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[PMID]:28745321
[Au] Autor:Andò S; Malivindi R; Catalano S; Rizza P; Barone I; Panza S; Rovito D; Emprou C; Bornert JM; Laverny G; Metzger D
[Ad] Endereço:Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Arcavacata di Rende (CS), Italy.
[Ti] Título:Conditional expression of Ki-Ras in the mammary epithelium of transgenic mice induces estrogen receptor alpha (ERα)-positive adenocarcinoma.
[So] Source:Oncogene;36(46):6420-6431, 2017 Nov 16.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Appropriate 'in vivo' models are crucial for studying breast cancer biology and evaluating the efficacy of therapeutic agents. Thus we engineered a novel transgenic mouse line expressing the human Ki-Ras bearing an activating mutation (Ki-Ras ) selectively in the mammary epithelium after lactation. These mice develop invasive ductal adenocarcinomas with 100% incidence within 3-9 months after Ki-Ras induction. Immunophenotyping revealed that the mammary tumors express luminal markers, are positive for estrogen and progesterone receptors, negative for HER2 and have a low proliferation index. Moreover, cell lines derived from such tumors are estrogen-responsive and, when transplanted into nude mice, form tumors that respond to the antiestrogen ICI 182780. In conclusion, the mammary tumors of these transgenic mice and the derived cell lines exhibit key features of the major form of human breast cancer, that is, luminal A subtype and thus have a high potential for breast cancer research and treatment.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Epitélio/metabolismo
Receptor alfa de Estrogênio/genética
Genes ras/genética
Glândulas Mamárias Animais/metabolismo
Neoplasias Mamárias Experimentais/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Animais
Estradiol/análogos & derivados
Estradiol/farmacologia
Antagonistas do Receptor de Estrogênio/farmacologia
Receptor alfa de Estrogênio/metabolismo
Feminino
Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Células MCF-7
Neoplasias Mamárias Experimentais/tratamento farmacológico
Neoplasias Mamárias Experimentais/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Nus
Camundongos Transgênicos
Mutação de Sentido Incorreto
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor Antagonists); 0 (Estrogen Receptor alpha); 22X328QOC4 (fulvestrant); 4TI98Z838E (Estradiol)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.252


  2 / 12052 MEDLINE  
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[PMID]:28985944
[Au] Autor:Fontana C; Kirsch A; Seidel C; Marpeaux L; Darne C; Gaté L; Remy A; Guichard Y
[Ad] Endereço:Institut National de Recherche et de Sécurité, Département de Toxicologie et de Biométrologie, 1 rue du Morvan, CS 60027, 54519 VandÅ“uvre Cedex, France.
[Ti] Título:In vitro cell transformation induced by synthetic amorphous silica nanoparticles.
[So] Source:Mutat Res;823:22-27, 2017 Nov.
[Is] ISSN:1873-135X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Synthetic amorphous silica nanoparticles (SAS) are among the most widely produced and used nanomaterials, but little is known about their carcinogenic potential. This study aims to evaluate the ability of four different SAS, two precipitated, NM-200 and NM-201, and two pyrogenic, NM-202 and NM-203, to induce the transformation process. For this, we used the recently developed in vitro Bhas 42 cell transformation assay (CTA). The genome of the transgenic Bhas 42 cells contains several copies of the v-Ha-ras gene, making them particularly sensitive to tumor-promoter agents. The Bhas 42 CTA, which includes an initiation assay and a promotion assay, was validated in our laboratory using known soluble carcinogenic substances. Its suitability for particle-type substances was verified by using quartz Min-U-Sil 5 (Min-U-Sil) and diatomaceous earth (DE) microparticles. As expected given their known transforming properties, Min-U-Sil responded positively in the Bhas 42 CTA and DE responded negatively. Transformation assays were performed with SAS at concentrations ranging from 2µg/cm to 80µg/cm . Results showed that all SAS have the capacity to induce transformed foci, interestingly only in the promotion assay, suggesting a mode of action similar to tumor-promoter substances. NM-203 exhibited transforming activity at a lower concentration than the other SAS. In conclusion, this study showed for the first time the transforming potential of different SAS, which act as tumor-promoter substances in the Bhas 42 model of cell transformation.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/metabolismo
Nanopartículas/toxicidade
Dióxido de Silício/toxicidade
[Mh] Termos MeSH secundário: Animais
Células 3T3 BALB
Carcinogênese/efeitos dos fármacos
Carcinogênese/metabolismo
Testes de Carcinogenicidade
Carcinógenos/toxicidade
Transformação Celular Neoplásica/induzido quimicamente
Genes ras
Camundongos
Tamanho da Partícula
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 7631-86-9 (Silicon Dioxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171008
[St] Status:MEDLINE


  3 / 12052 MEDLINE  
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[PMID]:28982179
[Au] Autor:Minchom A; Thavasu P; Ahmad Z; Stewart A; Georgiou A; O'Brien MER; Popat S; Bhosle J; Yap TA; de Bono J; Banerji U
[Ad] Endereço:The Lung Unit, Department of Medicine, The Royal Marsden, Sutton, United Kingdom.
[Ti] Título:A study of PD-L1 expression in KRAS mutant non-small cell lung cancer cell lines exposed to relevant targeted treatments.
[So] Source:PLoS One;12(10):e0186106, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We investigated PD-L1 changes in response to MEK and AKT inhibitors in KRAS mutant lung adenocarcinoma (adeno-NSCLC). PD-L1 expression was quantified using immunofluorescence and co-culture with a jurkat cell-line transfected with NFAT-luciferase was used to study if changes in PD-L1 expression in cancer cell lines were functionally relevant. Five KRAS mutant cell lines with high PD-L1 expression (H441, H2291, H23, H2030 and A549) were exposed to GI50 inhibitor concentrations of a MEK inhibitor (trametinib) and an AKT inhibitor (AZD5363) for 3 weeks. Only 3/5 (H23, H2030 and A549) and 2/5 cell lines (H441 and H23) showed functionally significant increases in PD-L1 expression when exposed to trametinib or AZD5363 respectively. PD-L1 overexpression is not consistent and is unlikely to be an early mechanism of resistance to KRAS mutant adeno-NSCLC treated with MEK or AKT inhibitors.
[Mh] Termos MeSH primário: Antígeno B7-H1/metabolismo
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Genes ras
Neoplasias Pulmonares/metabolismo
Mutação
[Mh] Termos MeSH secundário: Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular Tumoral
Técnicas de Cocultura
Seres Humanos
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (CD274 protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186106


  4 / 12052 MEDLINE  
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[PMID]:28982163
[Au] Autor:Brandt LP; Albers J; Hejhal T; Catalano A; Wild PJ; Frew IJ
[Ad] Endereço:Institute of Physiology, University of Zurich, Zurich, Switzerland.
[Ti] Título:Oncogenic HrasG12V expression plus knockdown of Cdkn2a using ecotropic lentiviral vectors induces high-grade endometrial stromal sarcoma.
[So] Source:PLoS One;12(10):e0186102, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The uterine corpus represents the most common site for tumour development in the female genital system. Uterine neoplasms are categorised as epithelial, mesenchymal, mixed epithelial-mesenchymal or trophoblastic tumours. In this study we employed a mouse genetic approach using the MuLE lentiviral gene regulatory system to functionally test the ability of ecotropic lentiviruses to model epithelial and mesenchymal uterine malignancies ex vivo and in vivo. We discovered that MuLE lentiviruses efficiently infect uterine stromal cells but not endometrial epithelial cells when injected into the uterus of cycling, pseudopregnant or ovarectomized mice. Consistent with this cellular infection spectrum, we show that intra-uterine injection of ecotropic MuLE viruses expressing oncogenic HrasG12V together with knockdown of Cdkn2a induce high-grade endometrial stromal sarcomas. These findings establish this approach as an efficient method of generating autochthonous mouse models of uterine sarcomas and in general for performing genetic manipulations of uterine stromal cells in vivo.
[Mh] Termos MeSH primário: Inibidor p16 de Quinase Dependente de Ciclina/genética
Neoplasias do Endométrio/genética
Genes ras
Vetores Genéticos
Lentivirus/genética
Sarcoma do Estroma Endometrial/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Neoplasias do Endométrio/patologia
Feminino
Técnicas de Silenciamento de Genes
Camundongos
Camundongos SCID
Sarcoma do Estroma Endometrial/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cdkn2a protein, mouse); 0 (Cyclin-Dependent Kinase Inhibitor p16)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186102


  5 / 12052 MEDLINE  
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[PMID]:28982154
[Au] Autor:Merchant M; Moffat J; Schaefer G; Chan J; Wang X; Orr C; Cheng J; Hunsaker T; Shao L; Wang SJ; Wagle MC; Lin E; Haverty PM; Shahidi-Latham S; Ngu H; Solon M; Eastham-Anderson J; Koeppen H; Huang SA; Schwarz J; Belvin M; Kirouac D; Junttila MR
[Ad] Endereço:Department of Translational Oncology, Genentech, Inc., South San Francisco, California, United States of America.
[Ti] Título:Combined MEK and ERK inhibition overcomes therapy-mediated pathway reactivation in RAS mutant tumors.
[So] Source:PLoS One;12(10):e0185862, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitogen-activated protein kinase (MAPK) pathway dysregulation is implicated in >30% of all cancers, rationalizing the development of RAF, MEK and ERK inhibitors. While BRAF and MEK inhibitors improve BRAF mutant melanoma patient outcomes, these inhibitors had limited success in other MAPK dysregulated tumors, with insufficient pathway suppression and likely pathway reactivation. In this study we show that inhibition of either MEK or ERK alone only transiently inhibits the MAPK pathway due to feedback reactivation. Simultaneous targeting of both MEK and ERK nodes results in deeper and more durable suppression of MAPK signaling that is not achievable with any dose of single agent, in tumors where feedback reactivation occurs. Strikingly, combined MEK and ERK inhibition is synergistic in RAS mutant models but only additive in BRAF mutant models where the RAF complex is dissociated from RAS and thus feedback productivity is disabled. We discovered that pathway reactivation in RAS mutant models occurs at the level of CRAF with combination treatment resulting in a markedly more active pool of CRAF. However, distinct from single node targeting, combining MEK and ERK inhibitor treatment effectively blocks the downstream signaling as assessed by transcriptional signatures and phospho-p90RSK. Importantly, these data reveal that MAPK pathway inhibitors whose activity is attenuated due to feedback reactivation can be rescued with sufficient inhibition by using a combination of MEK and ERK inhibitors. The MEK and ERK combination significantly suppresses MAPK pathway output and tumor growth in vivo to a greater extent than the maximum tolerated doses of single agents, and results in improved anti-tumor activity in multiple xenografts as well as in two Kras mutant genetically engineered mouse (GEM) models. Collectively, these data demonstrate that combined MEK and ERK inhibition is functionally unique, yielding greater than additive anti-tumor effects and elucidates a highly effective combination strategy in MAPK-dependent cancer, such as KRAS mutant tumors.
[Mh] Termos MeSH primário: MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Genes ras
MAP Quinase Quinase Quinases/metabolismo
Neoplasias/enzimologia
[Mh] Termos MeSH secundário: Western Blotting
Células HCT116
Seres Humanos
Neoplasias/genética
Neoplasias/terapia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.25 (MAP Kinase Kinase Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185862


  6 / 12052 MEDLINE  
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[PMID]:28957417
[Au] Autor:Brauswetter D; Gurbi B; Varga A; Várkondi E; Schwab R; Bánhegyi G; Fábián O; Kéri G; Vályi-Nagy I; Peták I
[Ad] Endereço:MTA-SE Pathobiochemistry Research Group, Budapest, Hungary.
[Ti] Título:Molecular subtype specific efficacy of MEK inhibitors in pancreatic cancers.
[So] Source:PLoS One;12(9):e0185687, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreatic cancer is an increasing cause of cancer related death worldwide. KRAS is the dominant oncogene in this cancer type and molecular rationale would indicate, that inhibitors of the downstream target MEK could be appropriate targeted agents, but clinical trials have failed so far to achieve statistically significant benefit in unselected patients. We aimed to identify predictive molecular biomarkers that can help to define subgroups where MEK inhibitors might be beneficial alone or in combination. Next-generation sequencing data of 50 genes in three pancreatic cancer cell lines (MiaPaCa2, BxPC3 and Panc1) were analyzed and compared to the molecular profile of 138 clinical pancreatic cancer samples to identify the molecular subtypes of pancreatic cancer these cell lines represent. Luminescent cell viability assay was used to determine the sensitivity of cell lines to kinase inhibitors. Western blot was used to analyze the pathway activity of the examined cell lines. According to our cell viability and pathway activity data on these model cell lines only cells harboring the rare G12C KRAS mutation and low EGFR expression are sensitive to single MEK inhibitor (trametinib) treatment. The common G12D KRAS mutation leads to elevated baseline Akt activity, thus treatment with single MEK inhibitors fails. However, combination of MEK and Akt inhibitors are synergistic in this case. In case of wild-type KRAS and high EGFR expression MEK inhibitor induced Akt phosphorylation leads to trametinib resistance which necessitates for MEK and EGFR or Akt inhibitor combination treatment. In all we provide strong preclinical rational and possible molecular mechanism to revisit MEK inhibitor therapy in pancreatic cancer in both monotherapy and combination, based on molecular profile analysis of pancreatic cancer samples and cell lines. According to our most remarkable finding, a small subgroup of patients with G12C KRAS mutation may still benefit from MEK inhibitor monotherapy.
[Mh] Termos MeSH primário: MAP Quinase Quinase Quinases/antagonistas & inibidores
Neoplasias Pancreáticas/patologia
Inibidores de Proteínas Quinases/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Genes ras
Seres Humanos
Mutação
Neoplasias Pancreáticas/metabolismo
Piridonas/farmacologia
Pirimidinonas/farmacologia
Receptor do Fator de Crescimento Epidérmico/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Pyridones); 0 (Pyrimidinones); 33E86K87QN (trametinib); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.25 (MAP Kinase Kinase Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185687


  7 / 12052 MEDLINE  
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[PMID]:28870789
[Au] Autor:Merx K; Martens UM; Kripp M; Hoehler T; Geissler M; Gaiser T; Mai S; Kienle P; Belle S; Plöger C; Hieber U; Wenz F; Post S; Hofheinz RD
[Ad] Endereço:III Medizinische Klinik, Universitätsmedizin Mannheim, Universität Heidelberg, Mannheim, Germany. Electronic address: kirsten.merx@umm.de.
[Ti] Título:Panitumumab in Combination With Preoperative Radiation Therapy in Patients With Locally Advanced RAS Wild-type Rectal Cancer: Results of the Multicenter Explorative Single-Arm Phase 2 Study NEORIT.
[So] Source:Int J Radiat Oncol Biol Phys;99(4):867-875, 2017 Nov 15.
[Is] ISSN:1879-355X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Studies investigating combinations of anti-epidermal growth factor receptor monoclonal antibodies such as panitumumab or cetuximab with standard chemoradiation therapy protocols in rectal cancer have yielded disappointing results. Because of the supposed negative interaction of epidermal growth factor receptor inhibition and chemoradiation therapy, we conducted a phase 2 study using single-agent panitumumab in combination with radiation therapy in patients with RAS wild-type locally advanced rectal cancer. METHODS AND MATERIALS: Patients with RAS wild-type locally advanced (clinical stage II or III) rectal cancer localized 0 to 12 cm from the anus were eligible for study participation. The primary objective of the study was to determine pathologic complete response (pCR). Secondary objectives comprised assessing the safety, surgical morbidity, clinical response, tumor downstaging, and tumor regression grading according to Dworak. RESULTS: A total of 54 patients with a median age of 58 years were treated. In 3.7% of patients, pCR was achieved. Downstaging of the primary tumor or lymph nodes was seen in 65% of patients. No grade ≥2 hematologic toxicity was seen. The most common grade ≥3 nonhematologic toxicities were skin toxicity (24%) and diarrhea (10%). CONCLUSIONS: Panitumumab in combination with radiation therapy as neoadjuvant treatment for locally advanced rectal cancer showed a favorable toxicity profile but failed to meet the predefined pCR rate to justify further clinical trials.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Antineoplásicos/uso terapêutico
Quimiorradioterapia/métodos
Genes ras
Neoplasias Retais/genética
Neoplasias Retais/terapia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Anticorpos Monoclonais/efeitos adversos
Antineoplásicos/efeitos adversos
Quimiorradioterapia/efeitos adversos
Diarreia/etiologia
Feminino
Seres Humanos
Infusões Intravenosas
Masculino
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Dosagem Radioterapêutica
Radioterapia de Intensidade Modulada/métodos
Neoplasias Retais/patologia
Pele/efeitos da radiação
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 6A901E312A (panitumumab)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE


  8 / 12052 MEDLINE  
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[PMID]:28721890
[Au] Autor:Sperduto PW; Jiang W; Brown PD; Braunstein S; Sneed P; Wattson DA; Shih HA; Bangdiwala A; Shanley R; Lockney NA; Beal K; Lou E; Amatruda T; Sperduto WA; Kirkpatrick JP; Yeh N; Gaspar LE; Molitoris JK; Masucci L; Roberge D; Yu J; Chiang V; Mehta M
[Ad] Endereço:Minneapolis Radiation Oncology, Minneapolis, Minnesota. Electronic address: psperduto@mropa.com.
[Ti] Título:The Prognostic Value of BRAF, C-KIT, and NRAS Mutations in Melanoma Patients With Brain Metastases.
[So] Source:Int J Radiat Oncol Biol Phys;98(5):1069-1077, 2017 Aug 01.
[Is] ISSN:1879-355X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Brain metastases are a common problem in patients with melanoma, but little is known about the effect of gene mutations on survival in these patients. METHODS AND MATERIALS: We created a retrospective multi-institutional database of 823 patients with melanoma and brain metastases diagnosed between 2006 and 2015. Clinical parameters, gene mutation status (BRAF, C-KIT, NRAS), and treatment were correlated with survival. Treatment patterns and outcomes were compared with a prior era (1985-2005). RESULTS: BRAF status was known in 584 of 823 patients (71%). BRAF, NRAS, and C-KIT mutations were present in 51%, 22%, and 11% of tested patients, respectively. The median time from primary diagnosis to brain metastasis was 32 months, and overall median survival (MS) from the time of initial treatment of brain metastases was 10 months. MS for BRAF-positive and BRAF-negative patients was 13 months and 9 months, respectively (P=.02). There was no significant difference in MS in patients with or without NRAS or C-KIT mutations. The time from primary diagnosis to brain metastasis did not vary by mutation and was not associated with survival after the diagnosis of brain metastases. MS for the 1985 to 2005 and 2006 to 2015 cohorts was 6.7 months and 10.0 months, respectively (P<.01). Reflecting treatment-trend changes, use of whole-brain radiation therapy decreased from 48% to 26% during this period. Among BRAF-positive patients, 71% received targeted BRAF and/or MEK inhibitors and 57% received some combination of targeted therapy, chemotherapy, and/or immunotherapy. CONCLUSIONS: For melanoma patients with brain metastases, BRAF-positive patients survive longer than BRAF-negative patients and overall survival has improved from 1985-2005 to 2006-2015.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/genética
Neoplasias Encefálicas/secundário
Genes ras
Melanoma/genética
Melanoma/secundário
Mutação
Proteínas Proto-Oncogênicas B-raf/genética
Proteínas Proto-Oncogênicas c-kit/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/uso terapêutico
Neoplasias Encefálicas/mortalidade
Neoplasias Encefálicas/terapia
Feminino
Seres Humanos
Imunoterapia
Modelos Lineares
Masculino
Melanoma/mortalidade
Melanoma/terapia
Meia-Idade
Terapia de Alvo Molecular
Prognóstico
Modelos de Riscos Proporcionais
Estudos Retrospectivos
Estatísticas não Paramétricas
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE


  9 / 12052 MEDLINE  
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[PMID]:28688743
[Au] Autor:Albertini AF; Raoux D; Neumann F; Rossat S; Tabet F; Pedeutour F; Duranton-Tanneur V; Kubiniek V; Vire O; Weinbreck N
[Ad] Endereço:Laboratoire Médipath, pôle d'excellence Jean-Louis, 263, Via Nova, 83600 Fréjus, France. Electronic address: af.albertini@medipath.com.
[Ti] Título:[Detection of RAS genes mutation using the Cobas method in a private laboratory of pathology: Medical and economical study in comparison to a public platform of molecular biology of cancer].
[Ti] Título:Analyse des mutations des gènes RAS par technique Cobas au sein d'une structure de pathologie libérale : étude médico-économique et moléculaire comparative avec une plateforme labellisée INCa..
[So] Source:Bull Cancer;104(7-8):662-674, 2017 Jul - Aug.
[Is] ISSN:1769-6917
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:In France, determination of the mutation status of RAS genes for predictive response to anti-EGFR targeted treatments is carried out by public platforms of molecular biology of cancer created by the French National Cancer Institute. This study aims to demonstrate the feasibility of these analyses by a private pathology laboratory (MEDIPATH) as per the requirements of accreditation. We retrospectively studied the mutation status of KRAS and NRAS genes in 163 cases of colorectal metastatic cancer using the Cobas technique. We compared our results to those prospectively obtained through pyrosequencing and allelic discrimination by the genetic laboratory of solid tumors at the Nice University Hospital (PACA-EST regional platform). The results of both series were identical: 98.7% positive correlation; negative correlation of 93.1%; overall correlation of 95.7% (Kappa=0.92). This study demonstrates the feasibility of molecular analysis in a private pathology laboratory. As this practice requires a high level of guarantee, its accreditation, according to the NF-EN-ISO15189 quality compliance French standard, is essential. Conducting molecular analysis in this context avoids the steps of routing the sample and the result between the pathology laboratory and the platform, which reduces the overall time of rendering the result. In conclusion, the transfer of some analysis from these platforms to private pathology laboratories would allow the platforms to be discharged from a part of routine testing and therefore concentrate their efforts to the development of new analyses constantly required to access personalized medicine.
[Mh] Termos MeSH primário: Acreditação
Neoplasias Colorretais/genética
Análise Mutacional de DNA/métodos
Genes ras
Laboratórios Hospitalares/normas
Mutação
[Mh] Termos MeSH secundário: Neoplasias Colorretais/patologia
Análise Mutacional de DNA/economia
Análise Mutacional de DNA/normas
Éxons
Estudos de Viabilidade
França
Seres Humanos
Laboratórios Hospitalares/economia
Estudos Prospectivos
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Reprodutibilidade dos Testes
Estudos Retrospectivos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170710
[St] Status:MEDLINE


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[PMID]:28649886
[Au] Autor:Giuliani J; Bonetti A
[Ad] Endereço:a Department of Oncology , Mater Salutis Hospital , Legnago , Italy.
[Ti] Título:Epidermal growth factor inhibitors in first-line for metastatic colorectal cancer with ras wild-type: a perspective based on pharmacological costs.
[So] Source:Expert Rev Pharmacoecon Outcomes Res;17(3):243-248, 2017 Jun.
[Is] ISSN:1744-8379
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: In light of the relevant expenses of pharmacological interventions it might be interesting to make a balance between the cost of the new drugs administered, such as EGFRIs (cetuximab and panitunumab) and the added value represented by the improvement of the clinical parameters of interest such as progression free survival (PFS). Areas covered: The analysis was conducted to assess the effect of front-line chemotherapy on the PFS, separately, on each arm of the evaluated trials. Only phase III randomized controlled trials (RCTs) were considered. We calculated the pharmacological costs necessary to get the benefit in PFS, for each trial. We have subsequently applied the European Society for Medical Oncology Magnitude of Clinical Benefit Scale (ESMO-MCBS) to the above phase III RCTs. Our analysis evaluated 9 phase III RCTs, including 7199 patients. ESMO-MCBS reached high scores (grade 4) for the CRYSTAL and PRIME trials. The combination of FOLFOX and panitunumab is associated with low difference per month-PFS gained (15 821.9 €) instead of FOLFIRI plus cetuximab (21 854.6 €) in KRAS wild-type patients. Expert commentary: Our data demonstrate a huge difference in cost per month of PFS gained in modern front-line treatments in mCRC with RAS wild-type.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Neoplasias Colorretais/tratamento farmacológico
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
[Mh] Termos MeSH secundário: Antineoplásicos/economia
Antineoplásicos/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/economia
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Ensaios Clínicos Fase III como Assunto
Neoplasias Colorretais/economia
Neoplasias Colorretais/patologia
Intervalo Livre de Doença
Custos de Medicamentos
Genes ras/genética
Seres Humanos
Metástase Neoplásica
Inibidores de Proteínas Quinases/administração & dosagem
Inibidores de Proteínas Quinases/economia
Inibidores de Proteínas Quinases/farmacologia
Ensaios Clínicos Controlados Aleatórios como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.1080/14737167.2017.1347504



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