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  1 / 72589 MEDLINE  
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[PMID]:29505523
[Au] Autor:Kang X; Zeng Y; Liang J; Li J; Ren D; Chai L; Sun Z; Yu S; Wu X; Han W; Wang W
[Ad] Endereço:Department of Dermatology.
[Ti] Título:Aberrations and clinical significance of BRAF in malignant melanoma: A series of 60 cases in Chinese Uyghur.
[So] Source:Medicine (Baltimore);97(1):e9509, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Malignant melanoma (MM) is a highly malignant melanocytic tumor, it occurs mostly in the skin, the mucous membrane close to the skin, but also in the tunicae rhagoides and the pia mater. The Uyghur is the largest ethnic group living in the Xinjiang Uyghur Autonomous Region of China, accounting for 46% of the total population of 20 million. Large-scale studies on MMs in Asian countries are limited. This study aimed to investigate BRAF mRNA expression and mutations in Chinese Uyghur patients with MMs and to identify the clinical features associated with these parameters.Formalin-fixed, paraffin wax-embedded tumor sections from 60 MMs were analyzed for BRAF expression using reverse transcription polymerase chain reaction (RT-PCR). Exons 11 and 15 of BRAF were analyzed for the presence of mutations using PCR and DNA sequencing. Sixty MMs were followed by mobile phone for survival analysis.BRAF mRNA expression was higher in MMs than in pigmented moles and normal skin tissues. Fourteen of 60 MMs had BRAF mutations. The frequency of BRAF mutations was significantly higher in patients younger than 60 years (10/28, 4/32, P = .02). A significant difference was observed in the frequency of BRAF mutations among specimens of mucosal, acral, chronic sun-induced damage (CSD), and non-CSD MMs (2/10, 3/19, 8/25, 1/6, P = .002). No significant association was found among BRAF mutations, sex, ulceration, or lymph node metastasis. MMs lymph node metastasis (hazard ratio 2.54 [95% confidence interval 1.062 - 6.066], P = .01) affected survival.This study indicated that BRAF mutations and expression might serve as independent adverse prognostic factors in melanoma.
[Mh] Termos MeSH primário: Melanoma/genética
Proteínas Proto-Oncogênicas B-raf/genética
Neoplasias Cutâneas/genética
[Mh] Termos MeSH secundário: Idoso
Grupo com Ancestrais do Continente Asiático/genética
China/epidemiologia
Feminino
Seres Humanos
Masculino
Melanoma/metabolismo
Melanoma/mortalidade
Meia-Idade
Mutação
Proteínas Proto-Oncogênicas B-raf/metabolismo
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/mortalidade
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009509


  2 / 72589 MEDLINE  
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[PMID]:29363351
[Au] Autor:Faghfuri E; Nikfar S; Niaz K; Faramarzi MA; Abdollahi M
[Ad] Endereço:a Pharmaceutical Biotechnology, Faculty of Pharmacy , Tehran University of Medical Sciences , Tehran , Iran.
[Ti] Título:Mitogen-activated protein kinase (MEK) inhibitors to treat melanoma alone or in combination with other kinase inhibitors.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):317-330, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Malignant melanoma (MM) is an aggressive disease with a rapidly rising incidence due to neoplasm of melanocytes. Molecular targeted therapies have demonstrated lower toxicity and improved overall survival versus conventional therapies of MM. The revealing of mutations in the BRAF/MEK/ERK pathway has led to the development of BRAF inhibitors such as vemurafenib and dabrafenib for the treatment of cutaneous MM. Though, progression of resistance to these agents has prompted attempts to target downstream proteins in this pathway. Trametinib, a MEK1/2 inhibitor, was approved in 2013 for the treatment of BRAF V600E/K mutation-positive unresectable or metastatic cutaneous melanoma patients. Areas covered: The aim of the current review is to present an update on the role of MEK in progressive melanomas and summarize latest results of clinical studies with innovative MEK inhibitors and/or combined approaches with other kinase inhibitors such as BRAF inhibitors in the treatment of MM. Expert opinion: Two combined treatments (i.e. trametinib plus dabrafenib and vemurafenib plus cobimetinib) target two different kinases in the BRAF/MEK/ERK pathway. The simultaneous prohibition of both MEK and BRAF is associated with more durable response rate than BRAF monotherapy and can overcome acquired resistance.
[Mh] Termos MeSH primário: Melanoma/tratamento farmacológico
Inibidores de Proteínas Quinases/administração & dosagem
Neoplasias Cutâneas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Resistência a Medicamentos Antineoplásicos
Seres Humanos
Melanoma/genética
Melanoma/patologia
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Terapia de Alvo Molecular
Mutação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas B-raf/genética
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1432593


  3 / 72589 MEDLINE  
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[PMID]:29185092
[Au] Autor:Ma M; Dai J; Xu T; Yu S; Yu H; Tang H; Yan J; Wu X; Yu J; Chi Z; Si L; Cui C; Sheng X; Kong Y; Guo J
[Ad] Endereço:Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Renal Cancer and Melanoma, Peking University Cancer Hospital and Institute, 52 Fucheng Road, Beijing, 100142, China.
[Ti] Título:Analysis of TSC1 mutation spectrum in mucosal melanoma.
[So] Source:J Cancer Res Clin Oncol;144(2):257-267, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Mucosal melanoma is a relatively rare subtype of melanoma for which no clearly established therapeutic strategy exists. The genes of the mTOR signalling pathway have drawn great attention as key targets for cancer treatment, including melanoma. In this study, we aimed to investigate the mutation status of the upstream mTOR regulator TSC1 and evaluated its correlation with the clinicopathological features of mucosal melanoma. METHODS: We collected 91 mucosal melanoma samples for detecting TSC1 mutations. All the coding exons of TSC1 were amplified by PCR and subjected to Sanger sequencing. Expression level of TSC1 encoding protein (hamartin) was detected by immunohistochemistry. The activation of mTOR pathway was determined by evaluating the phosphorylation status of S6RP and 4E-BP1. RESULTS: The overall mutation frequency of TSC1 was found to be 17.6% (16/91 patients). TSC1 mutations were more inclined to occur in advanced mucosal melanoma (stages III and IV). In the 16 patients with TSC1 mutations, 14 different mutations were detected, affecting 11 different exons. TSC1 mutations were correlated with upregulation of S6RP phosphorylation but were unrelated to 4E-BP1 phosphorylation or hamartin expression. Mucosal melanoma patients with TSC1 mutations had a worse outcome than patients without TSC1 mutations (24.0 versus 34.0 months, P = 0.007). CONCLUSIONS: Our findings suggest that TSC1 mutations are frequent in mucosal melanoma. TSC1 mutations can activate the mTOR pathway through phospho-S6RP and might be a poor prognostic predictor of mucosal melanoma. Our data implicate the potential significance of TSC1 mutations for effective and specific drug therapy for mucosal melanoma.
[Mh] Termos MeSH primário: Melanoma/genética
Mutação
Proteínas Supressoras de Tumor/genética
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Análise Mutacional de DNA
Feminino
Seres Humanos
Masculino
Melanoma/metabolismo
Melanoma/patologia
Meia-Idade
Membrana Mucosa/patologia
Estadiamento de Neoplasias
Fosfoproteínas/metabolismo
Prognóstico
Proteína S6 Ribossômica/metabolismo
Serina-Treonina Quinases TOR/metabolismo
Proteínas Supressoras de Tumor/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (EIF4EBP1 protein, human); 0 (Phosphoproteins); 0 (Ribosomal Protein S6); 0 (Tumor Suppressor Proteins); 0 (tuberous sclerosis complex 1 protein); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases)
[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:171130
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2550-z


  4 / 72589 MEDLINE  
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[PMID]:28468914
[Au] Autor:Engel C; Brügmann G; Lambing S; Mühlenbeck LH; Marx S; Hagen C; Horváth D; Goldeck M; Ludwig J; Herzner AM; Drijfhout JW; Wenzel D; Coch C; Tüting T; Schlee M; Hornung V; Hartmann G; Van den Boorn JG
[Ad] Endereço:Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital Bonn, Bonn, Germany.
[Ti] Título:RIG-I Resists Hypoxia-Induced Immunosuppression and Dedifferentiation.
[So] Source:Cancer Immunol Res;5(6):455-467, 2017 Jun.
[Is] ISSN:2326-6074
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A hypoxic tumor microenvironment is linked to poor prognosis. It promotes tumor cell dedifferentiation and metastasis and desensitizes tumor cells to type-I IFN, chemotherapy, and irradiation. The cytoplasmic immunoreceptor retinoic acid-inducible gene-I (RIG-I) is ubiquitously expressed in tumor cells and upon activation by 5'-triphosphate RNA (3pRNA) drives the induction of type I IFN and immunogenic cell death. Here, we analyzed the impact of hypoxia on the expression of RIG-I in various human and murine tumor and nonmalignant cell types and further investigated its function in hypoxic murine melanoma. 3pRNA-inducible RIG-I-expression was reduced in hypoxic melanoma cells compared with normoxic controls, a phenomenon that depended on the hypoxia-associated transcription factor HIF1α. Still, RIG-I functionality was conserved in hypoxic melanoma cells, whereas responsiveness to recombinant type-I IFN was abolished, due to hypoxia-induced loss of type I IFN receptor expression. Likewise, RIG-I activation in hypoxic melanoma cells, but not exposure to recombinant IFNα, provoked melanocyte antigen-specific CD8 T-cell and NK-cell attack. Scavenging of hypoxia-induced reactive oxygen species by vitamin C restored the inducible expression of RIG-I under hypoxia , boosted anti-melanoma NK- and CD8 T-cell attack, and augmented 3pRNA antitumor efficacy These results demonstrate that RIG-I remains operational under hypoxia and that RIG-I function is largely insensitive to lower cell surface expression of the IFNα receptor. RIG-I function could be fortified under hypoxia by the combined use of 3pRNA with antioxidants. .
[Mh] Termos MeSH primário: Hipóxia/metabolismo
Tolerância Imunológica
Melanoma/metabolismo
Receptores do Ácido Retinoico/metabolismo
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Ácido Ascórbico/farmacologia
Linhagem Celular
Linhagem Celular Tumoral
Feminino
Técnicas de Inativação de Genes
Seres Humanos
Camundongos Endogâmicos C57BL
RNA/farmacologia
Espécies Reativas de Oxigênio/metabolismo
Receptores do Ácido Retinoico/genética
Baço/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (RARRES3 protein, human); 0 (Reactive Oxygen Species); 0 (Receptors, Retinoic Acid); 63231-63-0 (RNA); PQ6CK8PD0R (Ascorbic Acid)
[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:170505
[St] Status:MEDLINE
[do] DOI:10.1158/2326-6066.CIR-16-0129-T


  5 / 72589 MEDLINE  
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[PMID]:28463413
[Au] Autor:da Silveira Nogueira Lima JP; Georgieva M; Haaland B; de Lima Lopes G
[Ad] Endereço:Drug Development Unit, Institute of Cancer Research, Sutton, United Kingdom.
[Ti] Título:A systematic review and network meta-analysis of immunotherapy and targeted therapy for advanced melanoma.
[So] Source:Cancer Med;6(6):1143-1153, 2017 Jun.
[Is] ISSN:2045-7634
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immune and BRAF-targeted therapies have changed the therapeutic scenario of advanced melanoma, turning the clinical decision-making a challenging task. This Bayesian network meta-analysis assesses the role of immunotherapies and targeted therapies for advanced melanoma. We retrieved randomized controlled trials testing immune, BRAF- or MEK-targeted therapies for advanced melanoma from electronic databases. A Bayesian network model compared therapies using hazard ratio (HR) for overall survival (OS), progression-free survival (PFS), and odds ratio (OR) for response rate (RR), along with 95% credible intervals (95% CrI), and probabilities of drugs outperforming others. We assessed the impact of PD-L1 expression on immunotherapy efficacy. Sixteen studies evaluating eight therapies in 6849 patients were analyzed. For OS, BRAF-MEK combination and PD-1 single agent ranked similarly and outperformed all other treatments. For PFS, BRAF-MEK combination surpassed all other options, including CTLA-4-PD-1 dual blockade hazard ratio (HR: 0.56; 95% CrI: 0.33-0.97; probability better 96.2%), whereas BRAF single agent ranked close to CTLA-4-PD-1 blockade. For RR, BRAF-MEK combination was superior to all treatments including CTLA-4-PD-1 (OR: 2.78; 1.18-6.30; probability better 97.1%). No OS data were available for CTLA-4-PD-1 blockade at the time of systematic review, although PFS and RR results suggested that this combination could also bring meaningful benefit. PD-L1 expression, as presently defined, failed to inform patient selection to PD-1-based immunotherapy. BRAF-MEK combination seemed an optimal therapy for BRAF-mutated patients, whereas PD-1 inhibitors seemed optimal for BRAF wild-type patients. Longer follow-up is needed to ascertain the role of CTLA-4-PD-1 blockade. Immunotherapy biomarkers remain as an unmet need.
[Mh] Termos MeSH primário: Antineoplásicos Imunológicos/uso terapêutico
Imunoterapia
Melanoma/terapia
Terapia de Alvo Molecular
[Mh] Termos MeSH secundário: Intervalo Livre de Doença
Seres Humanos
Melanoma/tratamento farmacológico
Ensaios Clínicos Controlados Aleatórios como Assunto
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents, Immunological)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.1002/cam4.1001


  6 / 72589 MEDLINE  
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[PMID]:28922786
[Au] Autor:Suciu S; Eggermont AMM; Lorigan P; Kirkwood JM; Markovic SN; Garbe C; Cameron D; Kotapati S; Chen TT; Wheatley K; Ives N; de Schaetzen G; Efendi A; Buyse M
[Ad] Endereço:European Organisation for Research and Treatment of Cancer Headquarters, Brussels, Belgium; Gustave Roussy Cancer Campus Grand Paris, Villejuif, France; The Christie NHS Foundation Trust, Manchester, UK; University of Pittsburgh Cancer Institute and School of Medicine, Pittsburgh, PA; Mayo Clinic Ro
[Ti] Título:Relapse-Free Survival as a Surrogate for Overall Survival in the Evaluation of Stage II-III Melanoma Adjuvant Therapy.
[So] Source:J Natl Cancer Inst;110(1), 2018 Jan 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: We assessed whether relapse-free survival (RFS; time until recurrence/death) is a valid surrogate for overall survival (OS) among resected stage II-III melanoma patients through a meta-analysis of randomized controlled trials. Methods: Individual patient data (IPD) on RFS and OS were collected from 5826 patients enrolled in 11 randomized adjuvant trials comparing interferon (IFN) to observation. In addition, IPD from two studies comparing IFN and vaccination in 989 patients were included. A two-level modeling approach was used for assessing Spearman's patient-level correlation (rho) of RFS and OS and the trial-level coefficient of determination (R²) of the treatment effects on RFS and on OS. The results were validated externally in 13 adjuvant studies without available IPD. We then tested the results on the European Organisation for Research and Treatment of Cancer (EORTC) 18071 double-blind trial comparing ipilimumab 10 mg/kg with placebo, which showed a statistically significant impact of the checkpoint inhibitor on RFS and OS. All statistical tests were two-sided. Results: With a median follow-up of seven years, 12 of 13 trials showed a consistency between the IFN vs No IFN differences regarding RFS (hazard ratio [HR]RFS = 0.88) and OS (HROS = 0.91), but the small trial, Eastern Cooperative Oncology Group 2696, was an outlier (HRRFS = 0.72 vs HROS = 1.11). Therefore, even if rho was high, R² was low and could not reliably be estimated. Based on the 12 trials, rho remained high (0.89), and the hazard ratios for RFS and OS were strongly correlated (R² = 0.91). The surrogate threshold effect for RFS was estimated to be 0.77. For the EORTC 18071 trial, the hazard ratio for RFS was 0.75, predicting an effect of ipilimumab on OS. This was subsequently confirmed (HROS = 0.72, 95.1% confidence interval = 0.58 to 0.88, P = .001). Conclusions: In high-risk stage II-III melanoma, RFS appeared to be a valid surrogate end point for OS for adjuvant randomized studies assessing interferon or a checkpoint inhibitor. In future similar adjuvant studies, a hazard ratio for RFS of 0.77 or less would predict a treatment impact on OS.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Antineoplásicos/uso terapêutico
Interferon-alfa/uso terapêutico
Melanoma/tratamento farmacológico
Melanoma/mortalidade
Neoplasias Cutâneas/tratamento farmacológico
Neoplasias Cutâneas/mortalidade
[Mh] Termos MeSH secundário: Quimioterapia Adjuvante
Intervalo Livre de Doença
Seres Humanos
Ipilimumab
Melanoma/patologia
Melanoma/cirurgia
Estadiamento de Neoplasias
Ensaios Clínicos Controlados Aleatórios como Assunto
Neoplasias Cutâneas/patologia
Neoplasias Cutâneas/cirurgia
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 0 (Interferon-alpha); 0 (Ipilimumab)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx133


  7 / 72589 MEDLINE  
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[PMID]:29295999
[Au] Autor:Han S; Ren Y; He W; Liu H; Zhi Z; Zhu X; Yang T; Rong Y; Ma B; Purwin TJ; Ouyang Z; Li C; Wang X; Wang X; Yang H; Zheng Y; Aplin AE; Liu J; Shao Y
[Ad] Endereço:Frontier Institute of Science and Technology, and Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, China.
[Ti] Título:ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma.
[So] Source:Nat Commun;9(1):28, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In human mutant BRAF melanoma cells, the stemness transcription factor FOXD3 is rapidly induced by inhibition of ERK1/2 signaling and mediates adaptive resistance to RAF inhibitors. However, the mechanism underlying ERK signaling control of FOXD3 expression remains unknown. Here we show that SOX10 is both necessary and sufficient for RAF inhibitor-induced expression of FOXD3 in mutant BRAF melanoma cells. SOX10 activates the transcription of FOXD3 by binding to a regulatory element in FOXD3 promoter. Phosphorylation of SOX10 by ERK inhibits its transcription activity toward multiple target genes by interfering with the sumoylation of SOX10 at K55, which is essential for its transcription activity. Finally, depletion of SOX10 sensitizes mutant BRAF melanoma cells to RAF inhibitors in vitro and in vivo. Thus, our work discovers a novel phosphorylation-dependent regulatory mechanism of SOX10 transcription activity and completes an ERK1/2/SOX10/FOXD3/ERBB3 axis that mediates adaptive resistance to RAF inhibitors in mutant BRAF melanoma cells.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica/genética
Melanoma/genética
Mutação
Proteínas Proto-Oncogênicas B-raf/genética
Fatores de Transcrição SOXE/genética
Neoplasias Cutâneas/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Inibidores Enzimáticos/farmacologia
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/metabolismo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Indóis/farmacologia
Melanoma/tratamento farmacológico
Melanoma/metabolismo
Camundongos Endogâmicos BALB C
Camundongos Nus
Fosforilação
Proteínas Proto-Oncogênicas B-raf/metabolismo
Interferência de RNA
Receptor ErbB-3/genética
Receptor ErbB-3/metabolismo
Fatores de Transcrição SOXE/metabolismo
Neoplasias Cutâneas/tratamento farmacológico
Neoplasias Cutâneas/metabolismo
Sulfonamidas/farmacologia
Sumoilação
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (FOXD3 protein, human); 0 (Forkhead Transcription Factors); 0 (Indoles); 0 (SOX10 protein, human); 0 (SOXE Transcription Factors); 0 (Sulfonamides); 207SMY3FQT (vemurafenib); EC 2.7.10.1 (ERBB3 protein, human); EC 2.7.10.1 (Receptor, ErbB-3); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02354-x


  8 / 72589 MEDLINE  
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[PMID]:29292905
[Au] Autor:Henriksson R; Falkenius J; Norin S; Öhman D; Abrahamsson M; Lindquist M; Lööv SÅ
[Ad] Endereço:Onkologi & Patologi - Regionalt Cancercentrum STOCKHOLM, Sweden Onkologi & Patologi - Regionalt Cancercentrum STOCKHOLM, Sweden.
[Ti] Título:Register för nya läkemedel i cancervården ger värdefull hjälp - Visar en bra bild av hur läkemedlen används ­ patienten kan följas i den kliniska vardagen..
[So] Source:Lakartidningen;114, 2017 Nov 06.
[Is] ISSN:1652-7518
[Cp] País de publicação:Sweden
[La] Idioma:swe
[Ab] Resumo:Register for new drugs in cancer care provides a picture of how the drugs are used in the daily clinical practice Today, an increasing number of cancer drugs are approved before traditional well-controlled phase 3 studies have been conducted and in many registration studies there is no participation of Swedish departments. This article describes the general experience of a caregiver initiated systematic follow-up of new cancer drugs that shows the possibility of obtaining a picture of the drug's use in routine care. From the register "New Pharmaceuticals in Cancer care", registrations from Stockholm-Gotland region are reported. The structure of the registry can be used with advantage in other therapeutic areas than cancer and can be supplemented with data from national and regional registers as well as quality registers including patient experiences. The knowledge is important to many actors in health care and can contribute to an evidence based, patient-safe and equal healthcare in accordance with current guidelines.
[Mh] Termos MeSH primário: Antineoplásicos
Neoplasias/tratamento farmacológico
Sistema de Registros
[Mh] Termos MeSH secundário: Androstenos/uso terapêutico
Antineoplásicos/administração & dosagem
Antineoplásicos/uso terapêutico
Bevacizumab/uso terapêutico
Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/mortalidade
Neoplasias Colorretais/tratamento farmacológico
Neoplasias Colorretais/mortalidade
Uso de Medicamentos
Seres Humanos
Ipilimumab/uso terapêutico
Masculino
Melanoma/tratamento farmacológico
Melanoma/mortalidade
Neoplasias/mortalidade
Cuidados Paliativos/métodos
Feniltioidantoína/análogos & derivados
Feniltioidantoína/uso terapêutico
Projetos Piloto
Neoplasias da Próstata/tratamento farmacológico
Neoplasias da Próstata/mortalidade
Rádio (Elemento)/uso terapêutico
Taxa de Sobrevida
Suécia/epidemiologia
Suspensão de Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androstenes); 0 (Antineoplastic Agents); 0 (Ipilimumab); 0 (MDV 3100); 0 (Radium-223); 2010-15-3 (Phenylthiohydantoin); 2S9ZZM9Q9V (Bevacizumab); G819A456D0 (abiraterone); W90AYD6R3Q (Radium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE


  9 / 72589 MEDLINE  
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[PMID]:29191943
[Au] Autor:Karimkhani C; Reddy BY; Dellavalle RP; Sundararajan S
[Ad] Endereço:Department of Dermatology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA ck2525@caa.columbia.edu.
[Ti] Título:Novel therapies for unresectable and metastatic melanoma.
[So] Source:BMJ;359:j5174, 2017 11 30.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Melanoma/secundário
Terapia de Alvo Molecular/métodos
Proteínas Proto-Oncogênicas B-raf/antagonistas & inibidores
Neoplasias Cutâneas/secundário
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/efeitos adversos
Anticorpos Monoclonais/uso terapêutico
Anticorpos Monoclonais Humanizados/efeitos adversos
Anticorpos Monoclonais Humanizados/uso terapêutico
Antineoplásicos Imunológicos/efeitos adversos
Antineoplásicos Imunológicos/uso terapêutico
Ensaios Clínicos Fase III como Assunto
Intervalo Livre de Doença
Quimioterapia Combinada
Feminino
Seres Humanos
Imunoterapia/economia
Imunoterapia/métodos
Ipilimumab/uso terapêutico
Melanoma/tratamento farmacológico
Melanoma/patologia
Melanoma/cirurgia
Meia-Idade
Terapia de Alvo Molecular/economia
Proteínas Proto-Oncogênicas B-raf/efeitos dos fármacos
Proteínas Proto-Oncogênicas B-raf/genética
Ensaios Clínicos Controlados Aleatórios como Assunto
Neoplasias Cutâneas/tratamento farmacológico
Neoplasias Cutâneas/imunologia
Neoplasias Cutâneas/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents, Immunological); 0 (Ipilimumab); 31YO63LBSN (nivolumab); DPT0O3T46P (pembrolizumab); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.j5174


  10 / 72589 MEDLINE  
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[PMID]:28460440
[Au] Autor:Massari NA; Nicoud MB; Sambuco L; Cricco GP; Martinel Lamas DJ; Herrero Ducloux MV; Blanco H; Rivera ES; Medina VA
[Ad] Endereço:Laboratory of Radioisotopes, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina.
[Ti] Título:Histamine therapeutic efficacy in metastatic melanoma: Role of histamine H4 receptor agonists and opportunity for combination with radiation.
[So] Source:Oncotarget;8(16):26471-26491, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aims of the work were to improve our knowledge of the role of H4R in melanoma proliferation and assess in vivo the therapeutic efficacy of histamine, clozapine and JNJ28610244, an H4R agonist, in a preclinical metastatic model of melanoma. Additionally, we aimed to investigate the combinatorial effect of histamine and gamma radiation on the radiobiological response of melanoma cells.Results indicate that 1205Lu metastatic melanoma cells express H4R and that histamine inhibits proliferation, in part through the stimulation of the H4R, and induces cell senescence and melanogenesis. Daily treatment with H4R agonists (1 mg/kg, sc) exhibited a significant in vivo antitumor effect and importantly, compounds reduced metastatic potential, particularly in the group treated with JNJ28610244, the H4R agonist with higher specificity. H4R is expressed in benign and malignant lesions of melanocytic lineage, highlighting the potential clinical use of histamine and H4R agonists. In addition, histamine increased radiosensitivity of melanoma cells in vitro and in vivo. We conclude that stimulation of H4R by specific ligands may represent a novel therapeutic strategy in those tumors that express this receptor. Furthermore, through increasing radiation-induced response, histamine could improve cancer radiotherapy for the treatment of melanoma.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Histamina/farmacologia
Melanoma/metabolismo
Melanoma/patologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Biomarcadores
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Senescência Celular/efeitos dos fármacos
Terapia Combinada
Modelos Animais de Doenças
Histamina/uso terapêutico
Seres Humanos
Imuno-Histoquímica
Indóis/farmacologia
Melanoma/terapia
Camundongos
Camundongos Nus
Metástase Neoplásica
Estadiamento de Neoplasias
Oximas/farmacologia
Radiação Ionizante
Receptores Histamínicos H4/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers); 0 (Indoles); 0 (JNJ28610244); 0 (Oximes); 0 (Receptors, Histamine H4); 820484N8I3 (Histamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15594



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