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[Title] Notch1 mediates growth suppression of papillary and follicular thyroid cancer cells by histone deacetylase inhibitors.

Here, we showed that although there was minimal Notch1 expression in follicular thyroid cancer FTC236 and papillary thyroid cancer DRO cells, transfection of constitutive Notch1 plasmid into these cells led to growth inhibition, down-regulation of cyclin D1, and up-regulation of p21.

Treatment of FTC236 cells with HDAC inhibitors valproic acid (1-4 mmol/L) or suberoyl bishydroxamic acid (10-30 micromol/L) induced functional Notch1 protein expression and suppressed cell growth in a dose-dependent manner.

These results indicate that HDAC inhibitors activate Notch1 signaling in thyroid cancer cells and lead to the suppression of proliferation by cell cycle arrest.

Our findings provide the first documentation of the role of Notch1 signaling as a tumor suppressor in DRO and FTC236 cells, suggesting that Notch1 activation may be a potential therapeutic target for papillary and follicular thyroid cancers.

[MeSH-major] Adenocarcinoma, Follicular / pathology. Carcinoma, Papillary / pathology. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Receptor, Notch1 / metabolism. Thyroid Neoplasms / pathology

[MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Proliferation / drug effects. Humans. Hydroxamic Acids / pharmacology. Plasmids / genetics. Transfection. Valproic Acid / pharmacology

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(PMID = 19190121.001).

[ISSN] 1535-7163

[Journal-full-title] Molecular cancer therapeutics

[ISO-abbreviation] Mol. Cancer Ther.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA117117; United States / NCI NIH HHS / CA / R21 CA117117-01A2; United States / NCI NIH HHS / CA / R01 CA109053; United States / NCI NIH HHS / CA / CA109053; United States / NIGMS NIH HHS / GM / R01 GM099705; United States / NCI NIH HHS / CA / R01 CA109053-01A2; United States / NCI NIH HHS / CA / R21 CA117117

[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 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Receptor, Notch1; 0 / suberoyl bis-hydroxamic acid; 614OI1Z5WI / Valproic Acid

[Other-IDs] NLM/ NIHMS92706; NLM/ PMC2673961

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Antisense p53 oligonucleotides inhibit proliferation and induce chemosensitivity in follicular thyroid cancer cells.

BACKGROUND: The potential of MTp53 knockout by oligodesoxyribonucleotide phosphothioates (ODNs) to affect proliferation, apoptosis and chemosensitivity in undifferentiated thyroid cancer (UTC) cells with a recessive MTp53 mutation was evaluated.

MATERIALS AND METHODS: Transient transfections with ODNs complementary to p53 and control ODN (HIV-RT) were carried out in FTC 133 cells.

In vitro proliferation was evaluated by cell counting of 10 random fields and by the MTT assay.

A single pulse of 100 microg/ml Cytarabine was added to each well and the cells were incubated for an additional day.

RESULTS: Transfection of UTC cells with ODN decreased the cell number by up to 70% (p < 0.002).

ODNs rendered FTC cells sensitive to treatment with Cytarabine, inducing apoptosis in 35% of cells, as compared to 17% of cells transfected with the reverse transcriptase gene of HIV (ODN-HIV) and less than 10% of non-transfected cells (p < 0.05).

CONCLUSION: Transient MTp53 knockout with ODNs complementary to p53 nucleotide sequences inhibited proliferation and increased chemosensitivity in the UTC cell line FTC133.

[MeSH-major] Adenocarcinoma, Follicular / genetics. Adenocarcinoma, Follicular / therapy. Genes, p53. Oligonucleotides, Antisense / genetics. Thyroid Neoplasms / genetics. Thyroid Neoplasms / therapy

[MeSH-minor] Apoptosis / genetics. Cell Growth Processes / genetics. Cell Line, Tumor. Combined Modality Therapy. Cytarabine / pharmacology. Humans. Point Mutation. Transfection

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(PMID = 16619520.001).

[ISSN] 0250-7005

[Journal-full-title] Anticancer research

[ISO-abbreviation] Anticancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

[Chemical-registry-number] 0 / Oligonucleotides, Antisense; 04079A1RDZ / Cytarabine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The effects of growth inhibitory peptide on follicular thyroid cancer cell growth, migration, and invasion.

AIMS AND BACKGROUND: Thyroid cancer is the most common endocrine neoplasm worldwide.

Although differentiated thyroid cancers are associated with a favorable survival, the prognosis worsens dramatically for patients with distant metastasis.

Metastases from follicular thyroid carcinoma (FTC) occur earlier and are more aggressive than those from papillary thyroid carcinoma.

For FTC that is resistant to radioactive iodine, new treatments are urgently needed.

However, the effects of GIP in FTC have not yet been studied.

The aim of this study was to investigate the antitumor ability of GIP in FTC.

METHODS AND STUDY DESIGN: Using both PBS and GIP control peptide as a negative control, the antiproliferative activity of GIP in the WRO human FTC cell line was determined using a tetrazolium-based colorimetric assay.

In addition, cell migration and invasion assays were used to measure tumor metastasis inhibition effects in vitro.

RESULTS: GIP did not inhibit WRO cell proliferation in a time- or dose-dependent manner.

Cell invasion was also significantly inhibited at 50 and 100 microM (67.1% and 39.0%, respectively; both P<0.05).

CONCLUSIONS: Although GIP failed to suppress FTC cell growth, it effectively interrupted both FTC cell migration and invasion abilities in vitro.

GIP may potentially serve as an anti-FTC metastasis agent aiding current chemotherapy regimens.

[MeSH-major] Adenocarcinoma, Follicular / drug therapy. Adenocarcinoma, Follicular / pathology. Antineoplastic Agents / pharmacology. Membrane Proteins / pharmacology. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / pathology

[MeSH-minor] Cell Movement / drug effects. Cell Survival / drug effects. Humans. Neoplasm Invasiveness. Tumor Cells, Cultured

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(PMID = 20845807.001).

[ISSN] 0300-8916

[Journal-full-title] Tumori

[ISO-abbreviation] Tumori

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Membrane Proteins; 0 / growth inhibitory proteins

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] FTC Versus Congress: The Biosimilars Debate.

The authors argue that the FTC's conclusion -that patent protection alone will fuel biotech R&D after passage of follow-on legislation - is shaky.

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(PMID = 22478787.001).

[ISSN] 1554-169X

[Journal-full-title] Biotechnology healthcare

[ISO-abbreviation] Biotechnol Healthc

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Other-IDs] NLM/ PMC2799095

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Evaluation of the PAX8/PPARG translocation in follicular thyroid cancer with a 4-color reverse-transcription PCR assay and automated high-resolution fragment analysis.

BACKGROUND: Molecular testing of thyroid malignancies, in combination with cytologic and histologic examination, is becoming increasingly attractive as a tool for refining traditional morphologic diagnosis.

The molecular changes associated with follicular thyroid carcinoma (FTC) are point mutations in RAS oncogenes or the presence of PAX8/PPARG (paired box 8/peroxisome proliferator-activated receptor gamma) rearrangement.

METHODS: We developed and validated a clinical assay for the detection of PAX8/PPARG rearrangements that uses a 4-color reverse-transcription PCR (RT-PCR) assay and high-resolution fragment analysis.

RESULTS: The RT-PCR assay is applicable for detecting the various described fusion transcripts of PAX8/PPARG in formalin-fixed, paraffin-embedded thyroid tissue and in fine-needle aspirate biopsy washes from thyroid nodules.

The analytical sensitivity of the assay is 1 abnormal cell in a background of 100-10 000 translocation-negative cells.

A comparison of the RT-PCR assay with dual-fusion fluorescence in situ hybridization showed an overall concordance of 95%.

With this assay, we obtained a prevalence for the PAX8/PPARG rearrangement in FTC of 62% (13 of 21 cases), compared with a 5% prevalence (3 of 55) for other follicular cell-derived neoplasms.

CONCLUSIONS: The introduction of this assay into clinical practice could provide useful information for the diagnosis and possibly for the prognosis and treatment of thyroid cancer in the future.

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[Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3286-94 [18593772.001]

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(PMID = 20056739.001).

[ISSN] 1530-8561

[Journal-full-title] Clinical chemistry

[ISO-abbreviation] Clin. Chem.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA080117; United States / NCI NIH HHS / CA / CA80117

[Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / PAX8 protein, human; 0 / PPAR gamma; 0 / Paired Box Transcription Factors

[Other-IDs] NLM/ NIHMS547600; NLM/ PMC3918957

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pathologic Fracture of the Femur as a Presenting Sign of Metastatic Follicular Carcinoma of the Thyroid.

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(PMID = 28958235.001).

[ISSN] 1555-9823

[Journal-full-title] The American surgeon

[ISO-abbreviation] Am Surg

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Gene-specific promoter hypermethylation without global hypomethylation in follicular thyroid cancer.

Genome-wide hypomethylation and hypermethylation at CpG promoters are common in cancer.

To date, little is known about global methylation changes in follicular thyroid cancer (FTC).

Two independent quantitative methods, bisulphite Pyrosequencing of Long Interspersed Nucleotide Elements-1 (LINE-1) and LUminometric Methylation Assay (LUMA) were used to quantify genome-wide methylation in 21 FTC and corresponding normal thyroid tissues.

Unexpectedly global methylation was not found significantly altered in tumors compared to normal thyroid by either LINE-1 (p=0.57) or LUMA (p=0.42), whilst the promoter of a tumor suppressor that is often epigenetically dysregulated, RASSF1A was found to be significantly hypermethylated by Pyrosequencing (p=0.0001).

In summary, the epigenetic inactivation of RASSF1A is a frequent event in FTC, but is not coupled to changes in global methylation.

[MeSH-major] Adenocarcinoma, Follicular / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic. Promoter Regions, Genetic. Thyroid Neoplasms / genetics

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(PMID = 18813801.001).

[ISSN] 1019-6439

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Greece

[Chemical-registry-number] 0 / RASSF1 protein, human; 0 / Tumor Suppressor Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Follow-up of papillary and follicular thyroid cancer--when and where?].

While papillary and follicular thyroid cancer usually has an excellent prognosis, recurrent and aggressive forms of the disease do occur.

Based on investigational results, the patients are divided into three groups: the cancer does not exist, may exist or remains.

In cancer-free patients, thyroxine therapy will be implemented as in ordinary hypothyreoidism.

[MeSH-major] Carcinoma, Papillary / radiotherapy. Carcinoma, Papillary / surgery. Iodine Radioisotopes / therapeutic use

[MeSH-minor] Ablation Techniques. Adenocarcinoma, Follicular. Combined Modality Therapy. Disease-Free Survival. Hormone Replacement Therapy. Humans. Thyroid Neoplasms / radiotherapy. Thyroid Neoplasms / surgery. Thyroxine / therapeutic use

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(PMID = 21125756.001).

[ISSN] 0012-7183

[Journal-full-title] Duodecim; lääketieteellinen aikakauskirja

[ISO-abbreviation] Duodecim

[Language] fin

[Publication-type] English Abstract; Journal Article

[Publication-country] Finland

[Chemical-registry-number] 0 / Iodine Radioisotopes; Q51BO43MG4 / Thyroxine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Operative strategy for follicular thyroid cancer in risk groups stratified by pTNM staging.

This study determined cancer survival rates and follow-up status at different pTNM stages to stratify risk groups in follicular thyroid carcinoma.

Two hundred and fourteen follicular thyroid cancer patients (167 females, 47 males) who underwent surgery and followed-up treatment at a single medical center were enrolled in this retrospective study.

Low risk for follicular thyroid cancer was defined as pT1N0M0. (Moderate-risk group) was defined as all other patients in pTNM stage I, and high risk as patients in stages II-IV.

After mean follow-up of 9.6+/-0.3 years, 1.6% (2/120), 21.9% (7/32), 5.6% (1/18) and 52.3% (23/44) of patients in pTNM stages I-IV, respectively, died of thyroid cancer.

Of 214 follicular thyroid cancer patients, 35 (16.4%), 85 (39.7%) and 94 (43.9%) were defined as low-, moderate- and high-risk groups at the time of surgery.

None of the low-risk patients died, and all achieved disease-free status.

In the moderate- and high-risk groups, 2.4% (2/85) and 27.7% (26/94) died of thyroid cancer.

The moderate- and high-risk groups underwent near-total thyroidectomy and (131)I therapies, and 15 of 107 (14.9%) died of thyroid cancer while 18 (16.8%) had persistent disease at the end of the study period.

In conclusion, the low-risk follicular thyroid cancer group as defined by pTNM staging had excellent prognosis.

Over one-fourth of the follicular thyroid cancer patients in the high-risk group died of thyroid cancer despite aggressive treatment.

[MeSH-major] Adenocarcinoma, Follicular / pathology. Adenocarcinoma, Follicular / therapy. Thyroid Neoplasms / pathology. Thyroid Neoplasms / therapy

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Disease-Free Survival. Female. Follow-Up Studies. Humans. Iodine Radioisotopes / therapeutic use. Male. Middle Aged. Neoplasm Staging. Radiotherapy, Adjuvant. Regression Analysis. Retrospective Studies. Risk Assessment. Thyroglobulin / blood. Thyroidectomy

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(PMID = 17600699.001).

[ISSN] 0960-7404

[Journal-full-title] Surgical oncology

[ISO-abbreviation] Surg Oncol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Iodine Radioisotopes; 9010-34-8 / Thyroglobulin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] I-131 accumulation in a benign cystic mesothelioma in a patient with follicular thyroid cancer.

Focal I-131 accumulation is generally a reliable indicator of functioning normal thyroid tissue or a differentiated thyroid cancer metastasis.

We report a case of focal I-131 accumulation in a benign cystic mesothelioma in a patient with follicular thyroid cancer.

[MeSH-major] Adenocarcinoma, Follicular / radionuclide imaging. Iodine Radioisotopes. Mesothelioma, Cystic / radionuclide imaging. Peritoneal Neoplasms / radionuclide imaging. Thyroid Nodule / radionuclide imaging. Tomography, Emission-Computed, Single-Photon / adverse effects

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(PMID = 18298317.001).

[ISSN] 1050-7256

[Journal-full-title] Thyroid : official journal of the American Thyroid Association

[ISO-abbreviation] Thyroid

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Iodine Radioisotopes

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Lymph node dissection in papillary and follicular thyroid cancer].

BACKGROUND: There is still unresolved debate about the optimal surgical management of papillary (PTC) and follicular (FTC) thyroid cancer regarding lymph node dissection.

PATIENTS AND METHODS: This study is based on 626 patients with PTC and 191 with FTC from a group of 1062 own patients with thyroid malignancies.

RESULTS: Tumors < or = 20 mm in size were found significantly more often in PTC than FTC (69.6% vs 28.3%, P<0.05).

Positive lymph nodes were found significantly more often in PTC than FTC as well (33.2% vs 5.2%, P<0.05).

In FTC positive lymph nodes occurred only in tumors >25 mm.

CONCLUSION: Due to prevalence and importance of lymph node metastasis differing between PTC and FTC, we recommend treating both tumor entities differently.

In small FTC it seems adequate to limit the operation to thyroidectomy without prophylactic lymph dissection.

[MeSH-major] Adenocarcinoma, Follicular / surgery. Carcinoma, Papillary / surgery. Lymph Node Excision / methods. Thyroid Neoplasms / surgery. Thyroidectomy / methods

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(PMID = 18317715.001).

[ISSN] 0009-4722

[Journal-full-title] Der Chirurg; Zeitschrift fur alle Gebiete der operativen Medizen

[ISO-abbreviation] Chirurg

[Language] ger

[Publication-type] English Abstract; Journal Article

[Publication-country] Germany

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Antisense p53 decreases production of VEGF in follicular thyroid cancer cells.

Inactivating mutations of wild-type p53 (WTp53) tumor suppressor gene are common in anaplastic thyroid cancer (ATC) and are associated with poor prognosis.

Therefore, the potential of MTp53 knockout by oligodeoxyribonucleotide phosphorothioates (ODNs) to affect VEGF production of undifferentiated thyroid cancer cells with a recessive MTp53 mutation was evaluated.

Transient transfection with 20 bp ODNs complementary to portions of exon 10 of p53 and a negative control ODN (HIV-RT) were carried out in FTC-133 cells.

In vitro secretion of VEGF protein was quantified by EIA and correlated to cell numbers, which was evaluated by in vitro MTT assay.

Transfection of undifferentiated thyroid cancer cells with ODN reduced VEGF secretion of FTC-133 cells following transfection by 34% as compared to the negative control (cells transfected with ODN-HIV; p = 0.03).

These results suggest that transient MTp53 knockout with ODNs complementary to p53 nucleotide sequences impair secretion of VEGF in the undifferentiated thyroid cancer cell line FTC-133.

[MeSH-major] Adenocarcinoma, Follicular / metabolism. Gene Silencing / physiology. Thyroid Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism. Vascular Endothelial Growth Factor A / biosynthesis

[MeSH-minor] Cell Survival. Humans. Oligodeoxyribonucleotides, Antisense / metabolism. Oligodeoxyribonucleotides, Antisense / pharmacology. Transfection. Tumor Cells, Cultured

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[Cites] J Surg Oncol. 1997 Sep;66(1):11-8 [9290687.001]

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(PMID = 16943578.001).

[ISSN] 1355-008X

[Journal-full-title] Endocrine

[ISO-abbreviation] Endocrine

[Language] eng

[Publication-type] Comparative Study; Evaluation Studies; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Oligodeoxyribonucleotides, Antisense; 0 / Tumor Suppressor Protein p53; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Of the 13 patients evaluable for response, stable disease was seen in 1 patient with follicular thyroid carcinoma and 1 with hepatocellular carcinoma for 51 and 164 days respectively.

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(PMID = 27961888.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Adrenal and renal metastases from follicular thyroid cancer.

Patients with differentiated thyroid cancer may have asymptomatic involvement of renal and/or adrenal gland, particularly if they are elderly and have associated metastases to other organs, which may remain undetected if these patients are not subjected to radioiodine treatment.

[MeSH-major] Adenocarcinoma, Follicular / secondary. Adrenal Gland Neoplasms / secondary. Kidney Neoplasms / secondary. Thyroid Neoplasms / surgery

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(PMID = 16249606.001).

[ISSN] 0007-1285

[Journal-full-title] The British journal of radiology

[ISO-abbreviation] Br J Radiol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Iodine Radioisotopes

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Importance of tumour size in papillary and follicular thyroid cancer.

BACKGROUND: The most controversial change in the new pathological tumour node metastasis (pTNM) classification of thyroid tumours is the extension of the pT1 classification to include tumours up to 20 mm.

METHODS: Four hundred and three patients with pT1 or pT2 differentiated thyroid carcinomas were divided into three groups according to tumour diameter (group 1, 10 mm or less; group 2, 11-20 mm; group 3, 21-40 mm).

They were analysed retrospectively with respect to carcinoma-specific and disease-free survival.

RESULTS: No patient in group 1 died from papillary thyroid carcinoma, compared with three patients in group 2 and six in group 3.

There was a statistically significant difference in carcinoma-specific survival between groups 1 and 2 (P = 0.033).

The difference in disease-free survival between groups 1 and 2 was significant (P = 0.025).

One patient in group 1, three in group 2 and four in group 3 died from follicular thyroid carcinoma, but there were no significant differences in survival between the three groups.

CONCLUSION: Extension of the pT1 classification to cover all tumours up to 20 mm does not appear to be justified for papillary thyroid carcinoma.

[MeSH-major] Carcinoma, Papillary / pathology. Carcinoma, Papillary, Follicular / pathology. Thyroid Neoplasms / pathology

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Follow-Up Studies. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Prognosis. Retrospective Studies. Thyroidectomy / methods. Treatment Outcome

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(PMID = 15685703.001).

[ISSN] 0007-1323

[Journal-full-title] The British journal of surgery

[ISO-abbreviation] Br J Surg

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Increased expression of valosin-containing protein (p97) is correlated with disease recurrence in follicular thyroid cancer.

BACKGROUND: Valosin-containing protein (VCP) is involved in the ubiquitin/proteasome-degradation pathway, which works in proliferation and antiapoptosis in human cancer cells.

Our previous study showed that VCP expression levels correlated with the recurrence and prognosis of several human cancers, such as hepatocellular carcinoma, gastric carcinoma, and colorectal carcinoma.

In this study, the correlation of VCP expression with the prognosis of differentiated thyroid carcinoma was examined.

METHODS: VCP expression in 332 patients who underwent operation for differentiated thyroid carcinoma--257 with papillary thyroid carcinoma and 75 with follicular thyroid carcinoma (FTC)--was analyzed by immunohistochemistry.

However, it correlated with neither any clinicopathologic factor nor prognosis in papillary thyroid carcinoma.

VCP expression correlated with extrathyroidal extension (P < .05), pT classification (P < .05), and lymph node metastasis (P < .01) in FTC.

Patients with low VCP expressing FTC showed better disease-free and overall survival rates than those with intermediate or high expression (P < .01 and P < .05, respectively).

Multivariate analysis revealed VCP expression and extracapsular extension to be independent prognostic factors for disease-free survival in cases of FTC.

CONCLUSIONS: The prognostic utility of VCP expression in FTC was demonstrated.

[MeSH-major] Adenocarcinoma, Follicular / metabolism. Cell Cycle Proteins / metabolism. Thyroid Neoplasms / metabolism

[MeSH-minor] Adenosine Triphosphatases. Adolescent. Adult. Aged. Aged, 80 and over. Carcinoma, Papillary / metabolism. Female. Humans. Immunohistochemistry. Lymphatic Metastasis. Male. Middle Aged. Multivariate Analysis. Prognosis

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(PMID = 16189643.001).

[ISSN] 1068-9265

[Journal-full-title] Annals of surgical oncology

[ISO-abbreviation] Ann. Surg. Oncol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Cell Cycle Proteins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / CDC48 protein

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Renal metastases from follicular thyroid cancer on SPECT/CT.

In well-differentiated thyroid carcinoma, only a subset of patients develop distant metastases, predominantly to the lungs and the skeletal system.

We report the case of a 64-year-old woman with a long history of follicular thyroid cancer who developed renal metastases.

Subsequent surgery and histopathologic analysis of the renal lesions confirmed the diagnosis.

[MeSH-major] Adenocarcinoma, Follicular / diagnosis. Adenocarcinoma, Follicular / secondary. Iodine Radioisotopes. Kidney Neoplasms / diagnosis. Kidney Neoplasms / secondary. Thyroid Neoplasms / diagnosis. Tomography, Emission-Computed, Single-Photon / methods. Tomography, X-Ray Computed / methods

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(PMID = 17710039.001).

[ISSN] 0363-9762

[Journal-full-title] Clinical nuclear medicine

[ISO-abbreviation] Clin Nucl Med

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Radiopharmaceuticals

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular prognostic markers in papillary and follicular thyroid cancer: Current status and future directions.

Gene expression profiling shows that, by gene signature, the difference between BRAF-positive and BRAF-negative PTC is so distinct that BRAF-positive cancer may be regarded as a molecular subtype of papillary thyroid cancer (PTC).

The frequency of BRAF mutation in PTC is high-45% on average, with values over 70-80% in some populations.

We estimate that 31% of all PTC patients and 39% of those diagnosed with stage I-II disease will face the risk of overtreatment if the decision will be based on the BRAF-positivity of their tumors.

Considering this, in the review we summarize the present status of knowledge on other prognosis-related gene expression changes in papillary and follicular cancer and relate them to he tumor's biology.

[MeSH-major] Adenocarcinoma, Follicular / metabolism. Carcinoma, Papillary / metabolism. Thyroid Neoplasms / metabolism

[MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Genetic Predisposition to Disease. Humans. Mutation. Prognosis. Proto-Oncogene Proteins B-raf / genetics. Proto-Oncogene Proteins B-raf / metabolism. ras Proteins / genetics. ras Proteins / metabolism

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[Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.

(PMID = 20138116.001).

[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; Review

[Publication-country] Ireland

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins

[Number-of-references] 259

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Comparison of seven serum thyroglobulin assays in the follow-up of papillary and follicular thyroid cancer patients.

BACKGROUND: Serum thyroglobulin (Tg) is the marker of differentiated thyroid cancer after initial treatment and TSH stimulation increases its sensitivity for the diagnosis of recurrent disease.

AIM: The goal of the study is to compare the diagnostic values of seven methods for serum Tg measurement for detecting recurrent disease both during L-T4 treatment and after TSH stimulation.

METHODS: Thyroid cancer patients who had no evidence of persistent disease after initial treatment (total thyroidectomy and radioiodine ablation) were studied at 3 months on L-T4 treatment (Tg1) and then at 9-12 months after withdrawal or recombinant human TSH stimulation (Tg2).

Using the two methods with a lowest functional sensitivity at 0.02 and 0.11 ng/ml resulted in a higher sensitivity for Tg1 (81% and 78%), but at the expense of a loss of specificity (42% and 63%); finally, for these two methods, using an optimized functional sensitivity according to receiver operating characteristic curves at 0.22 and 0.27 ng/ml resulted in a sensitivity at 65% and specificity at 85-87% for Tg1.

[MeSH-major] Carcinoma, Papillary, Follicular / blood. Carcinoma, Papillary, Follicular / radionuclide imaging. Chemistry, Clinical / methods. Thyroglobulin / analysis. Thyroglobulin / blood. Thyroid Neoplasms / blood. Thyroid Neoplasms / radionuclide imaging

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[CommentIn] Nat Clin Pract Endocrinol Metab. 2007 Nov;3(11):738-9 [17700550.001]

(PMID = 17426102.001).

[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; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers; 0 / Iodine Radioisotopes; 9010-34-8 / Thyroglobulin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Estradiol-induced proliferation of papillary and follicular thyroid cancer cells is mediated by estrogen receptors alpha and beta.

Premenopausal women are at highest risk for papillary and follicular thyroid carcinoma, implicating a role for estrogens in thyroid cancer.

The expression of estrogen receptors alpha and beta (ER), the effects of estradiol (E2), selective estrogen receptor modulators (SERMs) 4-hydroxytamoxifen and raloxifene, and ER subtype selective agonists were examined in NPA87 and KAT5 papillary and WRO follicular thyroid carcinoma cell lines.

All three thyroid cancer cell lines expressed full-length ERalpha and ERbeta proteins with cytoplasmic localization that was unaffected by E2.

ICI 182,780 (Fulvestrant, an ER antagonist), and inhibitors of non-genomic E2-activated MAPK and PI3K signaling blocked E2-induced cell proliferation.

SERMs acted in a cell line-specific manner.

No E2-induced estrogen response element (ERE)-driven reporter activity was observed in transiently transfected thyroid cancer cells.

In contrast, E2 did not increase progesterone receptor expression in the thyroid cancer cell lines.

GPR30 expression was lower in WRO than MCF-7 human breast cancer cells.

Overall, these findings suggest E2-mediated thyroid cancer cell proliferation involves ERalpha and ERbeta transcriptional and non-genomic signaling events.

[MeSH-major] Carcinoma / metabolism. Estradiol / pharmacology. Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Thyroid Neoplasms / metabolism

[MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans. Phosphorylation. RNA, Small Interfering / metabolism. Raloxifene Hydrochloride / pharmacology. Signal Transduction. Tamoxifen / analogs & derivatives. Tamoxifen / pharmacology

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(PMID = 20372779.001).

[ISSN] 1791-2423

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / R01 DK53220

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Greece

[Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / RNA, Small Interfering; 094ZI81Y45 / Tamoxifen; 17197F0KYM / afimoxifene; 22X328QOC4 / fulvestrant; 4F86W47BR6 / Raloxifene Hydrochloride; 4TI98Z838E / Estradiol

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Silencing of the maternally imprinted tumor suppressor ARHI contributes to follicular thyroid carcinogenesis.

The two most common subtypes of thyroid cancer, follicular thyroid carcinoma (FTC) and papillary thyroid carcinoma, have been extensively studied, but our fundamental understanding of the molecular events in thyroid epithelial oncogenesis is still limited.

Unreported data from our previous published global gene expression analysis revealed that the tumor suppressor gene aplysia ras homolog I (ARHI) is frequently underexpressed in FTCs.

In this study, we elucidated the frequency and mechanism of ARHI silencing in benign and malignant thyroid neoplasia.

We demonstrated that underexpression of ARHI occurs principally in FTCs (P = 0.0018), including its oncocytic variant (11 of 13), even at minimally invasive stage but not classic papillary thyroid carcinoma (two of seven) or follicular adenoma (FA) (three of 14).

FTCs show strong allelic imbalance with reduction in copy number/loss of heterozygosity (LOH) in 69%, compared with less than 10% for FAs.

In combination with our LOH data, bisulfite sequencing in a subset of samples revealed that FA displays a symmetric methylation pattern, likely representing one unmethylated allele and one presumptively imprinted allele, whereas FTC shows a virtually complete methylation pattern, representing LOH of the nonimprinted allele with only the hypermethylated allele remaining.

Furthermore, we showed that pharmacologic inhibition of histone deacetylation but not demethylation could reactivate ARHI expression in the FTC133 FTC cell line.

Therefore, our data suggest that silencing of the putative maternally imprinted tumor suppressor gene ARHI, primarily by large genomic deletion in conjunction with hypermethylation of the genomically imprinted allele, serves as a key early event in follicular thyroid carcinogenesis.

[MeSH-major] Azacitidine / analogs & derivatives. Gene Silencing. Genes, Tumor Suppressor. Genomic Imprinting / genetics. Thyroid Neoplasms / genetics. rho GTP-Binding Proteins / genetics

[MeSH-minor] Adenocarcinoma, Follicular / genetics. Adenocarcinoma, Follicular / pathology. Adenoma / genetics. Adenoma / pathology. Antimetabolites, Antineoplastic / pharmacology. Base Sequence. DNA Primers. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Loss of Heterozygosity. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 15546898.001).

[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 / P30 CA16059

[Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DIRAS3 protein, human; 0 / DNA Primers; 776B62CQ27 / decitabine; EC 3.6.5.2 / rho GTP-Binding Proteins; M801H13NRU / Azacitidine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Changing patterns in the incidence and survival of thyroid cancer with follicular phenotype--papillary, follicular, and anaplastic: a morphological and epidemiological study.

Thyroid carcinomas with follicular phenotype have demonstrated changing patterns over 30 years (1973-2003) according to data from the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute.

Papillary carcinomas have significantly increased.

They accounted for 74% of all cases of thyroid cancers in 1973 and 87% in 2003.

During this period, the incidence rate of papillary carcinoma (including the follicular variant) increased by 189%, the rate of follicular carcinoma remained stable, and the rate of anaplastic carcinoma decreased by 22%.

The rate of the follicular variant of papillary carcinoma alone increased by 173%.

Thyroid cancer was more common in whites than in blacks and in females more than in males.

Papillary carcinomas rapidly increased during adolescence and reached a peak around age 52-56, then declined.

Follicular carcinomas increased steadily, but at a lower rate until age 80.

After 1988, both papillary and follicular carcinomas, less than 2 cm, increased at the same rate as carcinomas larger than 2 cm.

However, papillary carcinomas less than 2 cm were more common.

Overall, the 10-year relative survival rate was greater than 90% for blacks and whites with the exception of follicular carcinoma in blacks.

The 10-year relative survival rate for anaplastic carcinoma in patients over 40 years of age was 4.7%.

The decrease in incidence rate of anaplastic carcinoma may be the result of the successful treatment of papillary and follicular carcinomas.

[MeSH-major] Adenocarcinoma, Follicular. Carcinoma, Papillary. Thyroid Neoplasms

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[Cites] Cancer Causes Control. 2000 Feb;11(2):163-70 [10710201.001]

[Cites] Clin Endocrinol (Oxf). 2004 Jan;60(1):21-8 [14678283.001]

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(PMID = 17652794.001).

[ISSN] 1046-3976

[Journal-full-title] Endocrine pathology

[ISO-abbreviation] Endocr. Pathol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 23

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Immunoexpression of TTF-1 and Ki-67 in a coexistent anaplastic and follicular thyroid cancer with rare long-life surviving.

We report the immunohistochemical diagnosis, including TTF-1 (thyroid transcription factor 1) and Ki-67, of a rare mixed thyroid neoplasm composed of minimally invasive well differentiated follicular areas and highly aggressive undifferentiated anaplastic areas.

Considering the dynamics of the disease and the multiple challenges presented by the patient: advanced age, tumor size, history of a longstanding goiter we decided to transfer her to the department of surgery.

The histopathological and immunohistochemical examination revealed a coexistent anaplastic and follicular thyroid carcinoma.

The proliferation index Ki-67, a cell proliferation marker, was found to be significantly higher in the anaplastic areas (30 +/- 5%) in the comparison with the follicular areas (2 +/- 1%).

The evaluation of the thyroid transcription factor 1 (TTF-1) expression revealed a correlation with the tumor cells aggressiveness accordingly to the cancer areas.

The patient is alive and more than five years after diagnosis she presented an increase of the serum thyroglobulin level suggesting, probably, a recurrence of the follicular form of the cancer.

According to our survey we suggest that in thyroid cancers TTF-1 and Ki-67 could provides useful information on the differentiation activities of thyroid tumor cells and may be helpful to distinguish well differentiated and undifferentiated areas in a mixed thyroid cancer.

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(PMID = 19141399.001).

[ISSN] 1897-5631

[Journal-full-title] Folia histochemica et cytobiologica

[ISO-abbreviation] Folia Histochem. Cytobiol.

[Language] ENG

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Poland

[Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [A case of follicular carcinoma of thyroid gland with concurrent tuberculous lymphadenitises].

We report a case of follicular carcinoma of the thyroid gland with concurrent tuberculous lymphadenitises as neck lymph node metastases of thyroid carcinoma.

A 71-year-old woman presented with multiple painless masses in the thyroid gland and painless lymphadenopathies in the right neck.

A diagnosis of thyroid cancer with lymph node metastases was made, and the patient underwent total thyroidectomy with neck dissection.

The histopathological diagnosis was follicular carcinoma and multiple nodes of adenomatous goiter of the thyroid gland, and tuberculous lymphadenitises of lymph nodes in the right neck.

The possibility of coexisting tuberculous lymphadenitis must thus be ruled out when we find painless lymph node swelling in aged patients with head and neck cancer including thyroid cancer.

[MeSH-major] Carcinoma, Papillary, Follicular / complications. Thyroid Neoplasms / complications. Tuberculosis, Lymph Node / complications

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(PMID = 17302297.001).

[ISSN] 0030-6622

[Journal-full-title] Nihon Jibiinkoka Gakkai kaiho

[ISO-abbreviation] Nippon Jibiinkoka Gakkai Kaiho

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Post-surgical use of radioiodine (131I) in patients with papillary and follicular thyroid cancer and the issue of remnant ablation: a consensus report.

OBJECTIVE: To determine, based on published literature and expert clinical experience, current indications for the post-surgical administration of a large radioiodine activity in patients with differentiated thyroid cancer.

RESULTS: There is general agreement that patients with unifocal microcarcinomas = 1 cm in diameter and no node or distant metastases have a <2% recurrence rate after surgery alone, and that post-surgical radioiodine confers recurrence and cause-specific survival benefits in patients, strongly suspected of having persistent disease or known to have tumor in the neck or distant sites.

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(PMID = 16260423.001).

[ISSN] 0804-4643

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

[Publication-type] Consensus Development Conference; Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Iodine Radioisotopes

[Number-of-references] 52

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Follicular thyroid carcinoma: From diagnosis to treatment.

Unusual presentations with bone, lung or soft tissue metastases in initial diagnosis of follicular thyroid carcinoma have been reported occasionally.

This implies how difficult it is to diagnosis this type of cancer at the pre-operative or intra-operative stage of treatment.

Fine needle aspiration cytology has been shown to be an ineffective method for diagnosing vascular or capsule invasion of follicular thyroid cancer.

Clinical application of various gene expressions in thyroid follicular tumors by needle aspiration using in situ hybridization requires further investigation.

Although radioactive iodide (131I) has been used as the standard treatment for follicular thyroid carcinoma with distant metastases, the effectiveness of 131I treatment for follicular thyroid carcinoma depends on the differentiation of cancer cells.

The possibility of 131I for thyroid remnant ablation replacing a secondary operation for follicular thyroid carcinoma has been debated.

Recent studies applied more expressions of sodium iodide symporters to attain the effect of 131I treatment and slow the proliferation of thyroid cancer cell which, in turn, slows the progression of follicular carcinoma.

Consensus for the surgical procedures for the specific prognostic risks for follicular thyroid carcinoma is needed.

Dedifferentiated, anti-angiogenic, or gene therapies for follicular thyroid cancer with distant metastases or anaplastic transformation comprise the principal directions in future research for this cancer.

[MeSH-major] Adenocarcinoma, Follicular / diagnosis. Adenocarcinoma, Follicular / therapy. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / therapy

[MeSH-minor] Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / pathology. Carcinoma, Papillary / therapy. Diagnostic Imaging. Humans. Iodine Radioisotopes / therapeutic use. Predictive Value of Tests. Thyroidectomy

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(PMID = 16807500.001).

[ISSN] 0918-8959

[Journal-full-title] Endocrine journal

[ISO-abbreviation] Endocr. J.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Japan

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Iodine Radioisotopes

[Number-of-references] 72

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Differentiation of metastatic follicular thyroid cancer from hepatocellular carcinoma using Hep Par 1.

Hepatocellular carcinoma usually arises in a cirrhotic liver.

The case is reported of a middle-aged woman presenting with multiple nodules on computed tomography with no clinically apparent primary for whom results of initial diagnostic investigations were potentially misleading.

[MeSH-major] Antibodies, Monoclonal. Carcinoma, Hepatocellular / diagnosis. Immunohistochemistry / methods. Liver Neoplasms / diagnosis. Neoplasm Proteins / analysis. Thyroid Neoplasms / diagnosis

[MeSH-minor] Adult. Diagnosis, Differential. Female. Humans

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(PMID = 17914993.001).

[ISSN] 0815-9319

[Journal-full-title] Journal of gastroenterology and hepatology

[ISO-abbreviation] J. Gastroenterol. Hepatol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Australia

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Neoplasm Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Comparison of clinical characteristics at diagnosis and during follow-up in 118 patients with Hurthle cell or follicular thyroid cancer.

BACKGROUND: Hurthle cell cancer (HCC) is considered by some to be a variant of follicular cancer (FC), but many think it is a distinct histologic tumor with a more aggressive behavior.

METHODS: The influence of age at diagnosis, tumor stage, gender, and extent of operation on disease-free interval and cause-specific mortality at 5 and 10 years after initial thyroidectomy was analyzed.

RESULTS: The 10-year disease-free interval was 75% for FC and 40.5% for HCC (P = .08).

The risk factors for HCC progression and survival were extrathyroidal invasion, presence of metastases at diagnosis, male gender, and extent of thyroidectomy, whereas for FC, the only significant risk factors were extrathyroidal invasion and presence of metastases at diagnosis.

[MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma, Follicular / diagnosis. Thyroid Neoplasms / diagnosis. Thyroidectomy

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Disease Progression. Disease-Free Survival. Female. Follow-Up Studies. Humans. Iodine Radioisotopes / therapeutic use. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Risk Factors. Sex Factors. Survival Analysis. Treatment Outcome

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(PMID = 18070728.001).

[ISSN] 1879-1883

[Journal-full-title] American journal of surgery

[ISO-abbreviation] Am. J. Surg.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Iodine Radioisotopes

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Follicular carcinoma of the thyroid and diffuse toxic goiter. Case report].

[Transliterated title] Cancer folicular de tiroides y bocio tóxico difuso. Reporte de un caso.

BACKGROUND: Follicular thyroid cancer rarely manifests itself as a distant metastatic lesion.

We report a case of a male with follicular thyroid cancer that presented as a distant metastatic lesion and diffuse toxic goiter.

CASE REPORT: A 50-year-old man was evaluated because of a soft, painless, pulsating sternal mass of 6 x 6 cm.

An incisional biopsy of the soft tissue showed metastatic thyroid follicular neoplasm.

A thyroid scan revealed uptake of (131)I in all thyroid areas of 36%.

Three months later, thyroid scan was negative and thyroglobulin was 17 ng/ml.

CONCLUSIONS: We report this case of follicular thyroid cancer because of its uncommon initial sternal presentation and soft tissue metastasis with diffuse toxic goiter.

[MeSH-major] Adenocarcinoma, Follicular / complications. Adenocarcinoma, Follicular / secondary. Bone Neoplasms / complications. Bone Neoplasms / secondary. Goiter / complications. Thyroid Neoplasms / complications. Thyroid Neoplasms / pathology

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(PMID = 17659173.001).

[ISSN] 0009-7411

[Journal-full-title] Cirugía y cirujanos

[ISO-abbreviation] Cir Cir

[Language] spa

[Publication-type] English Abstract; Journal Article

[Publication-country] Mexico

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Global variation in the pattern of differentiated thyroid cancer.

BACKGROUND: The prevalence of differentiated thyroid cancer (DTC) is increasing worldwide.

Iodine deficiency is a risk factor for follicular thyroid cancer (FTC).

METHODS: A retrospective review of thyroid cancer at tertiary centers in West Africa and the United States.

All patients diagnosed with thyroid cancer from 1980 to 2004 were retrieved from the West African Center's Cancer Registry Database.

In the American center, a review of patients undergoing surgery for thyroid cancer from 1997 to 2008 was performed.

RESULTS: At the African institution, 322 patients underwent thyroidectomy for cancer from 1980 to 2004.

Overall, 31.5% had papillary thyroid cancer (PTC), and 30.3% had FTC.

From 1980 to 1989, 27.3% had PTC and 35.8% had FTC.

From 1990 to 2004, 35.7% had PTC and 24.8% had FTC.

At the American institution, 105 patients underwent surgery for thyroid cancer from 1997 to 2008; 79% had PTC and 7.6% had FTC.

CONCLUSIONS: FTC is still common in developing countries, whereas PTC is the predominant subtype in developed countries.

[MeSH-major] Adenocarcinoma, Follicular / pathology. Carcinoma, Medullary / pathology. Carcinoma, Papillary / pathology. Neoplasm Staging / methods. Thyroid Neoplasms / pathology. Thyroidectomy / statistics & numerical data

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Disease Progression. Female. Humans. Incidence. Infant. Infant, Newborn. Male. Middle Aged. Nigeria / epidemiology. Prognosis. Retrospective Studies. SEER Program. United States / epidemiology. Young Adult

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[Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.

(PMID = 20887838.001).

[ISSN] 1879-1883

[Journal-full-title] American journal of surgery

[ISO-abbreviation] Am. J. Surg.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Multicenter Study

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Retinoic acid-mediated down-regulation of ENO1/MBP-1 gene products caused decreased invasiveness of the follicular thyroid carcinoma cell lines.

Retinoic acid (RA) acts as an anti-proliferative and redifferentiation agent in the therapy of thyroid carcinoma.

Our previous studies demonstrated that pretreatment of follicular thyroid carcinoma cell lines FTC-133 and FTC-238 resulted in decreased in vitro proliferation rates and reduced tumor cell growth of xenotransplants.

In addition to the previous results, we found that RA led to decreased vitality and invasiveness of FTC-133 and FTC-238 cells as they reacted with reduction of intracellular ATP levels and number of migrated cells respectively.

However, the molecular mechanisms by which RA mediates these effects are not well understood.

Two-dimensional (2D) screening of the proteins related to ATP metabolism and western blot analysis revealed alpha-enolase (ENO1) to be down-regulated in FTC-133 and FTC-238 cells after RA treatment.

Comparative 2D difference gel electrophoresis analysis of fluorescently labeled protein samples of RA-treated and untreated FTC-133 demonstrated a selective down-regulation of ENO1-A1 which we identified as a phosphoprotein.

Both, RA-mediated and specific knock-down of ENO1/MBP-1 resulted in the reduction of MYC oncoprotein, and simultaneously decreased proliferation rates of FTC-133 and FTC-238 cell lines.

In summary, the RA-mediated down-regulation of the ENO1 gene products and MYC oncoprotein provides a novel molecular mechanism facilitating the anti-proliferative effect of RA in human thyroid carcinoma cells and suggests new pathways for supportive RA therapies.

[MeSH-major] Biomarkers, Tumor / physiology. Cell Movement / drug effects. DNA-Binding Proteins / physiology. Gene Expression Regulation, Neoplastic / drug effects. Phosphopyruvate Hydratase / physiology. Thyroid Neoplasms / metabolism. Tretinoin / pharmacology. Tumor Suppressor Proteins / physiology

[MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Electrophoresis, Gel, Two-Dimensional. Humans. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

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(PMID = 19060179.001).

[ISSN] 1479-6813

[Journal-full-title] Journal of molecular endocrinology

[ISO-abbreviation] J. Mol. Endocrinol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; 5688UTC01R / Tretinoin; EC 4.2.1.11 / ENO1 protein, human; EC 4.2.1.11 / Phosphopyruvate Hydratase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Finding victory in legal defeat. FTC says ENH can keep Highland Park (Ill.) Hospital, but industry wary of what anti-competitive decision might mean.

FTC litigator Tom Brock, left, says the case turned on exorbitant price hikes the system extracted from managed-care plans.

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(PMID = 17958257.001).

[ISSN] 0160-7480

[Journal-full-title] Modern healthcare

[ISO-abbreviation] Mod Healthc

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Follicular thyroid carcinoma in an iodine-replete endemic goiter region: a prospectively collected, retrospectively analyzed clinical trial.

OBJECTIVE: To determine risk factors for presence of lymph node or distant metastases in patients with follicular thyroid cancer (FTC) at the time of diagnosis and whether there is a relationship between the type of tumor invasion and metastases.

SUMMARY BACKGROUND DATA: FTC often presents distant metastases at the initial diagnosis.

METHODS: The prognostic significance of gender (male vs. female), age (<or=40 years vs. <40 years), tumor size (<or=40 mm vs. >40 mm), number of lesions (uni- vs. multifocality), type of invasion (minimally invasive vs. widely invasive), and oncocytic changes (with vs. without) were analyzed in 207 patients, according to presence of lymph node and distant metastases at the time of initial surgery.

According to the type of invasion, the carcinoma-specific survival and the disease-free survival of minimally invasive (MI) and widely invasive (WI) FTC were estimated and compared.

Overall risk factors for the presence of lymph node metastases at the initial diagnosis were multifocality (P = 0.02) and widely invasion (P = 0.0001) and for distant metastases age >45 years (P = 0.007), tumor size larger than 40 mm (P = 0.03) and widely invasion (P = 0.0001).WI-FTC patients show larger tumors (P = 0.0001), older age (P = 0.0001), and are presented more frequently in recurrent goiter disease (P = 0.0001).

The estimated 10 years carcinoma-specific survival and disease-free survival for MI-tumors were significantly better than for WI-tumors (P = 0.0001).

CONCLUSIONS: Total thyroidectomy is recommended in all patients with FTC because of early distant metastases.

Patients with WI-FTC need a more aggressive surgical treatment because of higher tendency for lymph node metastases.

MI-FTC has an excellent prognosis with no sign of lymph node metastases, which emphasizes a limited need for nodal surgery.

[MeSH-major] Adenocarcinoma, Follicular / secondary. Adenocarcinoma, Follicular / surgery. Goiter, Endemic / complications. Thyroid Neoplasms / pathology. Thyroid Neoplasms / surgery

[MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Cohort Studies. Disease-Free Survival. Female. Humans. Lymph Node Excision. Male. Middle Aged. Neoplasm Invasiveness. Retrospective Studies. Risk Factors. Survival Rate. Thyroidectomy. Young Adult

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(PMID = 19474675.001).

[ISSN] 1528-1140

[Journal-full-title] Annals of surgery

[ISO-abbreviation] Ann. Surg.

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Endobronchial metastasis of follicular thyroid carcinoma presenting as hemoptysis: a case report.

Endobronchial metastasis secondary to follicular thyroid carcinoma is extremely rare.

Here, we report a case of follicular thyroid cancer in 58-year-old male who presented with hemoptysis.

Flexible fiberoptic bronchoscopy revealed a fragile polypoid mass 5 cm distal to the vocal cords; biopsy taken from this mass revealed follicular thyroid carcinoma.

[MeSH-major] Bronchial Neoplasms / secondary. Thyroid Neoplasms / pathology

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(PMID = 18417903.001).

[ISSN] 1998-4138

[Journal-full-title] Journal of cancer research and therapeutics

[ISO-abbreviation] J Cancer Res Ther

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] India

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] AKT activation promotes metastasis in a mouse model of follicular thyroid carcinoma.

The phosphatidylinositol 3-kinase/AKT pathway is crucial to many cell functions, and its dysregulation in tumors is a common finding.

The molecular basis of follicular thyroid cancer metastasis is not well understood but may also be influenced by AKT activation.

We previously created a knockin mutant mouse that expresses a mutant thyroid hormone receptor-beta gene (TRbetaPV mouse) that spontaneously develops thyroid cancer and distant metastasis similar to human follicular thyroid cancer.

In this study, we investigated whether our mouse model exhibits similar AKT activation as human follicular thyroid cancer.

Western blot analysis on thyroids from both wild-type and TRbeta(PV/PV) mice revealed elevation of activated AKT in TRbeta(PV/PV) mice.

Immunohistochemistry and confocal microscopy reveal activated AKT in both the thyroid and metastatic lesions of TRbeta(PV/PV) mice.

Whereas all three AKT isoforms were overexpressed in primary tumors from TRbeta(PV/PV) mice in the cytoplasm of thyroid cancer cells, only AKT1 was also found in the nucleus, matching the localization of activated AKT in a pattern similar to human follicular thyroid cancer.

We created primary thyroid cell lines derived from TRbeta(PV/PV) mice and found reduction of phosphorylated AKT levels or AKT downstream targets diminishes cell motility.

Activated AKT is common to both human and mouse follicular thyroid cancer and is correlated with increased cell motility in vitro and metastasis in vivo.

Thus, TRbeta(PV/PV) mice could be used to further dissect the detailed pathways underlying the progression and metastasis of follicular thyroid carcinoma.

[MeSH-major] Adenocarcinoma, Follicular / pathology. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Thyroid Neoplasms / pathology

[MeSH-minor] Animals. Cell Movement. Disease Models, Animal. Enzyme Activation. Humans. Kinetics. Mice. Neoplasm Metastasis. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt

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(PMID = 16002527.001).

[ISSN] 0013-7227

[Journal-full-title] Endocrinology

[ISO-abbreviation] Endocrinology

[Language] eng

[Grant] United States / Intramural NIH HHS / /

[Publication-type] Journal Article; Research Support, N.I.H., Intramural

[Publication-country] United States

[Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.1.- / Phosphatidylinositol 3-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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Connexin26 expression is associated with aggressive phenotype in human papillary and follicular thyroid cancers.

Connexin26 (Cx26), a component of GAP junctions and until recently believed to be a tumor suppressor gene, has been shown to play an important role in lymphatic invasion as well as lymph node and distant metastases in squamous lung cancer and breast cancer.

In the study presented here, we investigated Cx26 expression in human papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC) and its relationship with various clinicopathological parameters.

Of 69 PTCs, 33 were positive for Cx26 (47.8%), as were five of 11 FTCs (45.5%), all follicular thyroid adenomas (n=22) and normal thyroid tissues (n=20) were negative for Cx26.

A statistically significant association was observed between Cx26 expression and large tumor size (p=0.028 for PTC) and lymph node metastases (p=0.053 (marginally significant) for PTC and p=0.035 for FTC).

These results suggest that Cx26 may be implicated in the pathogenesis of PTC and FTC and is associated with the biologically aggressive phenotypes of these tumors.

[MeSH-major] Adenoma / genetics. Carcinoma, Papillary / genetics. Connexins / genetics. Thyroid Neoplasms / genetics

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(PMID = 18191019.001).

[ISSN] 0304-3835

[Journal-full-title] Cancer letters

[ISO-abbreviation] Cancer Lett.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Connexins; 127120-53-0 / connexin 26

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The Ras effector NORE1A is suppressed in follicular thyroid carcinomas with a PAX8-PPARgamma fusion.

NORE1A has not been studied in thyroid cancer.

OBJECTIVE: The objective of this study was to investigate whether NORE1A is involved in follicular thyroid cancer (FTC) development.

DESIGN: We analyzed NORE1A expression in 25 FTCs, eight follicular thyroid adenomas, and seven normal thyroid tissues by TaqMan quantitative RT-PCR.

No NORE1A promoter methylation was detected in the 32 thyroid tumors analyzed.

CONCLUSIONS: Our experiments demonstrate the suppression of NORE1A, a known Ras effector, in PAX8-PPARgamma carrying FTCs.

[MeSH-major] Adenocarcinoma, Follicular / genetics. Monomeric GTP-Binding Proteins / genetics. PPAR gamma / genetics. Paired Box Transcription Factors / genetics. RNA, Messenger / genetics. Thyroid Neoplasms / genetics

[MeSH-minor] Breast Neoplasms. Cell Line, Tumor. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. Exons. Female. Gene Expression Regulation, Neoplastic. Genes, Reporter. Humans. Promoter Regions, Genetic. Recombination, Genetic. Restriction Mapping. Reverse Transcriptase Polymerase Chain Reaction. Suppression, Genetic / genetics. Thyroidectomy

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(PMID = 16352687.001).

[ISSN] 0021-972X

[Journal-full-title] The Journal of clinical endocrinology and metabolism

[ISO-abbreviation] J. Clin. Endocrinol. Metab.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / PAX8 protein, human; 0 / PPAR gamma; 0 / Paired Box Transcription Factors; 0 / RASSF5 protein, human; 0 / RNA, Messenger; EC 3.6.5.2 / Monomeric GTP-Binding Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Follicular thyroid carcinoma: the role of histology and staging systems in predicting survival.

OBJECTIVE: To evaluate the risk factors including tumor histomorphology for survival specific to follicular thyroid carcinoma (FTC) and to apply commonly employed staging systems in predicting survival for patients with FTC.

SUMMARY BACKGROUND DATA: FTC is usually analyzed collectively with papillary thyroid carcinoma (PTC) in risk group analysis.

Risk factors and risk group analysis are important in the management of patients with FTC, although current published therapeutic guidelines call for total thyroidectomy followed by radioactive iodine (I) ablation for all FTC patients.

METHODS: Over a 40-year period, 156 patients surgically treated for FTC with an average follow-up of 14.4 years were retrospectively studied after histologic reclassification according to the type and degree of invasiveness of the tumor.

RESULTS: Seventeen (11%) patients had distant metastases at presentation, and bilateral thyroid resection was performed for 131 (84%) patients.

Seventeen (11%) patients died of recurrent or metastatic disease.

The overall and cancer-specific survival (CSS) rates at 10 years were 79% and 88%, respectively.

None of the patients with minimally invasive (n = 49) or angioinvasive (n = 23) carcinomas died compared with 17 of 84 patients with widely invasive carcinomas (P = 0.0007).

For patients who underwent curative treatment, old age and widely invasive carcinoma were risk factors for poor survival.

CONCLUSIONS: Commonly adopted staging systems can be applied specifically to patients with FTC.

The distinction of FTC in minimally invasive and widely invasive carcinoma based on the extent of invasiveness rather than vascular invasion is important in identifying low-risk FTC patients for a more conservative management.

[MeSH-major] Adenocarcinoma, Follicular / mortality. Adenocarcinoma, Follicular / pathology. Neoplasm Invasiveness / pathology. Neoplasm Staging / standards. Thyroid Neoplasms / mortality. Thyroid Neoplasms / pathology

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(PMID = 16244545.001).

[ISSN] 0003-4932

[Journal-full-title] Annals of surgery

[ISO-abbreviation] Ann. Surg.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Other-IDs] NLM/ PMC1409851

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The tumor suppressor PTEN inhibits EGF-induced TSP-1 and TIMP-1 expression in FTC-133 thyroid carcinoma cells.

In the present study, we found that epidermal growth factor (EGF) up-regulated TSP-1 expression in FTC-133 (primary tumor) but not in FTC-238 (lung metastasis) thyroid cancer cells.

In FTC-133 cells, EGF induced proliferation in a TSP-1- and TIMP-1-dependent manner.

In addition, we determined that re-expression of the tumor suppressor protein PTEN induced cell death, an effect that correlated with a block of Akt kinase phosphorylation.

EGF-induced TSP-1 and TIMP-1 promoter activity and protein expression were inhibited in FTC-133 cells stably expressing wtPTEN but not in cells expressing mutant PTEN.

Furthermore, we found that wtPTEN inhibited EGF--but not TSP-1--stimulated FTC-133 cell migration and also inhibited invasion induced by EGF and by TSP-1.

Finally, an antibody against TSP-1 reversed EGF-stimulated FTC-133 cell invasion as well as the constitutive invasive potential of FTC-238 cells.

Overall, our results suggest that PTEN can function as an important modulator of extracellular matrix proteins in thyroid cancer.

Therefore, analyzing differential regulation of TSP-1 by growth factors such as EGF can be helpful in understanding thyroid cancer development.

[MeSH-major] Carcinoma / metabolism. Epidermal Growth Factor / antagonists & inhibitors. Phosphoric Monoester Hydrolases / metabolism. Thrombospondin 1 / metabolism. Thyroid Neoplasms / metabolism. Tissue Inhibitor of Metalloproteinase-1 / metabolism. Tumor Suppressor Proteins / metabolism

[MeSH-minor] Apoptosis. Cell Line, Tumor. Cell Proliferation. Humans. MAP Kinase Kinase 1 / metabolism. PTEN Phosphohydrolase. Phosphatidylinositol 3-Kinases / metabolism. Promoter Regions, Genetic. Up-Regulation

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(PMID = 15707585.001).

[ISSN] 0014-4827

[Journal-full-title] Experimental cell research

[ISO-abbreviation] Exp. Cell Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Thrombospondin 1; 0 / Tissue Inhibitor of Metalloproteinase-1; 0 / Tumor Suppressor Proteins; 62229-50-9 / Epidermal Growth Factor; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genetic aspects of familial thyroid cancer.

Familial thyroid cancer is rare, accounting for <10% of thyroid cancer cases.

Activating germline point mutations in the RET proto-oncogene are associated with multiple endocrine neoplasia types 2A, 2B, and familial medullary thyroid cancer (FMTC)-around 3% of thyroid cancer cases.

Familial papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC) have been identified as a distinct group of familial thyroid cancers.

Sporadic nonmedullary thyroid cancer (NMTC) accounts for approximately 90% of all thyroid cancers-about 6% of NMTCs are familial (FNMTC).

Although multiple endocrine neoplasia types 2A and 2B and FMTC are well characterized, very little is known about the genetic predisposition to PTC and FTC.

[MeSH-major] Thyroid Neoplasms / genetics

[MeSH-minor] Carcinoma, Medullary / genetics. Carcinoma, Papillary / genetics. Humans. Multiple Endocrine Neoplasia Type 1 / genetics. Multiple Endocrine Neoplasia Type 2a / genetics. Multiple Endocrine Neoplasia Type 2b / genetics. Proto-Oncogene Proteins c-ret / genetics

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(PMID = 19465682.001).

[ISSN] 1549-490X

[Journal-full-title] The oncologist

[ISO-abbreviation] Oncologist

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / RET protein, human

[Number-of-references] 43

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Corticofugal shaping of frequency tuning curves in the central nucleus of the inferior colliculus of mice.

The latter was used here to measure how stimulation in the tonotopy of the mouse primary auditory cortex influences frequency tuning in the midbrain central nucleus of the inferior colliculus (ICC).

Shapes of collicular frequency tuning curves (FTCs) were quantified before and after cortical activation by measuring best frequencies, FTC bandwidths at various sound levels, level tolerance, Q-values, steepness of low- and high-frequency slopes, and asymmetries.

The changes were dependent not only on the relationship of physiological properties between the stimulated cortical neurons and recorded collicular neurons but also on the tuning curve class of the collicular neuron.

Cortical activation assimilated collicular FTC shapes; sharp and broad FTCs were changed to the shapes comparable to those of auditory nerve fibers.

Plasticity in the ICC was organized in a center (excitatory)-surround (inhibitory) way with regard to the stimulated location (i.e., the frequency) of cortical tonotopy.

This ensures, together with the spatial gradients of distribution of collicular FTC shapes, a sharp spectral filtering at the core of collicular frequency-band laminae and an increase in frequency selectivity at the periphery of the laminae.

Mechanisms of FTC plasticity were suggested to comprise both corticofugal and local ICC components of excitatory and inhibitory modulation leading to a temporary change of the balance between excitation and inhibition in the ICC.

[MeSH-minor] Acoustic Stimulation / methods. Action Potentials / physiology. Action Potentials / radiation effects. Analysis of Variance. Animals. Cell Count. Chi-Square Distribution. Dose-Response Relationship, Radiation. Electric Stimulation / methods. Female. Mice. Sensory Thresholds / physiology. Sensory Thresholds / radiation effects. Time Factors

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(PMID = 15331615.001).

[ISSN] 0022-3077

[Journal-full-title] Journal of neurophysiology

[ISO-abbreviation] J. Neurophysiol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Identification and functional characterization of isocitrate dehydrogenase 1 (IDH1) mutations in thyroid cancer.

In the present study, we investigated IDH1 and IDH2 mutations in follicular thyroid cancer (FTC) and anaplastic thyroid cancer (ATC), with the latter, like glioblastoma, having a rapidly aggressive and lethal clinical course.

By direct genomic DNA sequencing, we analyzed exon 4 of the IDH1 and IDH2 genes that harbored the mutation hot spots codon 132 and 172 of the two genes in glioblastoma, respectively, in 12 thyroid cancer cell lines, 20 FTC, and 18 ATC tumor samples.

A previously described IDH1 V71I mutation was found in a case of FTC and a case of ATC and no mutations were found in the cell lines.

The overall prevalence of mutations was thus 1/20 (5%) in FTC and 2/18 (11%) in ATC.

We did not find mutation in the IDH2 gene in these thyroid cancer cell lines and tumor samples.

Sequence alignment analysis of 16 species revealed that the novel IDH1 G123R mutation was located in a highly conserved region, raising the possibility of a serious functional consequence as could also be predicted by the occurrence of a positively charged amino acid from this mutation.

Thus, functionally relevant IDH1 mutations can also occur in thyroid cancer, particularly ATC, suggesting a potential tumorigenic role of the IDH1 system that could represent a new therapeutic target for thyroid cancer.

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[Copyright] 2010 Elsevier Inc. All rights reserved.

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(PMID = 20171178.001).

[ISSN] 1090-2104

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA134225-01A2; United States / NCI NIH HHS / CA / R01 CA113507; United States / NCI NIH HHS / CA / CA134225-01A2; United States / NCI NIH HHS / CA / R01CA134225-01; United States / NCI NIH HHS / CA / R01 CA134225

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human

[Other-IDs] NLM/ NIHMS182112; NLM/ PMC2838977

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genetic alterations in the phosphatidylinositol-3 kinase/Akt pathway in thyroid cancer.

BACKGROUND: Aberrant activation of the phosphatidylinositol-3 kinase (PI3K)/Akt pathway plays a fundamental role in thyroid tumorigenesis, particularly in follicular thyroid cancer (FTC) and aggressive thyroid cancer, such as anaplastic thyroid cancer (ATC).

As the drivers of this process, many genetic alterations activating the PI3K/Akt pathway have been identified in thyroid cancer in recent years.

These include PIK3CA mutations and genomic amplification/copy gain, Ras mutations, PTEN mutations, RET/PTC and PPARgamma/Pax8 rearrangements, as well as amplification/copy gain of PIK3CB, PDK1, Akt, and various receptor tyrosine kinase genes.

Most of these genetic alterations are particularly common in FTC and many of them are even more common in ATC; they are generally less common in papillary thyroid cancer (PTC), in which the MAP kinase (MAPK) pathway activated by the BRAF mutation instead plays a major role.

Many of these genetic alterations are mutually exclusive in differentiated thyroid tumors, but with increasing concurrence from benign tumors to FTC to ATC.

It is proposed that genetic alterations in the PI3K/Akt pathway promote thyroid cell transformation to FTC and that genetic alterations in the MAPK pathway promote cell transformation to PTC; accumulation of multiple genetic alterations that can activate both pathways promotes thyroid cancer aggressiveness and progression to ATC.

CONCLUSIONS: Genetic alterations are common in the PI3K/Akt pathway in thyroid cancer and play a fundamental role in the tumorigenesis and progression of this cancer.

This provides a strong basis for the emerging development of novel genetic-based diagnostic, prognostic, and therapeutic strategies for thyroid cancer.

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(PMID = 20578891.001).

[ISSN] 1557-9077

[Journal-full-title] Thyroid : official journal of the American Thyroid Association

[ISO-abbreviation] Thyroid

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01CA134225

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review

[Publication-country] United States

[Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt

[Other-IDs] NLM/ PMC2935335

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Diagnosis of thyroid follicular carcinoma by the vascular pattern and velocimetric parameters using high resolution pulsed and power Doppler ultrasonography.

The aim of this study was to define the preoperative diagnosis of thyroid follicular carcinoma by the vascular pattern and velocimetric parameters using high resolution pulsed and power Doppler ultrasonography (US).

We compared the vascular pattern and the velocimetric parameters, such as peak systolic velocity (Vmax), end-diastolic velocity (Vmin), pulsatility index (PI), or resistance index (RI) between follicular adenoma (FA, n = 25) and follicular carcinoma (FC, n = 10) and analysed them by means of receiver characteristics curves (ROC).

These color flow imagings by power Doppler US were suggested to be a reliable tool for the differential diagnosis of thyroid follicular tumor with a sensitivity of 87.5% and a specificity of 92%.

The diagnostic efficiency evaluated by ROC curves were 0.898 for PI, 0.876 for RI, and 0.888 for Vmax/Vmin, respectively.

In conclusion, the evaluation of the vascular pattern and the velocimetric parameters using pulsed and power Doppler ultrasound may provide important information that is useful in making correct differential diagnosis of malignant or benign thyroid follicular tumor preoperatively.

[MeSH-major] Adenocarcinoma, Follicular / blood supply. Adenocarcinoma, Follicular / ultrasonography. Thyroid Neoplasms / blood supply. Thyroid Neoplasms / ultrasonography. Ultrasonography, Doppler, Pulsed

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Blood Flow Velocity. Female. Humans. Logistic Models. Male. Middle Aged. ROC Curve. Sensitivity and Specificity

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(PMID = 15863949.001).

[ISSN] 0918-8959

[Journal-full-title] Endocrine journal

[ISO-abbreviation] Endocr. J.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Japan

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Randomized, double-blind study of emtricitabine (FTC) plus clevudine versus FTC alone in treatment of chronic hepatitis B.

Emtricitabine (FTC) is approved for the treatment of human immunodeficiency virus.

FTC and clevudine (CLV) have activity against hepatitis B virus (HBV).

This report summarizes the results of a double-blind, multicenter study of patients with chronic hepatitis B who had completed a phase 3 study of FTC and were randomized 1:1 to 200 mg FTC once daily (QD) plus 10 mg CLV QD or 200 mg FTC QD plus placebo for 24 weeks with 24 weeks of follow-up.

One hundred sixty-three patients were treated (82 with FTC plus CLV [FTC+CLV] and 81 with FTC); 72% were men, 53% were Asian, 47% were Caucasian, and 52% were hepatitis B e antigen positive, and the median baseline HBV DNA level was 6 log(10) copies/ml.

After 24 weeks of treatment, 74% (FTC+CLV) versus 65% (FTC alone) had serum HBV DNA levels of <4,700 copies/ml (P = 0.114) (Digene HBV Hybrid Capture II assay).

Twenty-four weeks posttreatment, the mean change in serum HBV DNA levels from baseline was -1.25 log(10) copies/ml (FTC+CLV), 40% had undetectable viremia (versus 23% for FTC alone), and 63% had normal alanine aminotransferase levels (versus 42% for FTC alone) (P < or = 0.025 for all endpoints).

In summary, after 24 weeks of treatment, no significant difference between arms was observed, but there was a significantly greater virologic and biochemical response 24 weeks posttreatment in the FTC+CLV arm.

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(PMID = 16641430.001).

[ISSN] 0066-4804

[Journal-full-title] Antimicrobial agents and chemotherapy

[ISO-abbreviation] Antimicrob. Agents Chemother.

[Language] eng

[Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antiviral Agents; 0 / Bicarbonates; 0 / Blood Glucose; 0 / DNA, Viral; 0 / Electrolytes; 0 / Hepatitis B e Antigens; 0 / Serum Albumin; 0W860991D6 / Deoxycytidine; 3083-77-0 / Arabinofuranosyluracil; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase; EC 2.7.3.2 / Creatine Kinase; EC 3.1.3.1 / Alkaline Phosphatase; EC 3.2.1.- / Amylases; G70B4ETF4S / Emtricitabine; IN51MVP5F1 / Clevudine; RFM9X3LJ49 / Bilirubin

[Other-IDs] NLM/ PMC1472200

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Vitamin D receptor polymorphisms in differentiated thyroid carcinoma.

To investigate the role of the VDR gene and its influence on 25(OH)D(3) and 1,25(OH)(2)D(3) plasma levels in thyroid carcinoma, we analyzed four VDR polymorphisms in patients and healthy controls (HC).

METHODS: Patients with thyroid carcinoma (n = 172) (n = 132 for papillary and n = 40 for follicular) and HC (n = 321) were genotyped for the ApaI (rs7975232), TaqI (rs731236), BsmI (rs1544410), and FokI (rs10735810) polymorphisms within the VDR gene and correlated with 25(OH)D(3) and 1,25(OH)(2)D(3) plasma levels.

RESULTS: The genotypes AA of the ApaI (rs7975232) and FF of the FokI (rs10735810) polymorphisms were significantly less frequent (12.5% vs. 35.2% and 25% vs. 42.1%, respectively, both corrected p [p(c)] = 0.04) in patients with follicular thyroid cancer (FTC) than in HC.

Additionally, the haplotypes, Ta (57.5% vs. 41.4%; p(c) = 0.0207), af (24.6% vs. 14.3%; p(c) = 0.0116), Tab (51.1% vs. 36.8%; p(c) = 0.0495), and Tabf (18.7% vs. 13.6%; p(c) = 0.0240) were more frequent, whereas the haplotypes AF (17.1% vs. 37.2%; p(c) = 0.0008), BF (11.4% vs. 31.9%; p(c) = 0.012), tF (7.9% vs. 25.5%; p(c) = 0.0016), and tABF (7.6% vs. 23%; p(c) = 0.0115) were less frequent in the FTC patients compared to HC.

Neither genotype nor haplotype frequencies differed between patients with papillary thyroid cancer (PTC) and HC.

Further, individuals with PTC and FTC had a significantly lower level of circulating 1,25(OH)(2)D(3) compared to controls.

CONCLUSIONS: Lower circulating levels of 1,25(OH)(2)D(3) are observed in patients with differentiated thyroid carcinoma.

Further, while the alleles AA and FF of the ApaI (rs7975232) and FokI (rs10735810) VDR polymorphisms and the haplotype tABF confer to protection from follicular carcinoma, the haplotype Tabf appeared to be associated with an increased FTC risk.

Since this is the first report associating VDR polymorphisms with thyroid carcinoma, these findings need to be confirmed in studies with larger numbers of patients.

[MeSH-major] Carcinoma, Papillary, Follicular / genetics. Polymorphism, Genetic / genetics. Receptors, Calcitriol / genetics. Thyroid Neoplasms / genetics

[MeSH-minor] Autoantibodies / immunology. Calcifediol / metabolism. Calcitriol / metabolism. Cell Differentiation. Female. Genotype. Haplotypes. Humans. Male. Neutrophil Infiltration. Thyroid Gland / immunology. Vitamin D / physiology

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(PMID = 19499989.001).

[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] 0 / Autoantibodies; 0 / Receptors, Calcitriol; 1406-16-2 / Vitamin D; FXC9231JVH / Calcitriol; P6YZ13C99Q / Calcifediol

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Radioactive iodine offers survival improvement in patients with follicular carcinoma of the thyroid.

BACKGROUND: The use of radioactive iodine (RAI) in patients with follicular thyroid carcinoma is well established.

It was used to identify patients with follicular thyroid carcinomas and the treatment that they received.

RESULTS: A total of 4317 patients were identified with follicular thyroid carcinoma.

Factors that were associated with increased risk of death included distant metastatic disease, cervical lymph node disease, and the lack of RAI use.

CONCLUSION: RAI provides survival benefit to some patients with follicular carcinoma of the thyroid.

The greatest improvements were seen in those patients with locoregional or distant disease spread.

[MeSH-major] Adenocarcinoma, Follicular / mortality. Adenocarcinoma, Follicular / radiotherapy. Iodine Radioisotopes / therapeutic use. Radiopharmaceuticals / therapeutic use. Thyroid Neoplasms / mortality. Thyroid Neoplasms / radiotherapy

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(PMID = 16360393.001).

[ISSN] 0039-6060

[Journal-full-title] Surgery

[ISO-abbreviation] Surgery

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Radiopharmaceuticals

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression of MGMT and its clinopathological significance in thyroid carcinoma.

OBJECTIVE: To study the expression of O(6)-methylguanine-DNA methyltransferase (MGMT) and its clinicopathological significance in thyroid cancer.

METHODS: Immunohistochemistry was used to determine the expression of MGMT in 61 thyroid cancer tissues, 21 thyroid adenomas, 15 Hashimoto's thyroiditis, 8 nodular goiter, and 12 peri-tumor tissues.

RESULTS: There was statistic difference in the expression of MGMT between the normal tissues and thyroid cancers (P<0.05).

Expression of MGMT increased from the normal tissue (16.67%, 10/12), nodular goiter (25.00%, 2/8), Hashimoto's thyroiditis (60.00%, 9/15), and thyroid adenoma (52.38%, 11/21)to thyroid cancer (60.66%, 38/61).

Expression of MGMT in papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC) had significant difference (P<0.05), and the expression level of MGMT decreased with the malignancy of thyroid cancer, such as in PTC (72.22%, 26/36), and FTC (50.00%, 8/16).

CONCLUSION: High expression of MGMT might be related to the malignancy of thyroid cancer, which may be one of the diagnosis indexes for thyroid cancer.

It will be a common clinical index in diagnosing thyroid cancer since there is no difference in MGMT expression among sexes, ages, and nationalities.

[MeSH-major] Biomarkers, Tumor / metabolism. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Thyroid Neoplasms / metabolism

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(PMID = 21200087.001).

[ISSN] 1672-7347

[Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences

[ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The role of the PAX8/PPARgamma fusion oncogene in the pathogenesis of follicular thyroid cancer.

When identified at early stages, most well-differentiated thyroid cancers are readily treated and yield excellent outcomes.

Follicular thyroid cancer (FTC) however, when diagnosed at a late stage, may be very resistant to treatment, and exhibits 10-year survival rates less than 40%.

Despite substantial progress in recent years, we still have limited understanding of the molecular and biological interrelationships between the various subtypes of benign and malignant follicular thyroid neoplasms.

In contrast to the wealth of information available regarding papillary thyroid carcinoma (PTC), the triggering mechanisms of FTC development and the major underlying genetic alterations leading to follicular thyroid carcinogenesis remain obscure.

Recent studies have focused on a chromosomal translocation, t(2;3) (q13;p25), fusing PAX8, a transcription factor that is essential for normal thyroid gland development, with the peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the steroid/thyroid nuclear receptor family.

This chromatin rearrangement results in the expression of a PAX8/PPARgamma fusion protein, designated PPFP, whose incidence is relatively common in FTC and may represent an initiating event in the genesis of FTC.

Here we review progress on the studies of PPFP that assess its involvement in FTC tumorigenesis.

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[Copyright] Copyright 2009 Elsevier Ireland Ltd. All rights reserved.

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(PMID = 19883731.001).

[ISSN] 1872-8057

[Journal-full-title] Molecular and cellular endocrinology

[ISO-abbreviation] Mol. Cell. Endocrinol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA080117-08; United States / NCI NIH HHS / CA / R01 CA080117-08

[Publication-type] Journal Article; Review

[Publication-country] Ireland

[Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / PAX8-PPARgamma fusion protein, human; 0 / PPAR gamma; 0 / Paired Box Transcription Factors

[Number-of-references] 85

[Other-IDs] NLM/ NIHMS161308; NLM/ PMC2849860

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Chemotherapy with doxorubicin in progressive medullary and thyroid carcinoma of the follicular epithelium.

Twenty-two patients (mean age 61) with metastasizing, progressive, nonradioiodine-accumulating thyroid carcinoma of the follicular epithelium were treated with doxorubicin between 2000 and 2005.

Tumors were histologically classified as follicular in 15 patients (68%) and papillary in 7 patients (32%).

In addition, nine patients (mean age 51 years) with medullary thyroid carcinoma were treated with doxorubicin between 1997 and 2005.

In patients with papillary or follicular thyroid carcinoma, 5% had a partial regression over 6 months, 42% had stable disease for a median of 7 months (range: 1-22), and 53% had continuous progression established over 5 months (range: 1-11).

In patients with medullary thyroid carcinoma, 11% had a partial regression over 6 months followed by stable disease for 3 months, 11% had stable disease over 7 months, and 79% demonstrated progressive disease established over 5 months (range: 2-12).

Doxorubicin can be a valid chemotherapy option, especially for advanced or metastatic thyroid carcinoma of the follicular epithelium.

[MeSH-major] Adenocarcinoma, Follicular / drug therapy. Antibiotics, Antineoplastic / therapeutic use. Doxorubicin / therapeutic use. Thyroid Neoplasms / drug therapy

[MeSH-minor] Adult. Aged. Carcinoma, Medullary / drug therapy. Carcinoma, Medullary / radiography. Carcinoma, Papillary / drug therapy. Carcinoma, Papillary / radiography. Female. Humans. Male. Middle Aged. Neoplasm Staging. Treatment Outcome

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(PMID = 18348081.001).

[ISSN] 0018-5043

[Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme

[ISO-abbreviation] Horm. Metab. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Thyroid hormone is a MAPK-dependent growth factor for thyroid cancer cells and is anti-apoptotic.

Thyroid hormone (l-thyroxine, T(4), or 3,5,3'-triiodo-l-thyronine, T(3)) treatment of human papillary and follicular thyroid cancer cell lines resulted in enhanced cell proliferation, measured by proliferating cell nuclear antigen (PCNA).

Thyroid hormone also induced activation of the Ras/MAPK (ERK1/2) signal transduction pathway.

ERK1/2 activation and cell proliferation caused by thyroid hormone were blocked by an iodothyronine analogue, tetraiodothyroacetic acid (tetrac), that inhibits binding of iodothyronines to the cell surface receptor for thyroid hormone on integrin alphaVbeta3.

A MAPK cascade inhibitor at MEK, PD 98059, also blocked hormone-induced cell proliferation.

We then assessed the possibility that thyroid hormone is anti-apoptotic.

We first established that resveratrol (10 microM), a pro-apoptotic agent in other cancer cells, induced p53-dependent apoptosis and c-fos, c-jun and p21 gene expression in both papillary and follicular thyroid cancer cells.

Resveratrol-induced gene expression and apoptosis were inhibited more than 50% by physiological concentrations of T(4).

Thus, plasma membrane-initiated activation of the MAPK cascade by thyroid hormone promotes papillary and follicular thyroid cancer cell proliferation in vitro.

[MeSH-major] Apoptosis / physiology. Growth Substances / metabolism. Mitogen-Activated Protein Kinases / physiology. Thyroid Neoplasms / metabolism. Thyroxine / metabolism. Triiodothyronine / metabolism

[MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans

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(PMID = 17174366.001).

[ISSN] 0039-128X

[Journal-full-title] Steroids

[ISO-abbreviation] Steroids

[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 / Growth Substances; 06LU7C9H1V / Triiodothyronine; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; Q51BO43MG4 / Thyroxine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Glycemic index, glycemic load and thyroid cancer risk.

BACKGROUND: Risk of thyroid cancer has already been related to refined cereals and starch food, but the association has not been studied in terms of glycemic index (GI) and glycemic load (GL).

PATIENTS AND METHODS: We analyzed data from a case-control study conducted in Italy from 1986 to 1992 and including 399 histologically confirmed and incident cases of thyroid cancer and 616 control subjects.

Information on dietary habits was derived through a food-frequency questionnaire and multivariate odds ratios (ORs) for GI and GL levels were estimated with adjustment for age, education, sex, area of residence, history of diabetes, body mass index, smoking, alcohol consumption, intake of fruit and vegetables, and noncarbohydrate energy intake.

The OR for highest tertile of GI compared with lowest one was 1.70 for papillary and 1.57 for follicular thyroid cancer.

The ORs for GL were 2.17 for papillary and 3.33 for follicular thyroid cancer.

CONCLUSION: Our study shows that high dietary levels of GI and GL are associated with thyroid cancer risk.

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(PMID = 17951595.001).

[ISSN] 1569-8041

[Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology

[ISO-abbreviation] Ann. Oncol.

[Language] ENG

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Blood Glucose; 0 / Dietary Carbohydrates