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[PMID]:29197967
[Au] Autor:Allegri L; Rosignolo F; Mio C; Filetti S; Baldan F; Damante G
[Ad] Endereço:Department of Medical Area, University of Udine, 33100, Udine, Italy.
[Ti] Título:Effects of nutraceuticals on anaplastic thyroid cancer cells.
[So] Source:J Cancer Res Clin Oncol;144(2):285-294, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The anaplastic thyroid carcinoma (ATC) is the most aggressive thyroid cancer with a high mortality rate. Since nutraceuticals may exert beneficial effects on tumor biology, here, effects of four of these compounds [resveratrol, genistein, curcumin and epigallocatechin-3-gallate (EGCG)] on ATC cell lines were investigated. METHODS: Two ATC-derived cell lines were used: SW1736 and 8505C. Cell viability and in vitro aggressiveness was tested by MTT and soft agar assays. Apoptosis was investigated by Western Blot, using an anti-cleaved-PARP antibody. mRNA and miRNA levels were quantified by real-time PCR. RESULTS: All tested nutraceuticals caused in both cell lines decrease of cell viability and increase of apoptosis. In contrast, only curcumin reduced in vitro aggressiveness in both SW1736 and 8505C cell lines, while genistein and EGCG determined a reduction of colony formation only in 8505C cells. Effects on genes related to the thyroid-differentiated phenotype were also tested: resveratrol and genistein administration determined the increment of almost all tested mRNAs in both cell lines. Instead curcumin and EGCG treatments had opposite effects in the two cell lines, causing the increment of almost all the mRNAs in 8505C cells and their reduction in SW1736. Finally, effects of nutraceuticals on levels of several miRNAs, known as important in thyroid cancer progression (hsa-miR-221, hsa-miR-222, hsa-miR-21, hsa-miR-146b, hsa-miR-204), were tested. Curcumin induced a strong and significant reduction of all miR analyzed, except for has-miR-204, in both cell lines. CONCLUSIONS: Altogether, our results clearly indicate the anti-cancer proprieties of curcumin, suggesting the promising use of this nutraceutical in ATC treatment. Resveratrol, genistein and EGCG have heterogeneous effects on molecular features of ATC cells.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Suplementos Nutricionais
Carcinoma Anaplásico da Tireoide/tratamento farmacológico
Neoplasias da Glândula Tireoide/tratamento farmacológico
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Catequina/análogos & derivados
Catequina/farmacologia
Diferenciação Celular/efeitos dos fármacos
Processos de Crescimento Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Curcumina/farmacologia
Genisteína/farmacologia
Seres Humanos
MicroRNAs/biossíntese
MicroRNAs/genética
Estilbenos/farmacologia
Carcinoma Anaplásico da Tireoide/genética
Carcinoma Anaplásico da Tireoide/patologia
Neoplasias da Glândula Tireoide/genética
Neoplasias da Glândula Tireoide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (MicroRNAs); 0 (Stilbenes); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); DH2M523P0H (Genistein); IT942ZTH98 (Curcumin); Q369O8926L (resveratrol)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2555-7


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[PMID]:29331658
[Au] Autor:Chatterjee S; Rhee Y; Chung PS; Ge RF; Ahn JC
[Ad] Endereço:Beckman Laser Institute Korea, Dankook University, Cheonan 31116, Republic of Korea.
[Ti] Título:Sulforaphene Enhances The Efficacy of Photodynamic Therapy In Anaplastic Thyroid Cancer Through Ras/RAF/MEK/ERK Pathway Suppression.
[So] Source:J Photochem Photobiol B;179:46-53, 2018 Feb.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Sulforaphene (SFE), a natural isothiocyanate from cruciferous vegetables has shown a potential anticancer effect against cervical and lung cancer. Palliative treatments like photodynamic therapy (PDT) are being implemented for a long time however, the results are still not promising in case of aggressive cancers like anaplastic thyroid cancer. The objective of this work is to establish an alternative method with the combination of photofrin-PDT and sulforaphene, a natural isothiocyanate from cruciferous vegetables, against human anaplastic thyroid cancer to enhance the efficacy of PDT. In this study, cell viability of FRO cells due to combination treatment was analyzed by MTT assay, Cell cycle arrest, MMP depolarization and ROS generation, analyzed by flow cytometry. Western blot analysis of various proliferative proteins was performed to assess the activity of combination treatment against FRO cells. From the results, sulforaphene alone showed no cytotoxicity against normal cells, however, combination of sulforaphene and photofrin mediated PDT showed a noticeable decrease in cell proliferation against FRO cells. Combination treatment synergistically caused cell cycle arrest via ROS generation and MMP depolarization. The expressions of Ras, MEK, ERK, B-Raf proteins significantly modulated due to combination treatment. PDT and SFE can induce apoptosis in anaplastic thyroid cancer cells individually but while treated in combination, it enhanced the apoptotic and anti-proliferative effect, much higher than the individual doses. In summary, our work designates sulforaphene as a unique natural enhancer of efficacy with PDT against anaplastic thyroid cancer.
[Mh] Termos MeSH primário: MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Isotiocianatos/farmacologia
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Fármacos Fotossensibilizantes/farmacologia
Transdução de Sinais/efeitos dos fármacos
Quinases raf/metabolismo
Proteínas ras/metabolismo
[Mh] Termos MeSH secundário: Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Éter de Diematoporfirina/farmacologia
Éter de Diematoporfirina/uso terapêutico
MAP Quinases Reguladas por Sinal Extracelular/antagonistas & inibidores
Seres Humanos
Isotiocianatos/uso terapêutico
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Fotoquimioterapia
Fármacos Fotossensibilizantes/uso terapêutico
Inibidores de Proteínas Quinases/farmacologia
Inibidores de Proteínas Quinases/uso terapêutico
Espécies Reativas de Oxigênio/metabolismo
Carcinoma Anaplásico da Tireoide/tratamento farmacológico
Carcinoma Anaplásico da Tireoide/metabolismo
Carcinoma Anaplásico da Tireoide/patologia
Neoplasias da Glândula Tireoide/tratamento farmacológico
Neoplasias da Glândula Tireoide/metabolismo
Neoplasias da Glândula Tireoide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Isothiocyanates); 0 (Photosensitizing Agents); 0 (Protein Kinase Inhibitors); 0 (Reactive Oxygen Species); 0 (sulphoraphene); 97067-70-4 (Dihematoporphyrin Ether); EC 2.7.11.1 (raf Kinases); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180115
[St] Status:MEDLINE


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[PMID]:29190616
[Au] Autor:Jin Z; Cheng X; Feng H; Kuang J; Yang W; Peng C; Shen B; Qiu W
[Ad] Endereço:Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
[Ti] Título:Apatinib Inhibits Angiogenesis Via Suppressing Akt/GSK3ß/ANG Signaling Pathway in Anaplastic Thyroid Cancer.
[So] Source:Cell Physiol Biochem;44(4):1471-1484, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Anaplastic thyroid carcinoma (ATC) is one of the most lethal human malignancies, and there is no efficient method to slow its process. Apatinib, a novel tyrosine kinase inhibitor (TKI), has been confirmed for its efficacy and safety in the treatment of advanced gastric carcinoma patients. However, the effects of Apatinib in ATC are still unknown. METHODS: In this study, we explored the effects and mechanisms of Apatinib on tumor growth and angiogenesis in vitro and in vitro in ATC cells. Angiogenesis antibodies array was utilized to detect the expression of angiogenesis-related genes after Apatinib treatment in ATC cells. In addition, we used Akt activator, Akt inhibitor and GSK3ß inhibitor to further study the mechanism for how Apatinib suppressed angiogenesis. RESULTS: Apatinib treatment could suppress the growth of ATC cells in a dose- and time-dependent manner via inducing apoptosis and blocking cell cycle progression at G0/G1 phase. Moreover, Apatinib treatment decreased the expression of angiogenin (ANG) and inhibited angiogenesis of ATC cells in vitro and in vitro. We further confirmed that recombinant human ANG (rhANG) significantly abrogated Apatinib-mediated anti-angiogenic ability in ATC cells. Additionally, Apatinib treatment decreased the level of p-Akt and p-GSK3ß. Moreover, the Apatinib-mediated decrease of ANG and anti-angiogenic ability were partly reversed when an Akt activator, SC79, was administered. Furthermore, the anti-angiogenic ability of Apatinib can be enhanced in the presence of Akt inhibitor, and the inhibition of GSK3ß attenuated the anti-angiogenic ability of Apatinib. CONCLUSION: Our results demonstrated that Apatinib treatment inhibited tumor growth, and Apatinib-induced suppression of Akt/GSK3ß/ANG signaling pathway may play an important role in the inhibition of angiogenesis in ATC, supporting a potential therapeutic approach for using Apatinib in the treatment of ATC.
[Mh] Termos MeSH primário: Antineoplásicos/toxicidade
Neovascularização Fisiológica/efeitos dos fármacos
Piridinas/toxicidade
Transdução de Sinais/efeitos dos fármacos
Carcinoma Anaplásico da Tireoide/patologia
Neoplasias da Glândula Tireoide/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Glicogênio Sintase Quinase 3 beta/antagonistas & inibidores
Glicogênio Sintase Quinase 3 beta/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/genética
Proteínas Recombinantes/farmacologia
Ribonuclease Pancreático/genética
Ribonuclease Pancreático/metabolismo
Carcinoma Anaplásico da Tireoide/metabolismo
Neoplasias da Glândula Tireoide/metabolismo
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Pyridines); 0 (Recombinant Proteins); 5S371K6132 (apatinib); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.27.- (angiogenin); EC 3.1.27.5 (Ribonuclease, Pancreatic)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1159/000485583


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[PMID]:28860443
[Au] Autor:Yamazaki H; Shimizu S; Iwasaki H; Yoshida T; Suganuma N; Yamanaka T; Kojima I; Masudo K; Toda S; Nakayama H; Masuda M
[Ad] Endereço:Dept. of Breast and Endocrine Surgery, Kanagawa Cancer Center.
[Ti] Título:[Efficacy and Safety of Lenvatinib for Unresectable Anaplastic Thyroid Cancer].
[So] Source:Gan To Kagaku Ryoho;44(8):695-697, 2017 Aug.
[Is] ISSN:0385-0684
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:The 208 trial showed that lenvatinib has a significant antitumor effect on unresectable anaplastic thyroid cancer(ATC). Herein, we present a retrospective review of data from 7 patients with unresectable ATC who received lenvatinib in our hospital between May 2015 and October 2016. Two patients were men and 5 were women. The median age was 78(range, 72-85)years, and 1 patient had Stage IV A disease, 1 had Stage IV B, and 5 had Stage IV C at diagnosis, respectively. Three patients experienced a partial response and 1 patient experienced stable disease. The response rate was 43%, and the disease control rate was 57%. The median progression-free survival(PFS)was 4.1(range, 1.1-12.2)months. Grade 3 and Grade 4 gastrointestinal hemorrhage were observed in 2patients and Grade 3 anorexia was observed in 1 patient. Further clinical research seems to be needed to establish a treatment strategy involving lenvatinib for ATC.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Compostos de Fenilureia/uso terapêutico
Quinolinas/uso terapêutico
Carcinoma Anaplásico da Tireoide/tratamento farmacológico
Neoplasias da Glândula Tireoide/tratamento farmacológico
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/efeitos adversos
Feminino
Seres Humanos
Masculino
Compostos de Fenilureia/efeitos adversos
Quinolinas/efeitos adversos
Neoplasias da Glândula Tireoide/patologia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Phenylurea Compounds); 0 (Quinolines); EE083865G2 (lenvatinib)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE


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[PMID]:28727740
[Au] Autor:Kalimuthu S; Oh JM; Gangadaran P; Zhu L; Lee HW; Jeon YH; Jeong SY; Lee SW; Lee J; Ahn BC
[Ad] Endereço:Department of Nuclear Medicine, Kyungpook National University School of Medicine/Hospital, Daegu, Republic of Korea.
[Ti] Título:Genetically engineered suicide gene in mesenchymal stem cells using a Tet-On system for anaplastic thyroid cancer.
[So] Source:PLoS One;12(7):e0181318, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Anaplastic thyroid cancer (ATC) is the most aggressive malignancy of the thyroid, during which undifferentiated tumors arise from the thyroid follicular epithelium. ATC has a very poor prognosis due to its aggressive behavior and poor response to conventional therapies. Gene-directed enzyme/prodrug therapy using genetically engineered mesenchymal stromal cells (MSC) is a promising therapeutic strategy. The doxycycline (DOX)-controlled Tet inducible system is the most widely utilized regulatory system and could be a useful tool for therapeutic gene-based therapies. For example, use a synthetic "tetracycline-on" switch system to control the expression of the therapeutic gene thymidine kinase, which converts prodrugs to active drugs. The aim of this study was to develop therapeutic MSCs, harboring an inducible suicide gene, and to validate therapeutic gene expression using optical molecular imaging of ATC. We designed the Tet-On system using a retroviral vector expressing herpes simplex virus thymidine kinase (HSV1-sr39TK) with dual reporters (eGFP-Fluc2). Mouse bone marrow-derived mesenchymal stromal cells (BM-MSC) were transduced using this system with (MSC-Tet-TK/Fluc2) or without (MSC-TK/Fluc) the Tet-On system. Transduced cells were screened and characterized. Engineered MSCs were co-cultured with ATC (CAL62/Rluc) cells in the presence of the prodrug ganciclovir (GCV) and stimulated with DOX. The efficiency of cell killing monitored by assessing Rluc (CAL62/Rluc) and Fluc (MSC-Tet-TK/Fluc and MSC-TK/Fluc) activities using IVIS imaging. Fluc activity increased in MSC-Tet-TK/Fluc cells in a dose dependent manner following DOX treatment (R2 = 0.95), whereas no signal was observed in untreated cells. eGFP could also be visualized after induction with DOX, and the HSV1-TK protein could be detected by western blotting. In MSC-TK/Fluc cells, the Fluc activity increased with increasing cell number (R2 = 0.98), and eGFP could be visualized by fluorescence microscopy. The Fluc activity and cell viability of MSC-Tet-TK/Fluc and MSC-TK/Fluc cells decreased significantly following GCV treatment. A bystander effect of the therapeutic cells confirmed in co-cultures of CAL62 cells, an anaplastic thyroid cancer cell line, with either MSC-Tet-TK/Fluc cells or MSC-TK/Fluc cells. The Rluc activity in MSC-Tet-TK/Fluc co-cultures, derived from the CAL62/Rluc cells, decreased significantly with GCV treatment of DOX treated cultures, whereas no significant changes were observed in untreated cultures. In addition, the Fluc activity of MSC-Tet-TK/Fluc cells also decreased significantly with DOX treatment whereas no signal was present in untreated cultures. A bystander effect also be demonstrated in co-cultures with MSC-TK/Fluc cells and CAL62/Rluc; both the Rluc activity and the Fluc activity were significantly decreased following GCV treatment. We have successfully developed a Tet-On system of gene-directed enzyme/prodrug delivery using MSCs. We confirmed the therapeutic bystander effect in CAL62/Rluc cells with respect to MSC-Tet-TK/Fluc and MSC-TK/Fluc cells after GCV treatment with and without DOX. Our results confirm the therapeutic efficiency of a suicide gene, with or without the Tet-On system, for ATC therapy. In addition, our findings provide an innovative therapeutic approach for using the Tet-On system to eradicate tumors by simple, repeated administration of MSC-Tet-TK/Fluc cells with DOX and GCV.
[Mh] Termos MeSH primário: Genes Transgênicos Suicidas
Carcinoma Anaplásico da Tireoide/terapia
[Mh] Termos MeSH secundário: Animais
Engenharia Genética/métodos
Terapia Genética/métodos
Vetores Genéticos
Seres Humanos
Células Mesenquimais Estromais/fisiologia
Camundongos
Retroviridae
Tetraciclina/farmacologia
Carcinoma Anaplásico da Tireoide/genética
Carcinoma Anaplásico da Tireoide/patologia
Ativação Transcricional/efeitos dos fármacos
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
F8VB5M810T (Tetracycline)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181318


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[PMID]:28707679
[Au] Autor:Molinaro E; Romei C; Biagini A; Sabini E; Agate L; Mazzeo S; Materazzi G; Sellari-Franceschini S; Ribechini A; Torregrossa L; Basolo F; Vitti P; Elisei R
[Ad] Endereço:Endocrine Unit, Department of Clinical and Experimental Medicine, University Hospital of Pisa.
[Ti] Título:Anaplastic thyroid carcinoma: from clinicopathology to genetics and advanced therapies.
[So] Source:Nat Rev Endocrinol;13(11):644-660, 2017 Nov.
[Is] ISSN:1759-5037
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Anaplastic thyroid carcinoma (ATC) is a rare malignancy, accounting for 1-2% of all thyroid cancers. Although rare, ATC accounts for the majority of deaths from thyroid carcinoma. ATC often originates in a pre-existing thyroid cancer lesion, as suggested by the simultaneous presence of areas of differentiated or poorly differentiated thyroid carcinoma. ATC is characterized by the accumulation of several oncogenic alterations, and studies have shown that an increased number of oncogenic alterations equates to an increased level of dedifferentiation and aggressiveness. The clinical management of ATC requires a multidisciplinary approach; according to recent American Thyroid Association guidelines, surgery, radiotherapy and/or chemotherapy should be considered. In addition to conventional therapies, novel molecular targeted therapies are the most promising emerging treatment modalities. These drugs are often multiple receptor tyrosine kinase inhibitors, several of which have been tested in clinical trials with encouraging results so far. Accordingly, clinical trials are ongoing to evaluate the safety, efficacy and effectiveness of these new agents. This Review describes the updated clinical and pathological features of ATC and provides insight into the molecular biology of this disease. The most recent literature regarding conventional, newly available and future therapies for ATC is also discussed.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Inibidores de Proteínas Quinases/uso terapêutico
Radioterapia
Carcinoma Anaplásico da Tireoide/terapia
Neoplasias da Glândula Tireoide/terapia
Tireoidectomia
[Mh] Termos MeSH secundário: Fatores Etários
Transtornos de Deglutição/etiologia
Dispneia/etiologia
GTP Fosfo-Hidrolases/genética
Rouquidão/etiologia
Seres Humanos
Proteínas de Membrana/genética
Cervicalgia/etiologia
Estadiamento de Neoplasias
Proteínas Proto-Oncogênicas B-raf/genética
Proteínas Proto-Oncogênicas p21(ras)/genética
Exposição à Radiação/estatística & dados numéricos
Sons Respiratórios/etiologia
Fatores de Risco
Estilbenos/uso terapêutico
Telomerase/genética
Tiazolidinedionas/uso terapêutico
Carcinoma Anaplásico da Tireoide/complicações
Carcinoma Anaplásico da Tireoide/genética
Carcinoma Anaplásico da Tireoide/patologia
Neoplasias da Glândula Tireoide/complicações
Neoplasias da Glândula Tireoide/genética
Neoplasias da Glândula Tireoide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Protein Kinase Inhibitors); 0 (Stilbenes); 0 (Thiazolidinediones); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.7.49 (TERT protein, human); EC 2.7.7.49 (Telomerase); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (NRAS protein, human); EC 3.6.5.2 (HRAS protein, human); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras)); I5590ES2QZ (fosbretabulin); M17ILL71MC (efatutazone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1038/nrendo.2017.76


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[PMID]:28635233
[Au] Autor:Wang JF; Zhu XH; Tan Z; Ge MH
[Ad] Endereço:Department of Head and Neck Surgery, Zhejiang Province Cancer Hospital, Hangzhou 310022, China.
[Ti] Título:[Clinical characteristics and prognosis of anaplastic thyroid carcinoma].
[So] Source:Zhonghua Zhong Liu Za Zhi;39(6):434-438, 2017 Jun 23.
[Is] ISSN:0253-3766
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the clinical characteristics, treatment outcomes and prognostic factors in patients with anaplastic thyroid cancer. Clinical data of 56 patients with anaplastic thyroid cancer at Zhejiang Cancer Hospital from January 2006 to June 2016 were retrospectively reviewed and followed up. Of the 56 patients, there were 24 male and 32 female. The median age was 65 years old. At diagnosis, 10 patients have different degrees of breathing difficulty; 8 patients have varying degrees of dysphagia, and 12 patients have hoarseness. Distant metastases were found in 23 patients at presentation. Patient staging was performed in accordance with the tumor-node-metastasis system as follows: stage â…£A ( =19), stage â…£B ( =14) and stage â…£C ( =23). The median survival time of 56 patients was 4.5 months.The overall 1-year survival rate was 5.4%. Univariate analysis showed that radiotherapy and multimodality therapy were prognostic factors for 1-year overall survival (both of <0.05). The overall 1-year survival rate of the patients who received precision radiotherapy was 16.7%, which was higher than who received the other radiation therapy (4.0%, =0.040). Furthermore, the overall 1-year survival rate of the patients who received surgery combined with radiotherapy was 12.5%, which was higher than who received the other treatments(4.2%, =0.040). Multivariate analysis indicated that radiotherapy was independently associated with improved survival ( =0.020). Patients with anaplastic thyroid cancer should receive multimodality therapies combining surgery with radiotherapy. Radiotherapy is independently associated with improved overall survival. Notably, the precision radiotherapy that based on image guidance has a significantly beneficial impact on the prognosis of patients.
[Mh] Termos MeSH primário: Carcinoma Anaplásico da Tireoide
[Mh] Termos MeSH secundário: Adulto
Idoso
Análise de Variância
Terapia Combinada
Feminino
Seres Humanos
Masculino
Meia-Idade
Estadiamento de Neoplasias
Prognóstico
Estudos Retrospectivos
Taxa de Sobrevida
Carcinoma Anaplásico da Tireoide/mortalidade
Carcinoma Anaplásico da Tireoide/radioterapia
Carcinoma Anaplásico da Tireoide/secundário
Carcinoma Anaplásico da Tireoide/cirurgia
Neoplasias da Glândula Tireoide/mortalidade
Neoplasias da Glândula Tireoide/patologia
Neoplasias da Glândula Tireoide/radioterapia
Neoplasias da Glândula Tireoide/cirurgia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0253-3766.2017.06.007


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[PMID]:28552827
[Au] Autor:Xu B; Scognamiglio T; Cohen PR; Prasad ML; Hasanovic A; Tuttle RM; Katabi N; Ghossein RA
[Ad] Endereço:Department of Pathology, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada, M4N 3M5.
[Ti] Título:Metastatic thyroid carcinoma without identifiable primary tumor within the thyroid gland: a retrospective study of a rare phenomenon.
[So] Source:Hum Pathol;65:133-139, 2017 Jul.
[Is] ISSN:1532-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metastatic papillary thyroid carcinoma (PTC) without an identifiable primary tumor despite extensive microscopic examination of the thyroid gland is a rare but true phenomenon.We retrieved 7 of such cases and described in detail the clinical and pathologic features of these tumors. BRAF V600E immunohistochemistry and Sequenom molecular profile were conducted in selected cases. All patients harbored metastatic disease in the central (n=3), lateral (n=3), or both neck compartments (n=1). The histotype of the metastatic disease was PTC (n=5), poorly differentiated thyroid carcinoma in association with a PTC columnar variant (n=1), and anaplastic thyroid carcinoma in association with a PTC tall cell variant (n=1). Fibrosis was present in the thyroid of 5 patients. All patients with PTC were alive without evidence of recurrence. The 76-year-old patient with poorly differentiated thyroid carcinoma did not recur and died of unknown causes. Finally, the patient with anaplastic thyroid carcinoma was alive with distant metastasis at last follow-up. The median follow-up for this cohort was 2.2years (range, 0.8-17). BRAF V600E was detected in 4 of 6 cases by immunohistochemistry. In conclusion, metastatic nodal disease without identifiable thyroid primary is a rare but real phenomenon of unknown mechanisms. Although most tumors are low grade and well differentiated, aggressive behavior due to poorly differentiated or anaplastic carcinoma can happen. Most cases are BRAF -positive thyroid tumors. A papillary carcinoma phenotype is found in all reported cases.
[Mh] Termos MeSH primário: Carcinoma/secundário
Neoplasias Primárias Desconhecidas/patologia
Carcinoma Anaplásico da Tireoide/secundário
Neoplasias da Glândula Tireoide/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais/genética
Carcinoma/genética
Carcinoma/terapia
Carcinoma Papilar
Diferenciação Celular
Análise Mutacional de DNA
Feminino
Predisposição Genética para Doença
Seres Humanos
Imuno-Histoquímica
Metástase Linfática
Masculino
Meia-Idade
Mutação
Gradação de Tumores
Neoplasias Primárias Desconhecidas/genética
Neoplasias Primárias Desconhecidas/terapia
Fenótipo
Proteínas Proto-Oncogênicas B-raf/genética
Estudos Retrospectivos
Carcinoma Anaplásico da Tireoide/genética
Carcinoma Anaplásico da Tireoide/terapia
Neoplasias da Glândula Tireoide/genética
Neoplasias da Glândula Tireoide/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE


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[PMID]:28546130
[Au] Autor:Nonaka D
[Ad] Endereço:Department of Histopathology, The Christie NHS Foundation Trust, Manchester M20 4BX, UK; Institute of Cancer Sciences, The University of Manchester, Manchester M20 4BX, UK. Electronic address: DNonaka@msn.com.
[Ti] Título:A study of FoxA1 expression in thyroid tumors.
[So] Source:Hum Pathol;65:217-224, 2017 Jul.
[Is] ISSN:1532-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:FoxA1 regulates a variety of tissues during embryogenesis and early life. In thyroid, FoxA1 expression has recently been shown in C cells and medullary thyroid carcinomas but not in follicular cells. FoxA1 has also been proposed as a potential oncogene in anaplastic thyroid carcinomas. However, FoxA1 expression has not been extensively investigated in a spectrum of thyroid nonneoplastic lesions and tumors. A variety of thyroid tumors and lesions and their morphologic mimics were stained with monoclonal anti-FoxA1 antibody. For the medullary carcinomas, its expression pattern was compared with those of other conventional markers. All 67 medullary thyroid carcinomas (100%), including 1 calcitonin-negative medullary carcinoma, showed diffuse and strong FoxA1 nuclear expression. The expression pattern was homogeneous throughout the tumor. Expressions of other markers in medullary thyroid carcinomas were as follows: calcitonin, 94.7%; CEA, 91.2%; and chromogranin, 100%, generally in variable intensity. FoxA1 was completely negative in follicular neoplasms, papillary thyroid carcinomas, and poorly differentiated carcinomas, whereas it was expressed in 55% of anaplastic thyroid carcinomas (33/60) in variable intensity. FoxA1 was also strongly expressed in C-cell hyperplasia as well as solid cell nests. No FoxA1 expression was seen in thyroid gland affected by nodular hyperplasia, Hashimoto thyroiditis, and Graves disease, or in paragangliomas or parathyroid lesions. FoxA1 discriminates between medullary thyroid carcinoma and tumors of follicular derivation with sensitivity and specificity greater than calcitonin and CEA; therefore, it may serve as a reliable ancillary marker for the diagnosis of medullary thyroid carcinoma because of its reliably uniform quality of staining.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Carcinoma Neuroendócrino/química
Fator 3-alfa Nuclear de Hepatócito/análise
Carcinoma Anaplásico da Tireoide/química
Neoplasias da Glândula Tireoide/química
[Mh] Termos MeSH secundário: Biópsia
Calcitonina/análise
Antígeno Carcinoembrionário/análise
Carcinoma Neuroendócrino/patologia
Carcinoma Neuroendócrino/cirurgia
Cromograninas/análise
Diagnóstico Diferencial
Seres Humanos
Hiperplasia
Imuno-Histoquímica
Valor Preditivo dos Testes
Carcinoma Anaplásico da Tireoide/patologia
Carcinoma Anaplásico da Tireoide/cirurgia
Neoplasias da Glândula Tireoide/patologia
Neoplasias da Glândula Tireoide/cirurgia
Análise Serial de Tecidos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Carcinoembryonic Antigen); 0 (Chromogranins); 0 (FOXA1 protein, human); 0 (Hepatocyte Nuclear Factor 3-alpha); 9007-12-9 (Calcitonin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE


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[PMID]:28423545
[Au] Autor:Teng L; Deng W; Lu J; Zhang J; Ren X; Duan H; Chuai S; Duan F; Gao W; Lu T; Wu H; Liang Z
[Ad] Endereço:Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China.
[Ti] Título:Hobnail variant of papillary thyroid carcinoma: molecular profiling and comparison to classical papillary thyroid carcinoma, poorly differentiated thyroid carcinoma and anaplastic thyroid carcinoma.
[So] Source:Oncotarget;8(13):22023-22033, 2017 Mar 28.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: As a rare but aggressive papillary thyroid carcinoma (PTC) variant, the genetic changes of hobnail variant of PTC (HVPTC) are still unclear. RESULTS: The prevalence of HVPTC was 1.69% (18/1062) of all PTC diagnosed in our cohort. 73 samples from 55 patients (17 HVPTC, 26 CPTC, 7 PDTC and 5 ATC) were successfully analyzed using targeted NGS with an 18-gene panel. Thirty-seven mutation variant types were identified among 11 genes. BRAF V600E mutation was the most common mutation, which is present in almost all HVPTC samples (16/17, 94%), most CPTC samples (20/26, 77%), and none of the ATC and PDTC samples. TERT promoter mutation (C228T) was identified in 2 ATC and one HVPTC patient. RAS and TP53 mutation are almost exclusively present among ATC and PDTC samples although TP53 mutation was also observed in 3 HVPTC patients. Six different GNAS mutations were identified among 8 CPTC patients (31%) and none of the HVPTC patients. The only patient who died of disease progression harbored concomitant TERT C228T mutation, BRAF V600E mutation and TP53 mutation. METHODS: HVPTC cases were identified from a group of 1062 consecutive surgical specimens diagnosed as PTC between 2000 and 2010. Targeted next-generation sequencing (NGS) was applied to investigate the mutation spectrum of HVPTC, compared to classical PTC (CPTC), poorly differentiated thyroid carcinoma (PDTC) and anaplastic thyroid carcinoma (ATC). CONCLUSION: As an aggressive variant of PTC, HVPTC has relatively specific molecular features, which is somewhat different from both CPTC and ATC/PDTC and may underlie its relatively aggressive behavior.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Carcinoma Papilar/genética
Perfilação da Expressão Gênica
Mutação
Proteínas Proto-Oncogênicas B-raf/genética
Carcinoma Anaplásico da Tireoide/genética
Neoplasias da Glândula Tireoide/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/patologia
Adulto
Idoso
Carcinoma Papilar/patologia
Diferenciação Celular
Progressão da Doença
Feminino
Seguimentos
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Seres Humanos
Masculino
Meia-Idade
Estadiamento de Neoplasias
Prognóstico
Regiões Promotoras Genéticas
Taxa de Sobrevida
Carcinoma Anaplásico da Tireoide/patologia
Neoplasias da Glândula Tireoide/patologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15786



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