Christopoulos G, Christopoulos A, Nylen ES, Snider RH Jr, Becker KL: Procalcitonin has bioactivity at calcitonin receptor family complexes: potential mediator implications in sepsis. Crit Care Med; 2008 May;36(5):1637-40
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  • Serum procalcitonin (ProCT) levels are markedly elevated in sepsis and correlate positively with severity of the illness and mortality, however, little is known about the biological activity of ProCT.
  • OBJECTIVE: To explore the biological activity of purified human ProCT at the calcitonin (CT) family of receptors.
  • DESIGN: Human ProCT was purified from the TT medullary thyroid carcinoma cell line.
  • Human CTa receptor or human CT receptor-like receptor (CLR) was transiently expressed in COS-7 cells alone or together with individual receptor activity-modifying proteins (RAMPs) to generate the CTa (CT) receptor, the AMY1 (amylin) receptor, the CGRP1 (CT gene-related peptide) receptor, and the AM1 and AM2 (adrenomedullin) receptors.
  • Biological activity of ProCT was assessed by measurement of cAMP accumulation.

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  • [CommentIn] Crit Care Med. 2008 May;36(5):1684-7 [18448945.001]
  • (PMID = 18434892.001).
  • [ISSN] 1530-0293
  • [Journal-full-title] Critical care medicine
  • [ISO-abbreviation] Crit. Care Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Precursors; 0 / Receptors, Calcitonin; 56645-65-9 / procalcitonin; 9007-12-9 / Calcitonin
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49. Rached E, Hard GC, Blumbach K, Weber K, Draheim R, Lutz WK, Ozden S, Steger U, Dekant W, Mally A: Ochratoxin A: 13-week oral toxicity and cell proliferation in male F344/n rats. Toxicol Sci; 2007 Jun;97(2):288-98
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  • [Title] Ochratoxin A: 13-week oral toxicity and cell proliferation in male F344/n rats.
  • Ochratoxin A (OTA) is nephrotoxic and a potent renal carcinogen.
  • Male rats are most susceptible to OTA toxicity, and chronic administration of OTA (70 and 210 microg/kg bw) for 2 years has been shown to induce high incidences of adenomas and carcinomas arising from the straight segment of the proximal tubule epithelium.
  • In contrast, treatment with a lower dose of 21 microg/kg bw did not result in increased tumor rates, suggesting a nonlinear dose response for renal tumor formation by OTA.
  • Since the mechanism of OTA carcinogenicity is still largely unknown, this study was conducted to investigate early functional and pathological effects of OTA and to determine if sustained stimulation of renal cell proliferation plays a role.
  • Cell proliferation in the renal cortex and outer stripe of the outer medulla (OSOM) was determined using bromodeoxyuridine incorporation and immunohistochemistry.
  • Histopathological examination showed renal alterations in mid- and high-dose-treated animals involving single-cell death and prominent nuclear enlargement within the straight proximal tubules.
  • Treatment with OTA at doses of 70 and 210 microg/kg bw led to a marked dose- and time-dependent increase in renal cell proliferation, extending from the medullary rays into the OSOM.
  • No effects were evident in kidneys of low-dose-treated animals or in the liver, which is not a target for OTA carcinogenicity.
  • A no observed effect level in this study was established at 21 microg/kg bw, correlating with the dose in the NTP 2-year bioassay that did not produce renal tumors.
  • The apparent correlation between enhanced cell turnover and tumor formation induced by OTA indicates that stimulation of cell proliferation may play an important role in OTA carcinogenicity and provides further evidence for an epigenetic, thresholded mechanism.
  • [MeSH-minor] Administration, Oral. Animals. Antimetabolites. Blood Cell Count. Body Weight / drug effects. Bromodeoxyuridine. Cell Proliferation / drug effects. Kidney / drug effects. Kidney / metabolism. Kidney / pathology. Liver / metabolism. Male. Organ Size / drug effects. Rats. Rats, Inbred F344. Tissue Distribution

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  • (PMID = 17344223.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites; 0 / Carcinogens; 0 / Ochratoxins; 1779SX6LUY / ochratoxin A; G34N38R2N1 / Bromodeoxyuridine
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50. Lee A, LiVolsi VA, Baloch ZW: Expression of DNA topoisomerase IIalpha in thyroid neoplasia. Mod Pathol; 2000 Apr;13(4):396-400
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  • It serves as a target for several useful antichemotherapeutic agents, such as etoposide (VP-16) and teniposide (VM26).
  • The topo II labeling index is defined as the number of topo II staining positive nuclei divided by the total number of tumor cells counted multiplied by 100.
  • The average labeling indexes for anaplastic carcinoma (7.8), tall cell variant of papillary carcinoma (4.8), follicular carcinoma (2.6), Hürthle cell carcinoma (3.4), and medullary carcinoma (2.4) were much higher than for papillary carcinoma (0.76), follicular adenoma (0.65), Hürthle cell adenoma (0.32), and normal thyroid (0.1).
  • This study suggests that immunohistochemical analysis of topo II correlates with thyroid tumor histology; it is more frequently expressed in tumors that are associated with aggressive clinical behavior.
  • It may help to define a role for anti-topoisomerase drugs in treatment of aggressive thyroid neoplasms.
  • [MeSH-major] DNA Topoisomerases, Type II / analysis. Isoenzymes / analysis. Thyroid Neoplasms / enzymology
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / pathology. Adenocarcinoma, Follicular / enzymology. Adenocarcinoma, Follicular / pathology. Antigens, Neoplasm. Carcinoma, Papillary / enzymology. Carcinoma, Papillary / pathology. DNA-Binding Proteins. Humans. Immunohistochemistry

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  • (PMID = 10786805.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / Isoenzymes; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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51. Hoegerle S, Altehoefer C, Ghanem N, Brink I, Moser E, Nitzsche E: 18F-DOPA positron emission tomography for tumour detection in patients with medullary thyroid carcinoma and elevated calcitonin levels. Eur J Nucl Med; 2001 Jan;28(1):64-71
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  • [Title] 18F-DOPA positron emission tomography for tumour detection in patients with medullary thyroid carcinoma and elevated calcitonin levels.
  • In spite of the availability of numerous procedures, diagnostic imaging of tumour manifestations in patients with medullary thyroid carcinoma and elevated calcitonin levels is often difficult.
  • After evaluation of the normal distribution of 18F-DOPA, 11 patients with medullary thyroid carcinoma were examined using 18F-DOPA PET.
  • All individual procedures were evaluated without reference to prior information.
  • Data assessment for each patient was based on cooperation between experienced radiologists and specialists in nuclear medicine, who considered all the available findings (histological results, imaging, follow-up studies).
  • The following sensitivities were calculated with respect to total tumour manifestations: 18F-DOPA PET 63%, 18F-FDG PET 44%, SRS 52%, morphological imaging 81%.
  • 18F-DOPA PET is a new functional imaging procedure for medullary thyroid carcinoma that seems to provide better results than SRS and 18F-FDG PET.
  • Moreover, the data indicate that no single procedure provides adequate diagnostic certainty.
  • Therefore, 18F-DOPA PET is a useful supplement to morphological diagnostic imaging, improving lymph node staging and enabling a more specific diagnosis of primary tumour and local recurrence.
  • [MeSH-major] Calcitonin / metabolism. Carcinoma, Medullary / metabolism. Carcinoma, Medullary / radionuclide imaging. Dihydroxyphenylalanine. Radiopharmaceuticals. Thyroid Neoplasms / metabolism. Thyroid Neoplasms / radionuclide imaging

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  • (PMID = 11202454.001).
  • [ISSN] 0340-6997
  • [Journal-full-title] European journal of nuclear medicine
  • [ISO-abbreviation] Eur J Nucl Med
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 2C598205QX / fluorodopa F 18; 63-84-3 / Dihydroxyphenylalanine; 9007-12-9 / Calcitonin
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52. Sofuni A, Iijima H, Moriyasu F, Nakayama D, Shimizu M, Nakamura K, Itokawa F, Itoi T: Differential diagnosis of pancreatic tumors using ultrasound contrast imaging. J Gastroenterol; 2005 May;40(5):518-25
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  • [Title] Differential diagnosis of pancreatic tumors using ultrasound contrast imaging.
  • BACKGROUND: The development of equipment and contrast agents for ultrasound imaging has contributed to major breakthroughs in the diagnosis of pancreatic tumors.
  • We aimed to determine the diagnostic effectiveness of contrast ultrasound with Levovist, using the Agent Detection Imaging (ADI) technique, in 50 patients with pancreatic tumors.
  • METHODS: We studied 50 cases of histologically proven pancreatic disease; 39 carcinomas, 2 endocrine tumors, 4 intraductal papillary mucinous carcinomas (IPMCs), and 5 cases of tumor-forming pancreatitis (TFP).
  • Vascular and perfusion images of contrast-enhanced ultrasound (CE-US) were used for the evaluation of tumor vascularity and parenchymal perfusion of the tumor, respectively.
  • The hemodynamics of the tumor, and the diagnostic capacity of CE-US were compared with those shown by computed tomography (CT).
  • The histological diagnosis in all cases was made from either biopsy or surgical specimens.
  • RESULTS: Thirty-four cases of pancreatic carcinoma (87%) showed a hypovascular and hypoperfusion pattern.
  • The endocrine tumors showed a heterogeneous hypervascular and hyperperfusion pattern.
  • All IPMC cases showed hypervascularity of the nodules inside the tumors.
  • When tumors showing a hypovascular or hypoperfusion pattern on CE-US were diagnosed as carcinomas, 34 of the 39 carcinomas (87%) fit this criterion, with a 95% confidence interval (CI) of 73%-96%, whereas, on CT, 31 of the 39 were diagnosed as carcinoma; (sensitivity, 79%).
  • Results of comparison between the CE-US findings and the histological diagnosis were as follows.
  • The one papillary adenocarcinoma showed a hypervascular and hyperperfusion pattern; the 32 well or moderately differentiated adenocarcinomas showed a hypovascular and hypoperfusion pattern; and in the poorly differentiated adenocarcinomas, 2 cases of scirrhous type showed a hypovascular and hypoperfusion pattern, and the 4 cases of medullary type showed an isovascular and isoperfusion pattern.
  • CONCLUSIONS: The differences in vascularity of pancreatic carcinomas depicted by CE-US were associated well with differences in histology.
  • CE-US, by the ADI technique, is useful for the diagnosis of pancreatic tumors.
  • [MeSH-major] Adenocarcinoma, Papillary / ultrasonography. Carcinoma, Pancreatic Ductal / ultrasonography. Contrast Media / pharmacology. Pancreatic Neoplasms / ultrasonography. Pancreatitis / ultrasonography
  • [MeSH-minor] Case-Control Studies. Confidence Intervals. Diagnosis, Differential. Female. Humans. Image Enhancement. Male. Neoplasm Staging. Probability. Sensitivity and Specificity. Single-Blind Method

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  • (PMID = 15942718.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Contrast Media
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53. Traugott A, Moley JF: Medullary thyroid cancer: medical management and follow-up. Curr Treat Options Oncol; 2005 Jul;6(4):339-46
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  • [Title] Medullary thyroid cancer: medical management and follow-up.
  • Medullary thyroid carcinoma (MTC) is a neuroendocrine malignancy that occurs in hereditary (25%) and sporadic (75%) clinical settings.
  • MTC is present in all patients with the multiple endocrine neoplasia type 2 (MEN 2) syndromes.
  • MTCs produce calcitonin, measurement of which indicates the presence of tumor in at-risk individuals and the effectiveness of therapy in treated patients.
  • Surgery is the mainstay of therapy for primary and recurrent disease.
  • Activating mutations in a tyrosine kinase receptor gene are present in the majority of MTCs, and experience with tyrosine kinase inhibitors and other agents in the setting of clinical trials is critical for the identification of effective systemic treatment.
  • [MeSH-major] Carcinoma, Medullary / therapy. Neoplasm Recurrence, Local / therapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Calcitonin / blood. Clinical Trials as Topic. Humans. Immunotherapy. Radiotherapy

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  • (PMID = 15967086.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 9007-12-9 / Calcitonin
  • [Number-of-references] 63
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54. Alfano L, Guida T, Provitera L, Vecchio G, Billaud M, Santoro M, Carlomagno F: RET is a heat shock protein 90 (HSP90) client protein and is knocked down upon HSP90 pharmacological block. J Clin Endocrinol Metab; 2010 Jul;95(7):3552-7
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  • [Title] RET is a heat shock protein 90 (HSP90) client protein and is knocked down upon HSP90 pharmacological block.
  • CONTEXT: Mutations of the RET receptor tyrosine kinase are associated to multiple endocrine neoplasia type 2 (MEN2) and sporadic medullary thyroid carcinoma (MTC).
  • DESIGN: 17-AAG effects were studied in RAT1 fibroblasts exogenously expressing MEN2-associated RET mutants and human MTC-derived cell lines.
  • RESULTS: 17-AAG induced a 26S proteasome-dependent degradation of wild-type RET and MEN2-associated RET mutants.
  • In human MTC cells carrying oncogenic RET mutants, HSP90 inhibition induced receptor degradation and signaling hindrance leading to cell cycle arrest.
  • [MeSH-major] HSP90 Heat-Shock Proteins / metabolism. Proto-Oncogene Proteins c-ret / metabolism
  • [MeSH-minor] Benzoquinones / pharmacology. Blotting, Western. Cell Line. Cells, Cultured. Enzyme Inhibitors / pharmacology. Humans. Lactams, Macrocyclic / pharmacology. Macrolides / pharmacology. Phosphorylation / genetics. Signal Transduction / drug effects. Transfection

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  • (PMID = 20444924.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Macrolides; 12772-57-5 / monorden; 4GY0AVT3L4 / tanespimycin; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human
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55. Do Cao C, Wémeau JL: [Current management of thyroid malignancies]. Presse Med; 2009 Feb;38(2):210-9
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  • The principal varieties are papillary and follicular, far ahead of medullary and anaplastic cancers and thyroid lymphomas.
  • Their management must be multidisciplinary for it requires competence in surgery, pathology, nuclear medicine and endocrinology.
  • [MeSH-major] Thyroid Neoplasms / therapy
  • [MeSH-minor] Aged. Carcinoma, Papillary / epidemiology. Combined Modality Therapy. Female. France / epidemiology. Humans. Incidence. Male. Middle Aged. Prognosis. Sex Characteristics. Survival Rate. Survivors

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  • (PMID = 19147329.001).
  • [ISSN] 2213-0276
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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56. Liu Z, Falola J, Zhu X, Gu Y, Kim LT, Sarosi GA, Anthony T, Nwariaku FE: Antiproliferative effects of Src inhibition on medullary thyroid cancer. J Clin Endocrinol Metab; 2004 Jul;89(7):3503-9
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  • [Title] Antiproliferative effects of Src inhibition on medullary thyroid cancer.
  • There is no effective treatment for recurrent or metastatic medullary thyroid cancer (MTC).
  • Hereditary MTC is associated with mutations in the RET protooncogene, which encodes for a tyrosine kinase.
  • Proliferation of the human MTC cell line, TT, was examined in the presence of a Src-specific tyrosine kinase inhibitor, PP2, or genistein.
  • Cell counts were performed with a Coulter counter or by flow cytometry.
  • A cell death ELISA was used to assess apoptosis.
  • The MAPK kinase inhibitor, PD098059, attenuated DNA synthesis, whereas genistein caused modest declines in cell count and DNA synthesis and minimal changes in apoptosis.
  • [MeSH-major] Carcinoma, Medullary / pathology. Enzyme Inhibitors / pharmacology. Phosphotransferases / antagonists & inhibitors. Proto-Oncogene Proteins / antagonists & inhibitors. Thyroid Neoplasms / pathology
  • [MeSH-minor] Apoptosis / drug effects. Cell Division / drug effects. Cell Line, Tumor. Enzyme Activation / drug effects. Flavonoids / pharmacology. Genistein / pharmacology. Humans. Imidazoles / pharmacology. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation / drug effects. Protein-Serine-Threonine Kinases / metabolism. Protein-Tyrosine Kinases. Proto-Oncogene Proteins c-akt. Pyridines / pharmacology. Pyrimidines / pharmacology. src-Family Kinases / antagonists & inhibitors

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  • (PMID = 15240638.001).
  • [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; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole; 0 / AG 1879; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Imidazoles; 0 / Proto-Oncogene Proteins; 0 / Pyridines; 0 / Pyrimidines; DH2M523P0H / Genistein; EC 2.7.- / Phosphotransferases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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57. Eng C: Common alleles of predisposition in endocrine neoplasia. Curr Opin Genet Dev; 2010 Jun;20(3):251-6
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  • The identification of germline high penetrance gain-of-function mutations in the RET proto-oncogene as causative of multiple endocrine neoplasia led to accurate molecular diagnosis, predictive testing and gene-informed preventative medicine.
  • Many syndromic endocrine neoplasias fell under this clinically utile model, although not all endocrine neoplasias were accounted for by these high penetrance predisposition genes associated with the validated practice of clinical cancer genetics.
  • The past decade has seen the identification of low penetrance alleles for various endocrine neoplasias, including medullary and epithelial thyroid carcinomas and isolated pituitary adenomas.
  • [MeSH-major] Endocrine Gland Neoplasms / genetics. Genetic Predisposition to Disease / genetics
  • [MeSH-minor] Alleles. Carcinoma, Medullary / genetics. Humans. Multiple Endocrine Neoplasia / genetics. Penetrance. Proto-Oncogene Proteins c-ret / genetics. Thyroid Neoplasms / genetics

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  • (PMID = 20211557.001).
  • [ISSN] 1879-0380
  • [Journal-full-title] Current opinion in genetics & development
  • [ISO-abbreviation] Curr. Opin. Genet. Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human
  • [Number-of-references] 50
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58. Zabel M, Gebarowska E, Drag-Zalesińska M, Wysocka T: Effect of calcitriol on proliferation of TT cells and on expression of calcitonin gene. Folia Histochem Cytobiol; 2002;40(2):187-8
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  • The absence of serum steroids was demonstrated to restrict proliferation of cultured TT cells (cell line originating from human thyroid medullary carcinoma) and supplementation with calcitriol was found to partially restore the proliferation.
  • Calcitriol stimulated TT cell proliferation by augmenting expression of proliferation-associated proteins and by restricting apoptosis.

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  • (PMID = 12056638.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Calcium Channel Agonists; 0 / Culture Media; 0 / RNA, Messenger; 83652-28-2 / Calcitonin Gene-Related Peptide; 9007-12-9 / Calcitonin; FXC9231JVH / Calcitriol
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59. Sherman SI: Advances in chemotherapy of differentiated epithelial and medullary thyroid cancers. J Clin Endocrinol Metab; 2009 May;94(5):1493-9
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  • [Title] Advances in chemotherapy of differentiated epithelial and medullary thyroid cancers.
  • CONTEXT: Systemic chemotherapies for advanced or metastatic thyroid carcinomas have been of only limited effectiveness.
  • For patients with differentiated or medullary carcinomas unresponsive to conventional treatments, novel therapies are needed to improve disease outcomes.
  • EVIDENCE ACQUISITION: The PubMed and Google Scholar search engines were used to identify publications and peer-reviewed meeting presentations addressing chemotherapy and targeted therapy for differentiated or medullary carcinoma.
  • EVIDENCE SYNTHESIS: Multiple novel therapies primarily targeting angiogenesis have entered clinical trials for metastatic thyroid carcinoma.
  • Partial response rates up to 30% have been reported in single agent studies, but prolonged disease stabilization is more commonly seen.
  • The most successful agents target the vascular endothelial growth factor receptors, with potential targets including the mutant kinases associated with papillary and medullary oncogenesis.
  • Two drugs approved for other malignancies, sorafenib and sunitinib, have had promising preliminary results reported, and are being used selectively for patients who do not qualify for clinical trials.
  • Randomized trials for several agents are underway that may lead to eventual drug approval for thyroid cancer.
  • CONCLUSION: Treatment for patients with metastatic or advanced thyroid carcinoma now emphasizes clinical trial opportunities for novel agents with considerable promise.
  • Alternative options now exist for use of tyrosine kinase inhibitors that are well tolerated and may prove worthy of regulatory approval for this disease.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Medullary / drug therapy. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Humans. Receptors, Cytoplasmic and Nuclear / drug effects

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  • (PMID = 19258410.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Cytoplasmic and Nuclear
  • [Number-of-references] 78
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60. Carlomagno F, Vitagliano D, Guida T, Ciardiello F, Tortora G, Vecchio G, Ryan AJ, Fontanini G, Fusco A, Santoro M: ZD6474, an orally available inhibitor of KDR tyrosine kinase activity, efficiently blocks oncogenic RET kinases. Cancer Res; 2002 Dec 15;62(24):7284-90
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  • RET/papillary thyroid carcinoma (PTC) oncogenes, generated by recombination of the tyrosine kinase-encoding domain of RET with different heterologous genes, are prevalent in papillary carcinomas of the thyroid.
  • Point mutations of RET cause multiple endocrine neoplasia type 2 (MEN2) familial cancer syndrome and are found in sporadic medullary thyroid carcinomas.
  • ZD6474 prevented the growth of two human PTC cell lines that carry spontaneous RET/PTC1 rearrangements.
  • Finally, it blocked anchorage-independent growth of RET/PTC3-transformed NIH3T3 fibroblasts and the formation of tumors after injection of NIH-RET/PTC3 cells into nude mice.
  • Thus, targeting RET oncogenes with ZD6474 might offer a potential treatment strategy for carcinomas sustaining oncogenic activation of RET.
  • [MeSH-major] Drosophila Proteins. Enzyme Inhibitors / pharmacology. Piperidines / pharmacology. Proto-Oncogene Proteins / antagonists & inhibitors. Quinazolines / pharmacology. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] 3T3 Cells. Animals. Carcinoma, Papillary / genetics. Carcinoma, Papillary / pathology. Carcinoma, Papillary / prevention & control. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / genetics. Mice. Mice, Inbred BALB C. Mice, Nude. Phosphorylation / drug effects. Proto-Oncogene Proteins c-ret. Signal Transduction / drug effects. Thyroid Neoplasms / genetics. Thyroid Neoplasms / pathology. Thyroid Neoplasms / prevention & control. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors


61. de Santis Feltran L, de Abreu Carvalhaes JT, Sesso R: Renal complications of sickle cell disease: managing for optimal outcomes. Paediatr Drugs; 2002;4(1):29-36
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  • [Title] Renal complications of sickle cell disease: managing for optimal outcomes.
  • A broad spectrum of renal changes is observed in patients with sickle cell anemia, and ideal therapeutic measures for the management of these alterations are still being studied.
  • The use of anti-inflammatory drugs is being studied in order to inhibit the prostaglandins involved in the process.
  • Increased renal blood flow, glomerular filtration rate, and filtration fraction are frequent findings.
  • Hematuria commonly occurs as a consequence of red blood cell sickling in the renal medulla, papillary necrosis, or even renal medullary carcinoma.
  • Nephropathy in patients with sickle cell anemia can be manifested by proteinuria and, more rarely, nephrotic syndrome.
  • Drugs such as prednisone and cyclophosphamide are ineffective for the treatment of patients with nephrotic syndrome.
  • Angiotensin converting enzyme inhibitors decrease proteinuria, but their long-term effect in preventing the progression of glomerular disease has not been established.
  • Chronic renal failure, although infrequent, may be one of the manifestations of this disease.
  • Hemodialysis and transplantation are satisfactory therapeutic options for patients with end-stage renal disease.
  • [MeSH-major] Anemia, Sickle Cell / complications. Kidney Diseases / therapy

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  • (PMID = 11817984.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 58
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62. Chow LQ, Eckhardt SG: Sunitinib: from rational design to clinical efficacy. J Clin Oncol; 2007 Mar 1;25(7):884-96
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  • Tyrosine kinase inhibitors such as SU6668 and SU5416 (semaxanib) demonstrated poor pharmacologic properties and limited efficacy; therefore, sunitinib was rationally designed and chosen for its high bioavailability and its nanomolar-range potency against the antiangiogenic receptor tyrosine kinases (RTKs)--vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR).
  • Sunitinib inhibits other tyrosine kinases including, KIT, FLT3, colony-stimulating factor 1 (CSF-1), and RET, which are involved in a number of malignancies including small-cell lung cancer, GI stromal tumors (GISTs), breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia types 2A and 2B, and familial medullary thyroid carcinoma.
  • Sunitinib demonstrated robust antitumor activity in preclinical studies resulting not only in tumor growth inhibition, but tumor regression in models of colon cancer, non-small-cell lung cancer, melanoma, renal carcinoma, and squamous cell carcinoma, which were associated with inhibition of VEGFR and PDGFR phosphorylation.
  • Clinical activity was demonstrated in neuroendocrine, colon, and breast cancers in phase II studies, whereas definitive efficacy has been demonstrated in advanced renal cell carcinoma and in imatinib-refractory GISTs, leading to US Food and Drug Administration approval of sunitinib for treatment of these two diseases.
  • Studies investigating sunitinib alone in various tumor types and in combination with chemotherapy are ongoing.
  • The clinical benchmarking of this small-molecule inhibitor of members of the split-kinase domain family of RTKs will lead to additional insights regarding the biology, potential biomarkers, and clinical utility of agents that target multiple signaling pathways in tumor, stromal, and endothelial compartments.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Indoles / therapeutic use. Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyrroles / therapeutic use
  • [MeSH-minor] Animals. Carcinoma, Renal Cell / drug therapy. Clinical Trials as Topic. Drug Design. Gastrointestinal Stromal Tumors / drug therapy. Humans. Kidney Neoplasms / drug therapy. Leukemia, Myeloid, Acute / drug therapy

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  • [CommentIn] J Clin Oncol. 2007 Jul 1;25(19):2858-9; author reply 2859-61 [17602094.001]
  • (PMID = 17327610.001).
  • [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; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Indoles; 0 / Protein Kinase Inhibitors; 0 / Pyrroles; 0 / sunitinib
  • [Number-of-references] 112
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63. Le Blanc M, Russo J, Kudelka AP, Smith JA: An in vitro study of inhibitory activity of gossypol, a cottonseed extract, in human carcinoma cell lines. Pharmacol Res; 2002 Dec;46(6):551-5
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  • [Title] An in vitro study of inhibitory activity of gossypol, a cottonseed extract, in human carcinoma cell lines.
  • Gossypol, a cottonseed extract, has been shown to have antiproliferative activity in a variety of cancer cell lines.
  • The objective of this study was to determine the inhibitory effects of gossypol on cell proliferation.
  • Five human carcinoma cell lines were evaluated including endometrial (RL95-2), ovarian (SKOV-3), medullary thyroid (TT), and adrenocortical (NCI-H295R and SW-13).
  • The results indicate that gossypol possesses antiproliferative action toward human carcinoma cells in vitro.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma / drug therapy. Carcinoma / pathology. Gossypol / pharmacology. Growth Inhibitors / pharmacology. Phytotherapy
  • [MeSH-minor] Cell Division / drug effects. Cell Division / physiology. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical / methods. Gossypium / metabolism. Humans. Plant Extracts / isolation & purification. Plant Extracts / pharmacology. Plant Extracts / therapeutic use. Seeds / metabolism. Tumor Cells, Cultured

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  • (PMID = 12457630.001).
  • [ISSN] 1043-6618
  • [Journal-full-title] Pharmacological research
  • [ISO-abbreviation] Pharmacol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Growth Inhibitors; 0 / Plant Extracts; KAV15B369O / Gossypol
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64. Lodish MB, Stratakis CA: RET oncogene in MEN2, MEN2B, MTC and other forms of thyroid cancer. Expert Rev Anticancer Ther; 2008 Apr;8(4):625-32
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  • Hereditary medullary thyroid carcinoma (MTC) is caused by specific autosomal dominant gain-of-function mutations in the RET proto-oncogene.
  • Genotype-phenotype correlations exist that help predict the presence of other associated endocrine neoplasms as well as the timing of thyroid cancer development.
  • The RET proto-oncogene has become the target for molecularly designed drug therapy.

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  • (PMID = 18402529.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / Z99 HD999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 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
  • [Number-of-references] 67
  • [Other-IDs] NLM/ NIHMS101681; NLM/ PMC2670186
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65. Carr LL, Mankoff DA, Goulart BH, Eaton KD, Capell PT, Kell EM, Bauman JE, Martins RG: Phase II study of daily sunitinib in FDG-PET-positive, iodine-refractory differentiated thyroid cancer and metastatic medullary carcinoma of the thyroid with functional imaging correlation. Clin Cancer Res; 2010 Nov 1;16(21):5260-8
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  • [Title] Phase II study of daily sunitinib in FDG-PET-positive, iodine-refractory differentiated thyroid cancer and metastatic medullary carcinoma of the thyroid with functional imaging correlation.
  • PURPOSE: We conducted a phase II study to assess the efficacy of continuous dosing of sunitinib in patients with flurodeoxyglucose positron emission tomography (FDG-PET)-avid, iodine-refractory well-differentiated thyroid carcinoma (WDTC) and medullary thyroid cancer (MTC) and to assess for early response per FDG-PET.
  • EXPERIMENTAL DESIGN: Patients had metastatic, iodine-refractory WDTC or MTC with FDG-PET-avid disease.
  • The primary end point was response rate per Response Evaluation Criteria in Solid Tumors (RECIST).
  • RESULTS: Thirty-five patients were enrolled (7 MTC, 28 WDTC), and 33 patients were evaluable for disease response.
  • There were 1 complete response (3%), 10 partial responses (28%), and 16 patients (46%) with stable disease.
  • Progressive disease was seen in 6 patients (17%).
  • The median percent change in average standardized uptake values was -11.7%, -13.9%, and 8.6% for patients with RECIST response, stable disease, and progressive disease, respectively.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20847059.001).
  • [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 / CA015704
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 9679TC07X4 / Iodine
  • [Other-IDs] NLM/ NIHMS236832; NLM/ PMC3063514
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66. Dill JA, Lee KM, Renne RA, Miller RA, Fuciarelli AF, Gideon KM, Chan PC, Burka LT, Roycroft JH: Alpha 2u-globulin nephropathy and carcinogenicity following exposure to decalin (decahydronaphthalene) in F344/N rats. Toxicol Sci; 2003 Apr;72(2):223-34
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  • (2) compare the kidney concentrations of decalin, 2-decalone, and alpha2u-globulin in males over 2 to 13 weeks of decalin exposure; and (3) correlate male rat nephropathy observed in the 13-week study with renal carcinogenicity in the two-year study.
  • F344 rats (M/F) were exposed via whole-body inhalation to 0, 25, 50, 100, 200, or 400 ppm decalin for 13 weeks.
  • Left kidneys were evaluated for histopathology and cell proliferation utilizing a proliferating cell nuclear antigen technique and counting proximal renal tubular epithelial cells to determine cell labeling indices.
  • Decalin exposure caused increases in kidney weight, urinalysis parameters (protein, AST, LDH), kidney alpha2u-globulin concentration, and proximal convoluted renal tubular cell proliferation in males.
  • These changes were accompanied by microscopic lesions (accumulation of hyaline droplets in cortical tubules, regeneration of proximal tubular epithelium, and granular casts in medullary tubules) clearly linked to alpha2u-globulin nephropathy.
  • For chronic exposure, F344 rats were exposed via whole-body inhalation to 0, 25, 50 (males only), 100, or 400 ppm decalin for two years.
  • Chronic exposure induced a spectrum of nonneoplastic and neoplastic lesions in the renal cortex of males, ranging from regenerative lesions of chronic nephropathy to tubular carcinomas.
  • Incidences of renal tubular adenoma, tubular carcinoma, combined tubular adenomas and carcinomas, cortical tubular hyperplasia, hyaline droplet accumulation, hyperplasia of pelvic epithelium, and mineralization in renal papilla were increased in exposed males compared to controls.
  • It was concluded that the carcinogenic effect on the renal cortical epithelium of male rats exposed to decalin was related to increased turnover of this epithelium, resulting from the cytotoxic effects of alpha2u-globulin accumulation in the renal cortical tubular cell cytoplasm.
  • [MeSH-major] Adenoma / chemically induced. Carcinogens / toxicity. Carcinoma / chemically induced. Kidney / drug effects. Kidney Neoplasms / chemically induced. Naphthalenes / toxicity
  • [MeSH-minor] Administration, Inhalation. Alpha-Globulins. Animals. Carcinogenicity Tests. Cell Division / drug effects. Dose-Response Relationship, Drug. Female. Hyalin / metabolism. Kidney Tubules, Proximal / drug effects. Kidney Tubules, Proximal / pathology. Male. Organ Size / drug effects. Rats. Rats, Inbred F344. Sex Factors. Solvents

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  • (PMID = 12660359.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / N01-ES-55392
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alpha-Globulins; 0 / Carcinogens; 0 / Naphthalenes; 0 / Solvents; 0 / alpha 2u globulin; 88451Q4XYF / decalin
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67. Stadler G, Wieser M, Steindl F, Grillari J, Katinger H, Pfragner R, Voglauer R: Development of standardized cell culture conditions for tumor cells with potential clinical application. Cytotherapy; 2007;9(5):488-98
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  • [Title] Development of standardized cell culture conditions for tumor cells with potential clinical application.
  • BACKGROUND: Tumor cell lines have enormous value for the study of different aspects of cancer biology and have also recently gained great importance in autologous cell-based anti-tumor therapies.
  • METHODS: To address this drawback, we aimed to develop a strategy for optimization of the culture medium for human medullary thyroid carcinoma (MTC) cell lines as a model system.
  • We combined the general cell screening system (GCSS), which continuously measured the growth behavior of cells in a 96-well plate format, with statistically based experimental designs.
  • RESULTS: The results obtained clearly demonstrated that, just by changing the composition of the basal medium, a significantly enhanced growth rate could be observed, and by subsequent addition of several substances a serum-free cell culture medium could be developed.
  • This medium allowed the propagation of two MTC cell lines comparable with conventionally used serum-supplemented medium.
  • DISCUSSION: We present a fast and easy way to screen for substances that are essential for tumor cell growth in vitro.
  • Furthermore, these tumor cells can be adapted to culture conditions that allow the use of the cells in safe cell-based therapies.
  • [MeSH-major] Carcinoma / metabolism. Cell Proliferation / drug effects. Drug Evaluation, Preclinical / methods. Thyroid Neoplasms / metabolism
  • [MeSH-minor] Cell Culture Techniques / methods. Cell Line, Tumor. Culture Media, Serum-Free / chemistry. Culture Media, Serum-Free / pharmacology. Culture Media, Serum-Free / standards. Humans

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  • (PMID = 17786610.001).
  • [ISSN] 1465-3249
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Serum-Free
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68. Furge KA, Dykema K, Petillo D, Westphal M, Zhang Z, Kort EJ, Teh BT: Combining differential expression, chromosomal and pathway analyses for the molecular characterization of renal cell carcinoma. Can Urol Assoc J; 2007 Jun;1(2 Suppl):S21-7
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  • [Title] Combining differential expression, chromosomal and pathway analyses for the molecular characterization of renal cell carcinoma.
  • This abnormal genetic makeup can have profound effects on cellular activities such as cell growth, cell survival and other regulatory processes.
  • Based on the pattern of gene expression, or molecular signatures of the tumours, we can distinguish or subclassify different types of cancers according to their cell of origin, behaviour, and the way they respond to therapeutic agents and radiation.
  • These approaches will lead to better molecular subclassification of tumours, the basis of personalized medicine.
  • These data are used to identify both cytogenetic abnormalities and molecular pathways that are deregulated in renal cell carcinoma (RCC).
  • For example, we have identified the deregulation of the VHL-hypoxia pathway in clear-cell RCC, as previously known, and the c-Myc pathway in aggressive papillary RCC.
  • Besides the more common clear-cell, papillary and chromophobe RCCs, we are currently characterizing the molecular signatures of rarer forms of renal neoplasia such as carcinoma of the collecting ducts, mixed epithelial and stromal tumours, chromosome Xp11 translocations associated with papillary RCC, renal medullary carcinoma, mucinous tubular and spindle-cell carcinoma, and a group of unclassified tumours.
  • Continued development and improvement in the field of molecular profiling will better characterize cancer and provide more accurate diagnosis, prognosis and prediction of drug response.

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  • (PMID = 18542781.001).
  • [ISSN] 1911-6470
  • [Journal-full-title] Canadian Urological Association journal = Journal de l'Association des urologues du Canada
  • [ISO-abbreviation] Can Urol Assoc J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC2422953
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69. Osborne ME, Brown RS, Hoskin PJ: Interaction of bisphosphonates with calcitonin in monitoring medullary carcinoma of the thyroid. Clin Oncol (R Coll Radiol); 2001;13(5):370-1
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  • [Title] Interaction of bisphosphonates with calcitonin in monitoring medullary carcinoma of the thyroid.
  • We report the case history of a patient with long standing recurrent medullary carcinoma of the thyroid.
  • Elevation of the serum marker calcitonin coincided with the introduction of biphosphonate therapy and recurrence of tumour was not established.
  • [MeSH-major] Calcitonin / blood. Carcinoma, Medullary / blood. Diphosphonates / blood. Thyroid Neoplasms / blood
  • [MeSH-minor] Adult. Drug Interactions. Female. Humans. Osteoporosis / drug therapy

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  • (PMID = 11716232.001).
  • [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] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Diphosphonates; 9007-12-9 / Calcitonin
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70. Ball DW: Medullary thyroid cancer: monitoring and therapy. Endocrinol Metab Clin North Am; 2007 Sep;36(3):823-37, viii
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  • [Title] Medullary thyroid cancer: monitoring and therapy.
  • This article summarizes the clinical features and molecular pathogenesis of medullary thyroid cancer (MTC) and focuses on the current use of molecular, biochemical, and imaging disease markers as a basis for selection of appropriate therapy.
  • (1) distinguishing MTC as early as possible from benign nodular disease and differentiated thyroid cancer to choose the appropriate initial surgery, (2) managing low-level residual cancer in otherwise asymptomatic individuals, and (3) treating progressive metastatic disease.
  • This article highlights early progress in targeted therapy of MTC and significant challenges in disease monitoring to appropriately select and evaluate patients being treated with these therapies.

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  • (PMID = 17673130.001).
  • [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 / CA096784-01; United States / NCI NIH HHS / CA / P50 CA096784; United States / NCI NIH HHS / CA / P50 CA096784-01
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers; 0 / Genetic Markers; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret
  • [Number-of-references] 60
  • [Other-IDs] NLM/ NIHMS29621; NLM/ PMC2806819
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71. Grozinsky-Glasberg S, Rubinfeld H, Nordenberg Y, Gorshtein A, Praiss M, Kendler E, Feinmesser R, Grossman AB, Shimon I: The rapamycin-derivative RAD001 (everolimus) inhibits cell viability and interacts with the Akt-mTOR-p70S6K pathway in human medullary thyroid carcinoma cells. Mol Cell Endocrinol; 2010 Feb 5;315(1-2):87-94
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  • [Title] The rapamycin-derivative RAD001 (everolimus) inhibits cell viability and interacts with the Akt-mTOR-p70S6K pathway in human medullary thyroid carcinoma cells.
  • Over-expression of the proto-oncogene Akt/PKB has been demonstrated in some neuroendocrine tumor models.
  • Akt may activate downstream proteins such as mTOR and p70S6K, inducing tumor proliferation.
  • The rapamycin-derivative RAD001, everolimus, interacts with this pathway by antagonizing mTOR, but its effects on neuroendocrine tumors are largely unknown.
  • We explored the mechanism of action of RAD001 on cell proliferation, hormonal secretion and on Akt/mTOR/p70S6K pathway activation, in a human medullary thyroid carcinoma (MTC) cell-line (TT) and in cells derived from human MTCs.
  • Treatment with RAD001 significantly inhibited cell viability in a dose- and time-dependent fashion, and diminished phosphorylation of Akt downstream targets, mTOR and p70S6K, in both TT cell-line and cultured human MTCs.
  • RAD001 induced cell-cycle arrest in the G(0)/G(1) phase in TT cells, but had no effect on apoptosis.
  • RAD001 seems to have potent anti-proliferative effect in human MTC cells, which suggest that clinical trials of this agent are of considerable interest.
  • [MeSH-major] Cell Survival / drug effects. Immunosuppressive Agents / pharmacology. Intracellular Signaling Peptides and Proteins / metabolism. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction / drug effects. Sirolimus / analogs & derivatives. Thyroid Neoplasms / metabolism
  • [MeSH-minor] Aged. Calcitonin / metabolism. Carcinoembryonic Antigen / metabolism. Cell Cycle / drug effects. Everolimus. Humans. Male. Middle Aged. Phosphorylation. TOR Serine-Threonine Kinases. Thyroid Gland / anatomy & histology. Thyroid Gland / pathology. Tumor Cells, Cultured

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  • [Copyright] 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19815051.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen; 0 / Immunosuppressive Agents; 0 / Intracellular Signaling Peptides and Proteins; 9007-12-9 / Calcitonin; 9HW64Q8G6G / Everolimus; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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72. Erlic Z, Hoffmann MM, Sullivan M, Franke G, Peczkowska M, Harsch I, Schott M, Gabbert HE, Valimäki M, Preuss SF, Hasse-Lazar K, Waligorski D, Robledo M, Januszewicz A, Eng C, Neumann HP: Pathogenicity of DNA variants and double mutations in multiple endocrine neoplasia type 2 and von Hippel-Lindau syndrome. J Clin Endocrinol Metab; 2010 Jan;95(1):308-13
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  • [Title] Pathogenicity of DNA variants and double mutations in multiple endocrine neoplasia type 2 and von Hippel-Lindau syndrome.
  • CONTEXT: Cancer genetics is fundamental for preventive medicine, in particular in pheochromocytoma-associated syndromes.
  • PATIENTS: Patients were registrants from the European-American Pheochromocytoma-Paraganglioma and German von Hippel-Lindau Disease Registries.
  • DESIGN: Analysis of germline mutation screening results for all pheochromocytoma-paraganglioma susceptibility genes, including RET [multiple endocrine neoplasia type 2 (MEN 2)] and VHL [von Hippel-Lindau disease (VHL)].
  • Cases in which more than one DNA variant was found were clinically reevaluated, and cosegregation of the disease with the variant was analyzed within the registrants' families.
  • None of the carriers of the RET variants who underwent prophylactic thyroidectomy showed medullary thyroid carcinoma.
  • Clinical reinvestigation of 18 variant carriers excluded MEN 2.
  • [MeSH-major] Genetic Predisposition to Disease. Germ-Line Mutation. Membrane Proteins / genetics. Multiple Endocrine Neoplasia Type 2a / genetics. Proto-Oncogene Proteins c-ret / genetics. von Hippel-Lindau Disease / genetics
  • [MeSH-minor] Adrenal Gland Neoplasms / genetics. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Paraganglioma / genetics. Pedigree. Pheochromocytoma / genetics


73. Woyach JA, Shah MH: New therapeutic advances in the management of progressive thyroid cancer. Endocr Relat Cancer; 2009 Sep;16(3):715-31
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  • The spectrum of thyroid cancers ranges from one of the most indolent to one of the most aggressive solid tumors identified.
  • Conventional therapies for thyroid cancers are based on the histologic type of thyroid cancers such as papillary or follicular thyroid cancer (differentiated thyroid cancer (DTC)), medullary thyroid cancer (MTC), or anaplastic thyroid cancer (ATC).
  • [MeSH-major] Antineoplastic Protocols. Carcinoma / therapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Animals. Carcinoma, Medullary / etiology. Carcinoma, Medullary / therapy. Carcinoma, Papillary / etiology. Carcinoma, Papillary / therapy. Clinical Trials as Topic / methods. Clinical Trials as Topic / trends. Disease Progression. Drug Evaluation, Preclinical / methods. Drug Evaluation, Preclinical / trends. Humans. Models, Biological

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  • (PMID = 19218279.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 106
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74. Baudin E, Droz JP, Paz-Ares L, van Oosterom AT, Cullell-Young M, Schlumberger M: Phase II study of plitidepsin 3-hour infusion every 2 weeks in patients with unresectable advanced medullary thyroid carcinoma. Am J Clin Oncol; 2010 Feb;33(1):83-8
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  • [Title] Phase II study of plitidepsin 3-hour infusion every 2 weeks in patients with unresectable advanced medullary thyroid carcinoma.
  • OBJECTIVES: To evaluate the antitumor response, time-to-event efficacy endpoints and toxicity of plitidepsin (Aplidin) 5 mg/m as a 3-hour intravenous (i.v.) infusion every 2 weeks in patients with unresectable advanced medullary thyroid carcinoma (MTC).
  • METHODS: Sixteen patients with MTC and disease progression or large tumor burden received plitidepsin.
  • Tumor response and time-related parameters were evaluated according to Response Evaluation Criteria in Solid Tumors.
  • No complete responses or partial responses (PR) were found, and 12 patients had stable disease for >8 weeks.
  • Marker response included 1 unconfirmed PR and 2 stabilizations for calcitonin, and 1 unconfirmed PR and 4 stabilizations for calcitonin and carcinoembryonic antigen.
  • CONCLUSIONS: Single-agent plitidepsin given as 3-hour i.v. infusions every 2 weeks was generally well tolerated but showed limited clinical activity in patients with unresectable advanced MTC.
  • [MeSH-major] Brain Stem Neoplasms / drug therapy. Depsipeptides / administration & dosage. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Female. Humans. Infusions, Intravenous. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate. Treatment Outcome

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  • (PMID = 19704366.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Depsipeptides; Y76ID234HW / aplidine
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75. Kunnimalaiyaan M, Vaccaro AM, Ndiaye MA, Chen H: Inactivation of glycogen synthase kinase-3beta, a downstream target of the raf-1 pathway, is associated with growth suppression in medullary thyroid cancer cells. Mol Cancer Ther; 2007 Mar;6(3):1151-8
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  • [Title] Inactivation of glycogen synthase kinase-3beta, a downstream target of the raf-1 pathway, is associated with growth suppression in medullary thyroid cancer cells.
  • Glycogen synthase kinase-3beta (GSK-3beta) is an important regulator of cell proliferation and survival.
  • In this study, we found that raf-1 activation in human medullary thyroid cancer cells, TT cells, resulted in phosphorylation of GSK-3beta.
  • Growth inhibition by GSK-3beta inactivation was found to be associated with cell cycle arrest due to an increase in the levels of cyclin-dependent kinase inhibitors such as p21, p27, and p15.
  • Additionally, LiCl-treated TT xenograft mice had a significant reduction in tumor volume compared with those treated with control.
  • [MeSH-major] Carcinoma, Medullary / prevention & control. Glycogen Synthase Kinase 3 / antagonists & inhibitors. Indoles / pharmacology. Maleimides / pharmacology. Proto-Oncogene Proteins c-raf / metabolism. Thyroid Neoplasms / prevention & control
  • [MeSH-minor] Adjuvants, Immunologic / pharmacology. Animals. Apoptosis / drug effects. Apoptosis / physiology. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Proliferation / drug effects. Chromogranin A / metabolism. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p15 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Humans. Lithium Chloride / pharmacology. Mice. Mice, Nude. NIH 3T3 Cells / drug effects. Phosphorylation. Signal Transduction / drug effects. Xenograft Model Antitumor Assays


76. Mitsiades CS, Poulaki V, McMullan C, Negri J, Fanourakis G, Goudopoulou A, Richon VM, Marks PA, Mitsiades N: Novel histone deacetylase inhibitors in the treatment of thyroid cancer. Clin Cancer Res; 2005 May 15;11(10):3958-65
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  • In this study, we characterized the effect of two HDAC inhibitors, suberoylanilide hydroxamic acid (SAHA) and m-carboxycinnamic acid bis-hydroxamide, on thyroid carcinoma cell lines, including lines originating from anaplastic and medullary carcinomas.
  • Transfection of Bcl-2 cDNA partially suppressed SAHA-induced cell death.
  • SAHA down-regulated the expression of the apoptosis inhibitors FLIP and cIAP-2 and sensitized tumor cells to cytotoxic chemotherapy and death receptor activation.
  • Our studies provide insight into the tumor type-specific mechanisms of antitumor effects of HDAC inhibitors and a framework for future clinical applications of HDAC inhibitors in patients with thyroid cancer, including histologic subtypes (e.g., anaplastic and medullary thyroid carcinomas) for which limited, if any, therapeutic options are available.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma / pathology. Cinnamates / pharmacology. Histone Deacetylase Inhibitors. Hydroxamic Acids / pharmacology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Apoptosis. Cell Death. Down-Regulation. Gene Expression Regulation, Neoplastic / drug effects. Humans. Tumor Cells, Cultured

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  • (PMID = 15897598.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cinnamates; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / carboxycinnamic acid bishydroxamide; 58IFB293JI / vorinostat
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77. Strock CJ, Park JI, Rosen DM, Ruggeri B, Denmeade SR, Ball DW, Nelkin BD: Activity of irinotecan and the tyrosine kinase inhibitor CEP-751 in medullary thyroid cancer. J Clin Endocrinol Metab; 2006 Jan;91(1):79-84
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  • [Title] Activity of irinotecan and the tyrosine kinase inhibitor CEP-751 in medullary thyroid cancer.
  • CONTEXT: Medullary thyroid cancer (MTC) is a cancer of the parafollicular C cells that commonly presents with an inherited or acquired RET gene mutation.
  • We studied the sensitivity of an MTC cell line and xenograft to irinotecan, alone and in combination with the tyrosine kinase inhibitor, CEP-751.
  • RESULTS: In TT cell culture and xenografts, irinotecan treatment was highly effective.
  • Treatment of TT cell xenografts resulted in durable complete remission in 100% of the mice, with median time to recurrence of 70 d for irinotecan alone and more than 130 d for irinotecan plus CEP-751.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Phytogenic / therapeutic use. Camptothecin / analogs & derivatives. Carbazoles / therapeutic use. Carcinoma, Medullary / drug therapy. Enzyme Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Blotting, Western. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Histones / biosynthesis. Histones / genetics. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Protein Kinases / biosynthesis. Protein Kinases / genetics. S Phase / drug effects. Signal Transduction / drug effects. Signal Transduction / physiology. Transplantation, Heterologous. cdc25 Phosphatases / biosynthesis. cdc25 Phosphatases / genetics

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  • (PMID = 16263812.001).
  • [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-96784
  • [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 / Antineoplastic Agents, Phytogenic; 0 / CEP 751; 0 / Carbazoles; 0 / Enzyme Inhibitors; 0 / H2AFX protein, human; 0 / Histones; 7673326042 / irinotecan; EC 2.7.- / Protein Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.1 / Checkpoint kinase 1; EC 3.1.3.16 / Cdc25a protein, mouse; EC 3.1.3.48 / CDC25A protein, human; EC 3.1.3.48 / cdc25 Phosphatases; XT3Z54Z28A / Camptothecin
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78. Sathornsumetee S, Rich JN: Vandetanib, a novel multitargeted kinase inhibitor, in cancer therapy. Drugs Today (Barc); 2006 Oct;42(10):657-70
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  • In addition to its antiangiogenic effects, vandetanib acts against EGFR, which is overexpressed or mutated in several solid tumors.
  • Furthermore, vandetanib exerts activity against oncogenic RET kinase, the overexpression of which is common in medullary and papillary thyroid carcinomas.
  • Therefore, the multitargeted kinase inhibitor vandetanib represents a new approach, targeting both tumor cells and tumor-associated endothelial cells.
  • Phase II clinical studies in patients with non-small-cell lung cancer have shown promising results, employing vandetanib as both monotherapy and in combination with docetaxel.
  • [MeSH-major] Neoplasms / drug therapy. Piperidines / therapeutic use. Quinazolines / therapeutic use. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors
  • [MeSH-minor] Animals. Clinical Trials as Topic. Drug Evaluation, Preclinical / methods. Humans. Molecular Structure. Treatment Outcome

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  • [Copyright] Copyright 2006 Prous Science. All rights reserved.
  • (PMID = 17136225.001).
  • [ISSN] 1699-3993
  • [Journal-full-title] Drugs of today (Barcelona, Spain : 1998)
  • [ISO-abbreviation] Drugs Today
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Piperidines; 0 / Quinazolines; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; YO460OQ37K / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine
  • [Number-of-references] 88
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79. Cakir M, Dworakowska D, Grossman A: Somatostatin receptor biology in neuroendocrine and pituitary tumours: part 1--molecular pathways. J Cell Mol Med; 2010 Nov;14(11):2570-84
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  • Neuroendocrine tumours (NETs) may occur at many sites in the body although the majority occur within the gastroenteropancreatic axis.
  • Non-gastroenteropancreatic NETs encompass phaeochromocytomas and paragangliomas, medullary thyroid carcinoma, anterior pituitary tumour, broncho-pulmonary NETs and parathyroid tumours.
  • Like most endocrine tumours, NETs also express somatostatin (SST) receptors (subtypes 1-5) whose ligand SST is known to inhibit endocrine and exocrine secretions and have anti-tumour effects.
  • SST is a potent anti-proliferative and anti-secretory agent for some NETs.
  • The successful therapeutic use of SST analogues in the treatment of these tumours depends on a thorough understanding of the diverse effects of SSTR subtypes in different tissues and cell types.
  • [MeSH-major] Neuroendocrine Tumors / metabolism. Pituitary Neoplasms / metabolism. Receptors, Somatostatin / metabolism

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  • [Copyright] © 2010 The Authors Journal compilation © 2010 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
  • (PMID = 20629989.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Somatostatin
  • [Other-IDs] NLM/ PMC4373477
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80. Rufini V, Treglia G, Perotti G, Leccisotti L, Calcagni ML, Rubello D: Role of PET in medullary thyroid carcinoma. Minerva Endocrinol; 2008 Jun;33(2):67-73
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  • [Title] Role of PET in medullary thyroid carcinoma.
  • In the diagnostic assessment of medullary thyroid carcinoma (MTC), nuclear medicine imaging provides its contribution mainly in the postoperative work-up to detect residual or recurrent tumor.
  • Moreover, the recent developments of hybrid machines allow to obtain images that simultaneously hold both anatomic (computed tomography) and functional (PET) information with great impact on diagnostic efficacy. (18)F-fluoro-deoxyglucose ((18)F-FDG) is the most frequently used PET tracer in oncology.
  • Preliminary reports of FDG-PET in MTC patients show encouraging results with a higher sensitivity in detecting local recurrent and metastatic disease when compared with single photon emission tracers.
  • However, (18)F-FDG uptake depends on lesion size and to some extent on the grade of differentiation and biologic aggressiveness of the tumor; so FDG-PET seems useful mainly in patients with very high calcitonin levels and high progression rate.
  • Like other neuroendocrine tumors, MTC is characterized by the presence of amine uptake mechanism and/or peptide receptors at the cell membrane allowing the clinical use of specific radiopharmaceuticals that reflect the different metabolic pathways of MTC, and in particular the synthesis, storage and release of hormones ((18)F-dihydroxyphenilalanine, (18)F-DOPA and (18)F-fluorodopamine, (18)F-FDA) and the expression of receptors ((68)Ga-labeled somatostatin analogs).
  • These tracers are currently under investigation and will further improve the diagnostic approach of MTC.
  • [MeSH-major] Carcinoma, Medullary / radionuclide imaging. Positron-Emission Tomography. Thyroid Neoplasms / radionuclide imaging

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  • (PMID = 18388854.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
  • [Number-of-references] 48
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81. Albadine R, Wang W, Brownlee NA, Toubaji A, Billis A, Argani P, Epstein JI, Garvin AJ, Cousi R, Schaeffer EM, Pavlovich C, Netto GJ: Topoisomerase II alpha status in renal medullary carcinoma: immuno-expression and gene copy alterations of a potential target of therapy. J Urol; 2009 Aug;182(2):735-40
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  • [Title] Topoisomerase II alpha status in renal medullary carcinoma: immuno-expression and gene copy alterations of a potential target of therapy.
  • PURPOSE: Renal medullary carcinoma is an aggressive renal neoplasm without currently available effective therapy to our knowledge.
  • Topoisomerase II alpha is a gyrase involved in cell proliferation, and DNA maintenance and repair.
  • Topoisomerase II alpha is a target of inhibiting agents such as anthracyclines.
  • Triggered by a recent response to topoisomerase II alpha inhibitors in a patient with renal medullary carcinoma, we evaluated topoisomerase II alpha expression in relation to the proliferation index and topoisomerase II alpha gene copy number status in a larger series of patients with renal medullary carcinoma.
  • MATERIALS AND METHODS: Archival tissues from 14 renal medullary carcinomas were retrieved from our 3 institutions.
  • The total number of topoisomerase II alpha and chromosome 17 centromere signals was counted in 150 cells per tumor and a topoisomerase II alpha-to-chromosome 17 centromere signal ratio was calculated in each tumor.
  • The percent of tumor cells with polysomic, eusomic or monosomic chromosome 17 status was also determined.
  • RESULTS: On immuno-expression analysis topoisomerase II alpha immunohistochemistry was technically inconclusive in 1 renal medullary carcinoma.
  • Topoisomerase II alpha was over expressed in 11 of 13 renal medullary carcinomas (85%) (median 50%, range 1% to 80%).
  • As expected, a high Ki67 proliferation index was noted in 13 of 14 tumors (median 87.5%, range 2% to 100%).
  • Ki67 expression was greater than topoisomerase II alpha expression in all 13 informative tumors.
  • On fluorescence in situ hybridization no topoisomerase II alpha amplification was detected in any of the 14 renal medullary carcinomas, including the 11 with topoisomerase II alpha over expression.
  • Topoisomerase II alpha gene deletions were noted in 4 tumors.
  • Two of 4 deletions were associated with chromosome 17 monosomy and 2 were in eusomic chromosome 17 tumors.
  • CONCLUSIONS: Topoisomerase II alpha is over expressed in 85% of renal medullary carcinomas, potentially supporting the use of topoisomerase II alpha inhibitor agents to treat this aggressive renal tumor.
  • Our findings suggest that topoisomerase II alpha over expression in our renal medullary carcinoma cohort was not due to gene amplification, but rather to transcriptional or post-transcriptional modifications.
  • The significance of the incidentally found topoisomerase II alpha deletions in 28% of renal medullary carcinomas requires further evaluation.
  • [MeSH-major] Antigens, Neoplasm / genetics. Carcinoma, Medullary / enzymology. Carcinoma, Medullary / genetics. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Kidney Neoplasms / enzymology. Kidney Neoplasms / genetics

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  • (PMID = 19539329.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058236
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Other-IDs] NLM/ NIHMS404080; NLM/ PMC3505671
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82. Sarlis NJ, Gourgiotis L: Molecular elements of apoptosis-regulating pathways in follicular thyroid cells: mining for novel therapeutic targets in the treatment of thyroid carcinoma. Curr Drug Targets Immune Endocr Metabol Disord; 2004 Sep;4(3):187-98
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  • [Title] Molecular elements of apoptosis-regulating pathways in follicular thyroid cells: mining for novel therapeutic targets in the treatment of thyroid carcinoma.
  • Apoptosis or programmed cell death occurs in both normal and pathological conditions, including cancer.
  • Dysregulation of apoptosis allows transformed cells to continually and uninhibitedly enter the cell cycle, thus perpetuating the sequence of mutation, genomic instability and, finally, oncogenesis.
  • The cell death machinery includes cell surface receptors, adaptor molecules, proteolytic enzymes, such as caspases, and a variety of mitochondrial proteins, which interact with each other in a complex fashion.
  • Recent advances in molecular techniques have shed light upon elements of the above pathways in assorted malignancies, including non-medullary thyroid carcinoma (ThyrCa).
  • A subgroup of ThyrCa patients is (or becomes over time) refractory to standard treatment modalities and eventually succumbs to their disease.
  • For such patients with clinically aggressive ThyrCa, novel therapeutic agents are urgently needed.
  • In this review, we outline the main molecular targets that play a role in apoptosis in ThyrCa cells, and discuss various options for promoting apoptosis, either by pharmacologic or gene transfer therapeutic interventions.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Adenocarcinoma, Follicular / pathology. Apoptosis / physiology. Drug Delivery Systems / methods. Signal Transduction / drug effects. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Humans. Thyroid Gland / drug effects. Thyroid Gland / metabolism. Thyroid Gland / pathology

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  • (PMID = 15379722.001).
  • [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] 162
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83. de Groot JW, Zonnenberg BA, Plukker JT, van Der Graaf WT, Links TP: Imatinib induces hypothyroidism in patients receiving levothyroxine. Clin Pharmacol Ther; 2005 Oct;78(4):433-8
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  • Interactions of imatinib with other drugs have been scarcely reported.
  • Eleven patients (1 with gastrointestinal stromal tumor and 10 with medullary thyroid carcinoma) received imatinib.
  • On average, thyrotropin (INN, thyrotrophin) levels increased to 384% +/- 228% of the upper limit in patients after thyroidectomy, whereas free thyroxine (fT4) and free tri-iodothyronine (fT3) values remained within the reference range (59% +/- 17% of the upper limit for fT4 and 63% +/- 4% of the upper limit for fT3).
  • [MeSH-major] Antineoplastic Agents / adverse effects. Hypothyroidism / chemically induced. Piperazines / adverse effects. Pyrimidines / adverse effects. Thyroxine / adverse effects
  • [MeSH-minor] Adult. Aged. Benzamides. Carcinoma, Medullary / drug therapy. Carcinoma, Medullary / surgery. Drug Synergism. Female. Gastrointestinal Stromal Tumors / drug therapy. Humans. Imatinib Mesylate. Male. Middle Aged. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / surgery. Thyroidectomy. Thyrotropin / blood. Triiodothyronine / blood

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  • (PMID = 16198662.001).
  • [ISSN] 0009-9236
  • [Journal-full-title] Clinical pharmacology and therapeutics
  • [ISO-abbreviation] Clin. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 06LU7C9H1V / Triiodothyronine; 8A1O1M485B / Imatinib Mesylate; 9002-71-5 / Thyrotropin; Q51BO43MG4 / Thyroxine
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84. Vitale G, Tagliaferri P, Caraglia M, Rampone E, Ciccarelli A, Bianco AR, Abbruzzese A, Lupoli G: Slow release lanreotide in combination with interferon-alpha2b in the treatment of symptomatic advanced medullary thyroid carcinoma. J Clin Endocrinol Metab; 2000 Mar;85(3):983-8
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  • [Title] Slow release lanreotide in combination with interferon-alpha2b in the treatment of symptomatic advanced medullary thyroid carcinoma.
  • Somatostatin analogs are promising agents in the treatment of medullary thyroid carcinoma.
  • We have evaluated the effects of the slow release somatostatin analog lanreotide in combination with interferon-alpha2b in seven patients with advanced and symptomatic medullary thyroid carcinoma.
  • The frequency and intensity of daily flushing episodes and bowel movements, the intensity of fatigue, weight, performance status, calcitonin levels, and change in tumor masses were recorded before and during treatment.
  • However, disease stabilization and minor tumor regression were observed in three of seven and two of seven patients, respectively.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Medullary / drug therapy. Interferon-alpha / therapeutic use. Peptides, Cyclic / therapeutic use. Somatostatin / analogs & derivatives. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Adult. Algorithms. Biomarkers, Tumor. Calcitonin / blood. Delayed-Action Preparations. Drug Combinations. Female. Humans. Lymph Node Excision. Male. Middle Aged. Recombinant Proteins. Thyroidectomy. Time Factors

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  • (PMID = 10720027.001).
  • [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
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Delayed-Action Preparations; 0 / Drug Combinations; 0 / Interferon-alpha; 0 / Peptides, Cyclic; 0 / Recombinant Proteins; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin; 9007-12-9 / Calcitonin; 99210-65-8 / interferon alfa-2b
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85. Izikson L, English JC 3rd, Zirwas MJ: The flushing patient: differential diagnosis, workup, and treatment. J Am Acad Dermatol; 2006 Aug;55(2):193-208
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  • [Title] The flushing patient: differential diagnosis, workup, and treatment.
  • However, in some cases, accurate diagnosis requires further laboratory, radiologic, or histopathologic studies to differentiate several important clinicopathologic entities.
  • If this work-up is unrevealing, rare causes, such as medullary carcinoma of the thyroid, pancreatic cell tumor, renal carcinoma, and others, should be considered.
  • LEARNING OBJECTIVE: At the completion of this learning activity, participants should be familiar with the mechanisms of flushing, its clinical differential diagnosis, the approach to establish a definitive diagnosis, and management of various conditions that produce flushing.
  • [MeSH-major] Flushing / etiology. Neoplasms / complications. Rosacea / complications
  • [MeSH-minor] Alcohol Drinking. Diagnosis, Differential. Drug Eruptions. Humans. Menopause. Mental Disorders / complications. Nervous System Diseases / complications. Nervous System Diseases / diagnosis

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  • (PMID = 16844500.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 101
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86. de Groot JW, Plaza Menacho I, Schepers H, Drenth-Diephuis LJ, Osinga J, Plukker JT, Links TP, Eggen BJ, Hofstra RM: Cellular effects of imatinib on medullary thyroid cancer cells harboring multiple endocrine neoplasia Type 2A and 2B associated RET mutations. Surgery; 2006 Jun;139(6):806-14
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  • [Title] Cellular effects of imatinib on medullary thyroid cancer cells harboring multiple endocrine neoplasia Type 2A and 2B associated RET mutations.
  • BACKGROUND: Activating mutations in the RET gene, which encodes a tyrosine kinase receptor, often cause medullary thyroid carcinoma (MTC).
  • We evaluated imatinib, a tyrosine kinase inhibitor currently used to treat chronic myelogenous leukemia and gastrointestinal stromal tumors, as a potential drug for systemic treatment of MTC, in 2 MTC-derived cell lines expressing multiple endocrine neoplasia-associated mutant RET receptors.
  • We determined the effects on cell proliferation by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay, and we used fluorescence-activated cell sorter analysis with annexin V/propidium iodide staining to study imatinib-induced cell-cycle arrest, apoptosis, and cell death.
  • Dose-dependent decreases in cell proliferation of both cell lines after exposure to imatinib with inhibitory concentration of 50% levels of 23 +/- 2 micromol/L and 25 +/- 4 micromol/L were seen.
  • These values are high, compared with those for chronic myelogenous leukemia and gastrointestinal stromal tumors.
  • We further could show that imatinib induced cell-cycle arrest, and apoptotic and nonapoptotic cell death.
  • CONCLUSIONS: Imatinib inhibits RET-mediated MTC cell growth affecting RET protein levels in vitro in a dose-dependent manner.
  • [MeSH-major] Carcinoma, Medullary / drug therapy. Multiple Endocrine Neoplasia Type 2a / genetics. Multiple Endocrine Neoplasia Type 2b / genetics. Mutation. Piperazines / pharmacology. Proto-Oncogene Proteins c-ret / genetics. Pyrimidines / pharmacology. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Humans. Imatinib Mesylate. Phosphorylation


87. Tomoda C, Moatamed F, Naeim F, Hershman JM, Sugawara M: Indomethacin inhibits cell growth of medullary thyroid carcinoma by reducing cell cycle progression into S phase. Exp Biol Med (Maywood); 2008 Nov;233(11):1433-40
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  • [Title] Indomethacin inhibits cell growth of medullary thyroid carcinoma by reducing cell cycle progression into S phase.
  • Indomethacin, a non-steroidal anti-inflammatory drug (NSAID), has been reported to inhibit the growth of medullary thyroid carcinoma (MTC) cells in vitro.
  • However, the mechanism of inhibition of MTC cell growth by indomethacin and its potency have yet to be revealed.
  • We examined the effect of indomethacin on three different MTC cell lines (TT cells, DRO 81-1 cells and HRO 85-1 cells) and two non-MTC cells.
  • The mechanism of indomethacin action in MTC cells was investigated by analyzing intracellular prostaglandin level, apoptosis, and cell cycle in TT cells.
  • Indomethacin inhibited cell growth of all three MTC cell lines but not normal thyroid cells or anaplastic thyroid carcinoma cells.
  • Indomethacin at 10 microM or greater showed a dose response inhibition of cell growth.
  • To examine whether prostaglandin depletion might determine the inhibition of MTC cell growth, we created different prostaglandin E2 (PGE2) levels in TT cells using three different NSAIDs.
  • A profound PGE2 depletion by indomethacin-ester, a potent cyclooxygenase (COX) II inhibitor, showed the least inhibition of cell growth.
  • Indomethacin, but not naproxen or indomethacin-ester, reduced cell cycle progression into S phase; this was unrelated to the degree of PGE2 depletion.
  • In conclusion, indomethacin has specific anti-tumor effect on MTC cells, probably by reducing cell cycle progression into S phase rather than by prostaglandin depletion.
  • Since no drug therapy is currently available for MTC, indomethacin may be one of the therapeutic candidates.
  • [MeSH-major] Carcinoma, Medullary / pathology. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cyclooxygenase Inhibitors / pharmacology. Indomethacin / pharmacology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Calcitonin / genetics. Carcinoembryonic Antigen / genetics. Cell Line. Dinoprostone / metabolism. Gene Expression / drug effects. Humans. Indoles / pharmacology. Phosphorylation. Pyrroles / pharmacology. Retinoblastoma Protein / metabolism. S Phase / drug effects

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  • (PMID = 18791128.001).
  • [ISSN] 1535-3702
  • [Journal-full-title] Experimental biology and medicine (Maywood, N.J.)
  • [ISO-abbreviation] Exp. Biol. Med. (Maywood)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carcinoembryonic Antigen; 0 / Cyclooxygenase Inhibitors; 0 / Indoles; 0 / Pyrroles; 0 / Retinoblastoma Protein; 0 / sunitinib; 9007-12-9 / Calcitonin; K7Q1JQR04M / Dinoprostone; XXE1CET956 / Indomethacin
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88. Karges W, Dralle H, Raue F, Mann K, Reiners C, Grussendorf M, Hüfner M, Niederle B, Brabant G, German Society for Endocrinology (DGE) - Thyroid Section: Calcitonin measurement to detect medullary thyroid carcinoma in nodular goiter: German evidence-based consensus recommendation. Exp Clin Endocrinol Diabetes; 2004 Jan;112(1):52-8
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  • [Title] Calcitonin measurement to detect medullary thyroid carcinoma in nodular goiter: German evidence-based consensus recommendation.
  • Serum calcitonin (CT) has become a very specific and sensitive marker for human medullary thyroid carcinoma (MTC), a neuroendocrine tumor affecting about 1 % of patients with nodular thyroid disease.
  • MTC is characterized by early micrometastasis and a lack of curative non-surgical treatment, so that early diagnosis is desirable.
  • To exclude MTC, serum CT should be determined in patients with nodular thyroid disease, using a two-site CT immunoassay.
  • If basal serum CT exceeds 10 pg/ml, CT should be analysed by pentagastrin stimulation testing, after renal insufficiency and proton pump inhibitor medication have been ruled out.
  • [MeSH-major] Calcitonin / blood. Carcinoma, Medullary / metabolism. Goiter, Nodular / metabolism. Thyroid Neoplasms / metabolism

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  • (PMID = 14758572.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 9007-12-9 / Calcitonin; EF0NX91490 / Pentagastrin
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89. Breeman WA, Fröberg AC, de Blois E, van Gameren A, Melis M, de Jong M, Maina T, Nock BA, Erion JL, Mäcke HR, Krenning EP: Optimised labeling, preclinical and initial clinical aspects of CCK-2 receptor-targeting with 3 radiolabeled peptides. Nucl Med Biol; 2008 Nov;35(8):839-49
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  • Medullary thyroid carcinoma (MTC) expresses CCK-2 receptors. (111)In-labeled DOTA-DGlu-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH(2) (DOTA-MG11), DOTA-DAsp-Tyr-Nle-Gly-Trp-Nle-Asp-Phe-NH(2) (DOTA-CCK), and (99m)Tc-labeled N(4)-Gly-DGlu-(Glu)(5)-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH(2) ((99m)Tc-Demogastrin 2) are analogs developed for CCK-2 receptor-targeted scintigraphy.
  • [MeSH-major] Carcinoma, Medullary / radionuclide imaging. Isotope Labeling. Radioligand Assay. Radiopharmaceuticals / metabolism. Receptor, Cholecystokinin B / metabolism. Thyroid Neoplasms / radionuclide imaging
  • [MeSH-minor] Adolescent. Adult. Aged. Autoradiography. Chromatography, High Pressure Liquid. Drug Stability. Female. Gastrins / metabolism. Humans. Male. Middle Aged

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  • (PMID = 19026945.001).
  • [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 / Gastrins; 0 / Radiopharmaceuticals; 0 / Receptor, Cholecystokinin B; 60748-07-4 / minigastrin
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90. Matuszczyk A, Petersenn S, Voigt W, Kegel T, Dralle H, Schmoll HJ, Bockisch A, Mann K: Chemotherapy with paclitaxel and gemcitabine in progressive medullary and thyroid carcinoma of the follicular epithelium. Horm Metab Res; 2010 Jan;42(1):61-4
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  • [Title] Chemotherapy with paclitaxel and gemcitabine in progressive medullary and thyroid carcinoma of the follicular epithelium.
  • Nine patients (mean age 53) with metastasizing, progressive, medullary (MTC), thyroid carcinoma and progressive, nonradioiodine accumulating thyroid carcinoma of the follicular epithelium (follicular carcinoma, FTC and papillary carcinoma, PTC) were treated with a combination of paclitaxel and gemcitabine between 2004 and 2006.
  • Tumors were histologically classified as follicular in 5 patients (56%), as papillary in 2 patients (22%), and medullary in 2 patients (22%).
  • All patients with papillary, follicular, or medullary thyroid carcinoma had continuous progression during restaging 14.8+/-8.8 weeks after initiation of chemotherapy, including one patient with stable disease after 3 cycles, but continuous progression after 6 cycles of chemotherapy.
  • Paclitaxel and gemcitabine are not a valid chemotherapy option, in particular in patients with progressive, nonradioiodine-accumulating follicular thyroid carcinoma, who were already treated by other chemotherapeutic agents.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Carcinoma, Medullary / drug therapy. Deoxycytidine / analogs & derivatives. Paclitaxel / therapeutic use. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Disease Progression. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Neoplasm Staging

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  • [Copyright] Georg Thieme Verlag KG Stuttgart New York.
  • (PMID = 19735058.001).
  • [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] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; P88XT4IS4D / Paclitaxel
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91. Eng C: Mendelian genetics of rare--and not so rare--cancers. Ann N Y Acad Sci; 2010 Dec;1214:70-82
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  • Identification and characterization of germline mutations in the RET proto-oncogene, encoding a receptor tyrosine kinase, as causing >90% of multiple endocrine neoplasia type 2 (MEN 2), an autosomal dominant disorder characterized by medullary thyroid cancer, pheochromocytoma, and hyperparathyroidism, heralded the era of evidence-based molecular diagnosis, predictive testing, genetic counseling, gene-informed cancer risk assessment, and preventative medicine.
  • Since then, many syndromic endocrine neoplasias have proven to fall under this clinically utile and actionable model, such as those caused by mutations in RET, VHL, or SDHB-D.
  • The familial risk associated with epithelial (nonmedullary) thyroid carcinoma is among the highest of all solid tumors, yet only a few highly penetrant heritable epithelial thyroid cancer syndrome exist.
  • [MeSH-major] Germ-Line Mutation. Neoplastic Syndromes, Hereditary / genetics. Proto-Oncogene Proteins / genetics

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  • [Copyright] © 2010 New York Academy of Sciences.
  • (PMID = 20946573.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins
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92. Schlumberger M, Carlomagno F, Baudin E, Bidart JM, Santoro M: New therapeutic approaches to treat medullary thyroid carcinoma. Nat Clin Pract Endocrinol Metab; 2008 Jan;4(1):22-32
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  • [Title] New therapeutic approaches to treat medullary thyroid carcinoma.
  • Medullary thyroid carcinoma (MTC) accounts for up to 8% of all thyroid cancers.
  • Although primary surgery is curative in the vast majority of patients treated at an early stage, disease can persist or recur with deleterious effects on quality of life.
  • No comprehensive clinical trial data are available on conventional cytotoxic agents for the treatment of MTC.
  • Patients with distant metastases, in particular, might benefit from several novel compounds directed against angiogenesis and molecular targets in tumor cells, such as products of the proto-oncogene RET and mutants of it, and other signaling components.
  • [MeSH-major] Carcinoma, Medullary / therapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Combined Modality Therapy / trends. Humans. Thyroidectomy


93. He X, Wei Q, Zhang X, Xiao J, Jin X, Zhu Y, Cui B, Ning G: Immunohistochemical expression of CXCR4 in thyroid carcinomas and thyroid benign lesions. Pathol Res Pract; 2010 Oct 15;206(10):712-5
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  • [Title] Immunohistochemical expression of CXCR4 in thyroid carcinomas and thyroid benign lesions.
  • In different tumor entities, expression of the chemokine receptor 4 (CXCR4) has been linked to tumor dissemination and poor prognosis.
  • The aim of this study was to examine the immunohistochemical expression of CXCR4 in thyroid carcinomas and thyroid benign lesions.
  • Using monoclonal anti-CXCR4 antibody, we performed immunohistochemical staining on tissue sections from 134 cases obtained from Ruijin Hospital affiliated with Shanghai Jiaotong University School of Medicine (Shanghai, China) between 2000 and 2007.
  • In our study, the CXCR4 expression of the thyroid carcinoma group (including 16 papillary thyroid carcinomas, 18 follicular thyroid carcinomas, 9 poorly differentiated thyroid carcinomas, and 7 medullary thyroid carcinomas) was found to be higher than in the benign lesion group (including 19 cases of Hashimoto's thyroiditis, 15 nodular goiters, and 50 follicular adenomas) (p<0.0001).
  • Within the carcinoma group, the more malignant thyroid carcinoma group (including 9 poorly differentiated thyroid carcinomas and 7 medullary thyroid carcinomas) showed a higher ratio of CXCR4 positivity compared to the less malignant thyroid carcinoma group (including 16 papillary thyroid carcinomas and 18 follicular thyroid carcinomas) (p<0.0001).
  • Our study suggests that CXCR4 expression might be a frequent and cancer-specific event in thyroid carcinoma, and it might be involved in malignancy transformation during the progression of thyroid carcinoma.
  • [MeSH-major] Biomarkers, Tumor / analysis. Immunohistochemistry. Receptors, CXCR4 / analysis. Thyroid Diseases / immunology
  • [MeSH-minor] Adenocarcinoma, Follicular. Adolescent. Adult. Aged. Carcinoma. Carcinoma, Neuroendocrine. Cell Differentiation. Child. Female. Goiter, Nodular / immunology. Hashimoto Disease / immunology. Humans. Male. Middle Aged. Neoplasm Invasiveness. Thyroid Neoplasms / immunology. Thyroid Neoplasms / pathology. Young Adult

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  • [Copyright] Copyright © 2010 Elsevier GmbH. All rights reserved.
  • (PMID = 20646838.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CXCR4 protein, human; 0 / Receptors, CXCR4; Thyroid cancer, medullary; Thyroid cancer, papillary
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94. Gilliam LK, Kohn AD, Lalani T, Swanson PE, Vasko V, Patel A, Livingston RB, Pickett CA: Capecitabine therapy for refractory metastatic thyroid carcinoma: a case series. Thyroid; 2006 Aug;16(8):801-10
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  • [Title] Capecitabine therapy for refractory metastatic thyroid carcinoma: a case series.
  • OBJECTIVE: There are few effective therapies for metastatic medullary (MTC) or radioiodine-resistant follicular thyroid carcinomas (FTC).
  • DESIGN: We retrospectively analyzed five cases of metastatic thyroid carcinoma, three MTCs and two radioiodine-resistant FTCs, treated with capecitabine alone or in combination with other chemotherapeutics.
  • Patients were selected for treatment based on low tumor TS immunohistochemical staining (< or =5%).
  • Therapeutic response was assessed by imaging studies and serum tumor markers: calcitonin and carcinoembryonic antigen (MTC), and thyroglobulin (FTC).
  • MAIN OUTCOME: Two of three patients with MTC had stable disease or disease regression on capecitabine.
  • Both patients with FTC initially had stable disease on capecitabine.
  • One patient, who was treated with capecitabine in combination first with doxorubicin and then etoposide, had an initial decrease in tumor burden, followed by stable disease for 2.8 years.
  • The second patient had stable disease, but capecitabine was discontinued after 11 months because of hand/foot syndrome.
  • CONCLUSIONS: This series demonstrates promising results for the use of capecitabine in treatment of MTC and radioiodine-resistant FTC, for which there is a limited repertoire of therapeutic agents.
  • [MeSH-major] Deoxycytidine / analogs & derivatives. Fluorouracil / analogs & derivatives. Iodine Radioisotopes / pharmacology. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Adult. Antimetabolites, Antineoplastic / pharmacology. Capecitabine. Carcinoembryonic Antigen / metabolism. Dihydrouracil Dehydrogenase (NADP) / metabolism. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Retrospective Studies. Thymidine Phosphorylase / metabolism. Thyroglobulin / metabolism

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  • (PMID = 16910885.001).
  • [ISSN] 1557-9077
  • [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
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Carcinoembryonic Antigen; 0 / Iodine Radioisotopes; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; 9010-34-8 / Thyroglobulin; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); EC 2.4.2.4 / Thymidine Phosphorylase; U3P01618RT / Fluorouracil
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95. Santarpia L, Ye L, Gagel RF: Beyond RET: potential therapeutic approaches for advanced and metastatic medullary thyroid carcinoma. J Intern Med; 2009 Jul;266(1):99-113
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  • [Title] Beyond RET: potential therapeutic approaches for advanced and metastatic medullary thyroid carcinoma.
  • Medullary thyroid carcinoma (MTC) is a rare calcitonin-producing neuroendocrine tumour that originates from the parafollicular C-cells of the thyroid gland.
  • The RET proto-oncogene encodes the RET receptor tyrosine kinase, which has essential roles in cell survival, differentiation and proliferation.
  • Activating mutations of RET are associated with the pathogenesis of MTC and have been demonstrated in nearly all hereditary and in 30-50% of sporadic MTC cases, making this receptor an excellent target for small-molecule inhibitors for this tumour.
  • Clinical trials of small organic inhibitors of tyrosine kinase receptors (TKIs) targeting the RET receptor have shown efficacy for treatment of metastatic MTC with 30-50% of patients responding to these agents.
  • Despite the importance of the RET receptor in MTC, it is clear that other signal transduction pathways, tyrosine kinase receptors, and tumour suppressor genes are involved in MTC tumourigenesis and progression.
  • Finally, there is evidence that immunological-based therapy using dendritic cell vaccination strategies have been effective for reducing tumour mass in a small number of patients.
  • The identification of additional MTC-specific tumour antigens and a better understanding of specific epitopes in these tumour antigens may lead to improvement of response rates.
  • [MeSH-major] Carcinoma, Medullary / therapy. Proto-Oncogene Proteins c-ret / physiology. Thyroid Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Cell Transformation, Neoplastic. Humans. Protein Kinase Inhibitors / pharmacology. Signal Transduction

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  • (PMID = 19522829.001).
  • [ISSN] 1365-2796
  • [Journal-full-title] Journal of internal medicine
  • [ISO-abbreviation] J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret
  • [Number-of-references] 109
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96. Stein R, Goldenberg DM: A humanized monoclonal antibody to carcinoembryonic antigen, labetuzumab, inhibits tumor growth and sensitizes human medullary thyroid cancer xenografts to dacarbazine chemotherapy. Mol Cancer Ther; 2004 Dec;3(12):1559-64
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  • [Title] A humanized monoclonal antibody to carcinoembryonic antigen, labetuzumab, inhibits tumor growth and sensitizes human medullary thyroid cancer xenografts to dacarbazine chemotherapy.
  • A variety of observations have shown that carcinoembryonic antigen (CEA) is associated with growth and metastasis of cancers, including correlation of CEA serum levels with poor clinical outcome, mediation of cell-cell adhesion by CEA, and involvement of CEA in the immune recognition of tumors and apoptotic pathways.
  • The purpose of this study was to investigate the effect that an anti-CEA monoclonal antibody (MAb) may have on the growth of medullary thyroid cancer (MTC), a CEA-expressing tumor, alone and in combination with chemotherapy.
  • Using the TT MTC cell line grown s.c., we compared tumor growth in untreated mice with that of mice given the humanized anti-CEA MAb labetuzumab or an isotype-matched control MAb.
  • The effects of time of administration post-tumor injection, MAb dose response, specificity of response, and combination with dacarbazine (DTIC) chemotherapy were studied.
  • The humanized anti-CEA MAb, labetuzumab, has direct, specific, antitumor effects in this model, without conjugation to a cytotoxic agent.
  • In addition, labetuzumab sensitizes these tumor cells to chemotherapy with an effective drug in this model, DTIC, without increased toxicity.
  • Significant delays in tumor growth were caused by the MAb therapy or chemotherapy alone; however, the combination of these agents was significantly more effective than either agent given as a monotherapy or use of an irrelevant MAb in this model.
  • The superiority of the combined modality treatment argues for the integration of CEA MAb therapy into chemotherapeutic regimens for MTC management and possibly other CEA-expressing neoplasms.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents, Alkylating / therapeutic use. Carcinoembryonic Antigen / immunology. Carcinoma, Medullary / drug therapy. Dacarbazine / therapeutic use. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Mice. Mice, Nude. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 15634649.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents, Alkylating; 0 / Carcinoembryonic Antigen; 7GR28W0FJI / Dacarbazine
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97. Schmidt M, Eschner W, Dietlein M, Theissen P, Schicha H: [Established nuclear medicine techniques for tumour diagnosis (tumour SPECT): can they still compete with (18)F-FDG-PET?]. Nuklearmedizin; 2005 Feb;44(1):37-48; quiz N2-3
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  • [Title] [Established nuclear medicine techniques for tumour diagnosis (tumour SPECT): can they still compete with (18)F-FDG-PET?].
  • [Transliterated title] Konventionelle nuklearmedizinische Tumordiagnostik (Tumor-SPECT): Was ist angesichts von (18)F-FDG-PET noch aktuell?
  • This overview presents the indications of tumour SPECT in contrast to tumour PET using (18)F-FDG.
  • A number of diagnostic SPECT radiopharmaceuticals have been used for years in oncology and are widely available in nuclear medicine departments.
  • Today, tumour SPECT has to compete with tumour PET using (18)F-FDG.
  • Therefore, PET is better than SPECT in localising a tumour, if the special tumour entity accumulates (18)F-FDG.
  • SPECT radiopharmaceuticals are still up to date for examination of tumour entities which do not accumulate (18)F-FDG (e. g. neuroendocrine tumours) and in clinical problem solving if (18)F-FDG-PET is not regarded as superior (e. g. search for recurrent medullary thyroid carcinoma) or in the management of tumours with overlapping diagnosis and therapy as it is the case for differentiated thyroid carcinomas ((123)I/(131)I-NaI), phaeochromozytomas, and neuroblastomas ((123)I/(131)I-MIBG), carcinoids, gastroenteropancreatic tumours, paragangliomas, and Merkel-cell tumours (somatostatin receptor scintigraphy).
  • [MeSH-major] Fluorodeoxyglucose F18. Neoplasms / radionuclide imaging. Nuclear Medicine / methods. Positron-Emission Tomography / methods. Tomography, Emission-Computed, Single-Photon / methods

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  • (PMID = 15711728.001).
  • [ISSN] 0029-5566
  • [Journal-full-title] Nuklearmedizin. Nuclear medicine
  • [ISO-abbreviation] Nuklearmedizin
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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98. American Thyroid Association Guidelines Task Force, Kloos RT, Eng C, Evans DB, Francis GL, Gagel RF, Gharib H, Moley JF, Pacini F, Ringel MD, Schlumberger M, Wells SA Jr: Medullary thyroid cancer: management guidelines of the American Thyroid Association. Thyroid; 2009 Jun;19(6):565-612
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  • [Title] Medullary thyroid cancer: management guidelines of the American Thyroid Association.
  • BACKGROUND: Inherited and sporadic medullary thyroid cancer (MTC) is an uncommon and challenging malignancy.
  • The American Thyroid association (ATA) chose to create specific MTC Clinical Guidelines that would bring together and update the diverse MTC literature and combine it with evidence-based medicine and the knowledge and experience of a panel of expert clinicians.
  • RESULTS: Clinical topics addressed in this scholarly dialog included: initial diagnosis and therapy of preclinical disease (including RET oncogene testing and the timing of prophylactic thyroidectomy), initial diagnosis and therapy of clinically apparent disease (including preoperative testing and imaging, extent of surgery, and handling of devascularized parathyroid glands), initial evaluation and treatment of postoperative patients (including the role of completion thyroidectomy), management of persistent or recurrent MTC (including the role of tumor marker doubling times, and treatment of patients with distant metastases and hormonally active metastases), long-term follow-up and management (including the frequency of follow-up and imaging), and directions for future research.
  • [MeSH-major] Carcinoma, Medullary / therapy. Thyroid Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Humans. Terminology as Topic


99. de Groot JW, Links TP, Plukker JT, Lips CJ, Hofstra RM: RET as a diagnostic and therapeutic target in sporadic and hereditary endocrine tumors. Endocr Rev; 2006 Aug;27(5):535-60
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  • [Title] RET as a diagnostic and therapeutic target in sporadic and hereditary endocrine tumors.
  • The RET gene encodes a receptor tyrosine kinase that is expressed in neural crest-derived cell lineages.
  • The RET receptor plays a crucial role in regulating cell proliferation, migration, differentiation, and survival through embryogenesis.
  • Germline point mutations are found in the cancer syndromes multiple endocrine neoplasia (MEN) type 2, including MEN 2A and 2B, and familial medullary thyroid carcinoma.
  • The identification of mutations associated with these syndromes has led to genetic testing to identify patients at risk for MEN 2 and familial medullary thyroid carcinoma and subsequent implementation of prophylactic thyroidectomy in mutation carriers.
  • In addition, more than 10 somatic rearrangements of RET have been identified from papillary thyroid carcinomas.
  • Recently, various kinds of therapeutic approaches, such as tyrosine kinase inhibition, gene therapy with dominant negative RET mutants, monoclonal antibodies against oncogene products, and nuclease-resistant aptamers that recognize and inhibit RET have been developed.
  • [MeSH-major] Endocrine Gland Neoplasms / diagnosis. Endocrine Gland Neoplasms / genetics. Endocrine Gland Neoplasms / therapy. Proto-Oncogene Proteins c-ret / genetics
  • [MeSH-minor] Animals. Fetal Development / genetics. Gene Targeting. Genetic Therapy. Haplotypes. Humans. Ligands. Models, Biological. Multiple Endocrine Neoplasia Type 2a / diagnosis. Multiple Endocrine Neoplasia Type 2a / genetics. Multiple Endocrine Neoplasia Type 2a / therapy. Polymorphism, Genetic. Signal Transduction / drug effects

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  • (PMID = 16849421.001).
  • [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 / Ligands; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human
  • [Number-of-references] 305
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100. Harris PE: The management of thyroid cancer in adults: a review of new guidelines. Clin Med (Lond); 2002 Mar-Apr;2(2):144-6
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  • The central tenet of the guidelines is that thyroid cancer is a disease which requires specialist care from a multidisciplinary team, including an endocrinologist, nuclear medicine physician, thyroid surgeon and endocrine pathologist.
  • The guidelines are comprehensive and detailed, covering differentiated (papillary and follicular) and medullary cancer of the thyroid.
  • [MeSH-major] Carcinoma, Medullary / therapy. Carcinoma, Papillary, Follicular / therapy. Thyroid Neoplasms / therapy

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  • (PMID = 11991098.001).
  • [ISSN] 1470-2118
  • [Journal-full-title] Clinical medicine (London, England)
  • [ISO-abbreviation] Clin Med (Lond)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 7
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