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[PMID]:29019889
[Au] Autor:Luo W; Li YL; Chen YJ; Xiang Q; Chen H
[Ad] Endereço:aDepartment of Respiratory Medicine, The People's Hospital of Leshan, Leshan bDepartment of Respiratory and Critical Care Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan cThe First Affiliated Hospital of Chongqing Medical University, Chongqing, P.R. China.
[Ti] Título:High dose of nimustine as an add-on treatment for small cell lung cancer with intracranial metastasis: A case report and literature review.
[So] Source:Medicine (Baltimore);96(41):e8218, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Small cell lung cancer (SCLC) characterized by high degree of malignancy and rapid tumor progression. Intracranial metastases often appear at the time of the initial diagnosis or treatment. Besides of radiotherapy, chemotherapy is supposed to have limited effect. PATIENT CONCERNS: A 66-year-old male had blurred vision and unsteady step with moderate headache, nausea, vomit. DIAGNOSES: The patient was diagnosed with SCLC with intracranial metastases. INTERVENTIONS: High dose of nimustine (ACNU) (300 mg/m) add to the regimen containing carboplatin and irinotecan. OUTCOMES: Although the patient suffered severe myelosuppression, the intracranial lesion almost disappeared and maintained half a year. LESSONS: ACNU at a dose of 200 mg/m might be tolerable in combination with other chemotherapeutic drugs for the treatment of SCLC with intracranial metastases besides radiotherapy.
[Mh] Termos MeSH primário: Neoplasias Encefálicas
Neoplasias Pulmonares/patologia
Nimustina
Carcinoma de Pequenas Células do Pulmão/patologia
[Mh] Termos MeSH secundário: Idoso
Antineoplásicos/administração & dosagem
Antineoplásicos/efeitos adversos
Protocolos Antineoplásicos
Encéfalo/diagnóstico por imagem
Neoplasias Encefálicas/patologia
Neoplasias Encefálicas/secundário
Neoplasias Encefálicas/terapia
Quimiorradioterapia/métodos
Relação Dose-Resposta a Droga
Seres Humanos
Masculino
Estadiamento de Neoplasias
Exame Neurológico/métodos
Nimustina/administração & dosagem
Nimustina/efeitos adversos
Resultado do Tratamento
Transtornos da Visão/diagnóstico
Transtornos da Visão/etiologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0S726V972K (Nimustine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008218


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[PMID]:28247160
[Au] Autor:Ogita S; Endo T; Sugiyama S; Saito R; Inoue T; Sumiyoshi A; Nonaka H; Kawashima R; Sonoda Y; Tominaga T
[Ad] Endereço:Department of Neurosurgery, Graduate School of Medicine, Tohoku University, 1-1 Seiryo Aoba, Sendai, Japan, 980-8574.
[Ti] Título:Convection-enhanced delivery of a hydrophilic nitrosourea ameliorates deficits and suppresses tumor growth in experimental spinal cord glioma models.
[So] Source:Acta Neurochir (Wien);159(5):939-946, 2017 May.
[Is] ISSN:0942-0940
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Convection-enhanced delivery (CED) is a technique allowing local infusion of therapeutic agents into the central nervous system, circumventing the blood-brain or spinal cord barrier. OBJECTIVE: To evaluate the utility of nimustine hydrochloride (ACNU) CED in controlling tumor progression in an experimental spinal cord glioma model. METHODS: Toxicity studies were performed in 42 rats following the administration of 4 µl of ACNU CED into the mid-thoracic spinal cord at concentrations ranging from 0.1 to 10 mg/ml. Behavioral analyses and histological evaluations were performed to assess ACNU toxicity in the spinal cord. A survival study was performed in 32 rats following the implantation of 9 L cells into the T8 spinal cord. Seven days after the implantation, rats were assigned to four groups: ACNU CED (0.25 mg/ml; n = 8); ACNU intravenous (i.v.) (0.4 mg; n = 8); saline CED (n = 8); saline i.v. (n = 8). Hind limb movements were evaluated daily in all rats for 21 days. Tumor sizes were measured histologically. RESULTS: The maximum tolerated ACNU concentration was 0.25 mg/ml. Preservation of hind limb motor function and tumor growth suppression was observed in the ACNU CED (0.25 mg/ml) and ACNU i.v. groups. Antitumor effects were more prominent in the ACNU CED group especially in behavioral analyses (P < 0.05; log-rank test). CONCLUSIONS: ACNU CED had efficacy in controlling tumor growth and preserving neurological function in an experimental spinal cord tumor model. ACNU CED can be a viable treatment option for spinal cord high-grade glioma.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Sistemas de Liberação de Medicamentos/métodos
Glioma/tratamento farmacológico
Nimustina/administração & dosagem
Neoplasias da Medula Espinal/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Convecção
Masculino
Nimustina/uso terapêutico
Ratos
Ratos Endogâmicos F344
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0S726V972K (Nimustine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE
[do] DOI:10.1007/s00701-017-3123-2


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[PMID]:27943283
[Au] Autor:van de Ven M; van der Burg E; van der Gulden H; Klarenbeek S; Bouwman P; Jonkers J
[Ad] Endereço:Division of Molecular Pathology and Cancer Genomics Netherlands, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
[Ti] Título:Prophylactic window therapy with the clinical poly(ADP-ribose) polymerase inhibitor olaparib delays BRCA1-deficient mammary tumour formation in mice.
[So] Source:J Pathol;241(4):511-521, 2017 Mar.
[Is] ISSN:1096-9896
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Women with heterozygous germline mutations in the BRCA1 tumour suppressor gene are strongly predisposed to developing early-onset breast cancer through loss of the remaining wild-type BRCA1 allele and inactivation of TP53. Although tumour prevention strategies in BRCA1-mutation carriers are still limited to prophylactic surgery, several therapeutic strategies have been developed to target the DNA repair defects (also known as 'BRCAness') of BRCA1-deficient tumours. In particular, DNA-damaging agents such as platinum drugs and poly(ADP-ribose) polymerase (PARP) inhibitors show strong activity against BRCA1-mutated tumours. However, it is unclear whether drugs that target BRCAness can also be used to prevent tumour formation in BRCA1-mutation carriers, especially as loss of wild-type BRCA1 may not be the first event in BRCA1-associated tumourigenesis. We performed prophylactic treatments in a genetically engineered mouse model in which de novo development of BRCA1-deficient mammary tumours is induced by stochastic loss of BRCA1 and p53. We found that prophylactic window therapy with nimustine, cisplatin or olaparib reduced the amount and size of mammary gland lesions, and significantly increased the median tumour latency. Similar results were obtained with intermittent prophylactic treatment with olaparib. Importantly, prophylactic window therapy with nimustine and cisplatin resulted in an increased fraction of BRCA1-proficient mammary tumours, suggesting selective survival and malignant transformation of BRCA1-proficient lesions upon prophylactic treatment with DNA-damaging agents. Prophylactic therapy with olaparib significantly prolonged mammary tumour-free survival without any significant increase in the fraction of BRCA1-proficient tumours, warranting the evaluation of this PARP inhibitor in prophylactic trials in BRCA1-mutation carriers. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Neoplasias Mamárias Animais/tratamento farmacológico
Ftalazinas/farmacologia
Piperazinas/farmacologia
Inibidores de Poli(ADP-Ribose) Polimerases/farmacologia
Proteínas Supressoras de Tumor/genética
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Cisplatino/farmacologia
Reparo do DNA
Modelos Animais de Doenças
Feminino
Mutação em Linhagem Germinativa
Seres Humanos
Neoplasias Mamárias Animais/patologia
Neoplasias Mamárias Animais/prevenção & controle
Camundongos
Nimustina/farmacologia
Ftalazinas/uso terapêutico
Piperazinas/uso terapêutico
Inibidores de Poli(ADP-Ribose) Polimerases/uso terapêutico
Poli(ADP-Ribose) Polimerases/genética
Poli(ADP-Ribose) Polimerases/metabolismo
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Brca1 protein, mouse); 0 (Phthalazines); 0 (Piperazines); 0 (Poly(ADP-ribose) Polymerase Inhibitors); 0 (Tumor Suppressor Proteins); 0S726V972K (Nimustine); EC 2.4.2.30 (Poly(ADP-ribose) Polymerases); Q20Q21Q62J (Cisplatin); WOH1JD9AR8 (olaparib)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE
[do] DOI:10.1002/path.4857


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[PMID]:27725524
[Au] Autor:Aoki T; Arakawa Y; Ueba T; Oda M; Nishida N; Akiyama Y; Tsukahara T; Iwasaki K; Mikuni N; Miyamoto S
[Ad] Endereço:Department of Neurosurgery, National Hospital Organization, Kyoto Medical Center.
[Ti] Título:Phase I/II Study of Temozolomide Plus Nimustine Chemotherapy for Recurrent Malignant Gliomas: Kyoto Neuro-oncology Group.
[So] Source:Neurol Med Chir (Tokyo);57(1):17-27, 2017 Jan 15.
[Is] ISSN:1349-8029
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The objective of this phase I/II study was to examine the efficacy and toxicity profile of temozolomide (TMZ) plus nimustine (ACNU). Patients who had received a standard radiotherapy with one or two previous chemo-regimens were enrolled. In phase I, the maximum-tolerated dose (MTD) by TMZ (150 mg/m /day) (Day 1-5) plus various doses of ACNU (30, 35, 40, 45 mg/m /day) (Day 15) per 4 weeks was defined on a standard 3 + 3 design. In phase II, these therapeutic activity and safety of this regimen were evaluated. Forty-nine eligible patients were enrolled. The median age was 50 years-old. Eighty percent had a KPS of 70-100. Histologies were glioblastoma (73%), anaplastic astrocytoma (22%), anaplastic oligodendroglioma (4%). In phase I, 15 patients were treated at four cohorts by TMZ plus ACNU. MTD was TMZ (150 mg/m ) plus ACNU (40 mg/m ). In phase II, 40 patients were treated at the dose of cohort 3 (MTD). Thirty-five percent of patients experienced grade 3 or 4 toxicities, mainly hematologic. The overall response rate was 11% (4/37). Sixty-eight percent (25/37) had stable disease. Twenty-two percent (8/37) showed progression. Progression-free survival (PFS) rates at 6 and 12 months were 24% (95% CI, 12-35%) and 8% (95% CI, 4-15%). Median PFS was 13 months (95% CI, 9.2-17.2 months). Overall survival (OS) at 6 and 12 were 78% (95% CI, 67-89%) and 49% (95% CI, 33-57%). Median OS was 11.8 months (95% CI, 8.2-14.5 months). This phase I/II study showed a moderate toxicity in hematology and may has a promising efficacy in OS, without inferiority in PFS.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/uso terapêutico
Neoplasias Encefálicas/tratamento farmacológico
Dacarbazina/análogos & derivados
Glioma/tratamento farmacológico
Recidiva Local de Neoplasia/tratamento farmacológico
Nimustina/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Dacarbazina/uso terapêutico
Feminino
Seres Humanos
Japão
Masculino
Meia-Idade
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0S726V972K (Nimustine); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161012
[St] Status:MEDLINE
[do] DOI:10.2176/nmc.oa.2016-0162


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[PMID]:27756356
[Au] Autor:Musha A; Saitoh JI; Shirai K; Yokoo S; Ohno T; Nakano T
[Ad] Endereço:Gunma University Heavy Ion Medical Center, 3-39-22 Showa-machi, Maebashi, Gunma, Japan. musha@gunma-u.ac.jp.
[Ti] Título:Oral mucosal melanoma treated with carbon ion radiotherapy: a case report.
[So] Source:J Med Case Rep;10(1):284, 2016 Oct 18.
[Is] ISSN:1752-1947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Oral mucosal melanoma is a rare disease with a relatively poor prognosis. Carbon ion radiotherapy has been shown to be effective against radiotherapy-resistant tumors owing to its excellent dose concentration and high biological effect. CASE PRESENTATION: Our patient was a 66-year-old Japanese man with oral mucosal melanoma of his right maxillary gingiva (T4aN0M0). He received carbon ion radiotherapy at 57.6 Gy (relative biological effectiveness) in 16 fractions for 4 weeks. Concomitant chemotherapy (dacarbazine + nimustine + vincristine) was administered at the same time as carbon ion radiotherapy initiation. Two courses of adjuvant chemotherapy were given after carbon ion radiotherapy. Although he experienced grade 2 acute oral mucositis, his symptoms improved within a few weeks of undergoing carbon ion radiotherapy. He was alive at the time of reporting, 35 months after treatment, without any recurrence. Late toxicity has not been observed. CONCLUSIONS: Carbon ion radiotherapy for oral mucosal melanoma resulted in a good local effect.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/administração & dosagem
Radioterapia com Íons Pesados
Melanoma/radioterapia
Mucosa Bucal/patologia
Neoplasias Bucais/radioterapia
Recidiva Local de Neoplasia/prevenção & controle
Lesões por Radiação/patologia
[Mh] Termos MeSH secundário: Idoso
Terapia Combinada
Dacarbazina/administração & dosagem
Radioterapia com Íons Pesados/efeitos adversos
Radioterapia com Íons Pesados/métodos
Seres Humanos
Masculino
Melanoma/patologia
Mucosa Bucal/efeitos da radiação
Neoplasias Bucais/patologia
Membrana Mucosa/patologia
Membrana Mucosa/efeitos da radiação
Nimustina/administração & dosagem
Dosagem Radioterapêutica
Resultado do Tratamento
Vincristina/administração & dosagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0S726V972K (Nimustine); 5J49Q6B70F (Vincristine); 7GR28W0FJI (Dacarbazine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170512
[Lr] Data última revisão:
170512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE


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[PMID]:27381626
[Au] Autor:Ter Brugge P; Kristel P; van der Burg E; Boon U; de Maaker M; Lips E; Mulder L; de Ruiter J; Moutinho C; Gevensleben H; Marangoni E; Majewski I; Józwiak K; Kloosterman W; van Roosmalen M; Duran K; Hogervorst F; Turner N; Esteller M; Cuppen E; Wesseling J; Jonkers J
[Ad] Endereço:Affiliations of authors: Division of Molecular Pathology and Cancer Genomics Centre Netherlands (PtB, PK, EvdB, UB, MdM, EL, LM, JdR, JW, JJ), Division of Molecular Carcinogenesis (IM), Department of Epidemiology and Biostatistics (KJ), and Family Cancer Clinic and Department of Pathology (FH), The
[Ti] Título:Mechanisms of Therapy Resistance in Patient-Derived Xenograft Models of BRCA1-Deficient Breast Cancer.
[So] Source:J Natl Cancer Inst;108(11), 2016 Nov.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Although BRCA1-deficient tumors are extremely sensitive to DNA-damaging drugs and poly(ADP-ribose) polymerase (PARP) inhibitors, recurrences do occur and, consequently, resistance to therapy remains a serious clinical problem. To study the underlying mechanisms, we induced therapy resistance in patient-derived xenograft (PDX) models of BRCA1-mutated and BRCA1-methylated triple-negative breast cancer. METHODS: A cohort of 75 mice carrying BRCA1-deficient breast PDX tumors was treated with cisplatin, melphalan, nimustine, or olaparib, and treatment sensitivity was determined. In tumors that acquired therapy resistance, BRCA1 expression was investigated using quantitative real-time polymerase chain reaction and immunoblotting. Next-generation sequencing, methylation-specific multiplex ligation-dependent probe amplification (MLPA) and Target Locus Amplification (TLA)-based sequencing were used to determine mechanisms of BRCA1 re-expression in therapy-resistant tumors. RESULTS: BRCA1 protein was not detected in therapy-sensitive tumors but was found in 31 out of 42 resistant cases. Apart from previously described mechanisms involving BRCA1-intragenic deletions and loss of BRCA1 promoter hypermethylation, a novel resistance mechanism was identified in four out of seven BRCA1-methylated PDX tumors that re-expressed BRCA1 but retained BRCA1 promoter hypermethylation. In these tumors, we found de novo gene fusions that placed BRCA1 under the transcriptional control of a heterologous promoter, resulting in re-expression of BRCA1 and acquisition of therapy resistance. CONCLUSIONS: In addition to previously described clinically relevant resistance mechanisms in BRCA1-deficient tumors, we describe a novel resistance mechanism in BRCA1-methylated PDX tumors involving de novo rearrangements at the BRCA1 locus, demonstrating that BRCA1-methylated breast cancers may acquire therapy resistance via both epigenetic and genetic mechanisms.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Resistência a Medicamentos Antineoplásicos/genética
Fusão Gênica
Genes BRCA1
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
Neoplasias de Mama Triplo Negativas/genética
[Mh] Termos MeSH secundário: Animais
Proteína BRCA1/deficiência
Cisplatino/uso terapêutico
Metilação de DNA
Feminino
Expressão Gênica
Seres Humanos
Melfalan/uso terapêutico
Camundongos
Mutação
Transplante de Neoplasias
Nimustina/uso terapêutico
Ftalazinas/uso terapêutico
Piperazinas/uso terapêutico
Regiões Promotoras Genéticas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (BRCA1 Protein); 0 (Phthalazines); 0 (Piperazines); 0S726V972K (Nimustine); Q20Q21Q62J (Cisplatin); Q41OR9510P (Melphalan); WOH1JD9AR8 (olaparib)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160707
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djw148


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[PMID]:27014877
[Au] Autor:Zhang Q; Gao M; Luo G; Han X; Bao W; Cheng Y; Tian W; Yan M; Yang G; An J
[Ad] Endereço:Department of Pharmacology, State University of New York, Upstate Medical University, Syracuse, New York, United States of America.
[Ti] Título:Enhancement of Radiation Sensitivity in Lung Cancer Cells by a Novel Small Molecule Inhibitor That Targets the ß-Catenin/Tcf4 Interaction.
[So] Source:PLoS One;11(3):e0152407, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Radiation therapy is an important treatment choice for unresectable advanced human lung cancers, and a critical adjuvant treatment for surgery. However, radiation as a lung cancer treatment remains far from satisfactory due to problems associated with radiation resistance in cancer cells and severe cytotoxicity to non-cancer cells, which arise at doses typically administered to patients. We have recently identified a promising novel inhibitor of ß-catenin/Tcf4 interaction, named BC-23 (C21H14ClN3O4S), which acts as a potent cell death enhancer when used in combination with radiation. Sequential exposure of human p53-null non-small cell lung cancer (NSCLC) H1299 cells to low doses of x-ray radiation, followed 1 hour later by administration of minimally cytotoxic concentrations of BC-23, resulted in a highly synergistic induction of clonogenic cell death (combination index <1.0). Co-treatment with BC-23 at low concentrations effectively inhibits Wnt/ß-catenin signaling and down-regulates c-Myc and cyclin D1 expression. S phase arrest and ROS generation are also involved in the enhancement of radiation effectiveness mediated by BC-23. BC-23 therefore represents a promising new class of radiation enhancer.
[Mh] Termos MeSH primário: Antineoplásicos/química
Fatores de Transcrição de Zíper de Leucina e Hélice-Alça-Hélix Básicos/metabolismo
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Neoplasias Pulmonares/metabolismo
Nimustina/química
Tolerância a Radiação/efeitos dos fármacos
Fatores de Transcrição/metabolismo
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Ligação Competitiva
Carcinoma Pulmonar de Células não Pequenas/terapia
Ciclo Celular
Linhagem Celular Tumoral/efeitos dos fármacos
Linhagem Celular Tumoral/efeitos da radiação
Ciclina D1/metabolismo
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Luciferases/metabolismo
Neoplasias Pulmonares/terapia
Células-Tronco Neoplásicas/citologia
Proteínas Proto-Oncogênicas c-myc/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Espectrometria de Fluorescência
Fator de Transcrição 4
Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Basic Helix-Loop-Helix Leucine Zipper Transcription Factors); 0 (CCND1 protein, human); 0 (CTNNB1 protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (Reactive Oxygen Species); 0 (TCF4 protein, human); 0 (Transcription Factor 4); 0 (Transcription Factors); 0 (beta Catenin); 0S726V972K (Nimustine); 136601-57-5 (Cyclin D1); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160326
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0152407


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[PMID]:26881613
[Au] Autor:Lou M; Zhao Y
[Ti] Título:Satisfactory therapy results of combining nimustine with nicardipine against glioma at advanced stage.
[So] Source:J Cancer Res Ther;11(4):1030, 2015 Oct-Dec.
[Is] ISSN:1998-4138
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:Glioblastoma multiforme (GBM) is one of the most frequent brain cancers with a very poor prognosis. According to cancer stem cell (CSC) theory, therapies that are more specifically directed against CSCs might result in much more durable responses. Recently, we treated a case of GBM basing on the conception of CSC and gained a better clinic outcome. A 37-year-old male patient complained weakness of left limbs for 1 month. Magnetic resonance imaging (MRI) showed extensive lesions in the right hemisphere. We performed an intracranial tumor partial resection and the postoperative pathological diagnose was GBM. 1 month later, he received monthly chemotherapies with the combination of nimustine and nicardipine for totally 4 times. At the last chemotherapy, MRI scan showed the cancer almost completely disappeared with significantly improved clinic condition. The combination therapy of chemotherapeutics and nicardipine may be a promising treatment for patients of GBM at advanced stage.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/tratamento farmacológico
Glioblastoma/tratamento farmacológico
Nicardipino/uso terapêutico
Nimustina/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Anti-Hipertensivos/uso terapêutico
Antineoplásicos/uso terapêutico
Neoplasias Encefálicas/patologia
Quimioterapia Combinada
Glioblastoma/patologia
Seres Humanos
Masculino
Prognóstico
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Antineoplastic Agents); 0S726V972K (Nimustine); CZ5312222S (Nicardipine)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160217
[St] Status:MEDLINE
[do] DOI:10.4103/0973-1482.154033


  9 / 760 MEDLINE  
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[PMID]:26418950
[Au] Autor:Tomicic MT; Meise R; Aasland D; Berte N; Kitzinger R; Krämer OH; Kaina B; Christmann M
[Ad] Endereço:Department of Toxicology, University Medical Center Mainz, D-55131 Mainz, Germany.
[Ti] Título:Apoptosis induced by temozolomide and nimustine in glioblastoma cells is supported by JNK/c-Jun-mediated induction of the BH3-only protein BIM.
[So] Source:Oncotarget;6(32):33755-68, 2015 Oct 20.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The outcome of cancer therapy strongly depends on the complex network of cell signaling pathways, including transcription factor activation following drug exposure. Here we assessed whether and how the MAP kinase (MAPK) cascade and its downstream target, the transcription factor AP-1, influence the sensitivity of malignant glioma cells to the anticancer drugs temozolomide (TMZ) and nimustine (ACNU). Both drugs induce apoptosis in glioma cells at late times following treatment. Activation of the MAPK cascade precedes apoptosis, as shown by phosphorylation of Jun kinase (JNK) and c-Jun, a main component of AP-1. Pharmacological inhibition and siRNA mediated knockdown of JNK and c-Jun reduced the level of apoptosis in LN-229 glioma cells treated with TMZ or ACNU. Analyzing the underlying molecular mechanism, we identified the pro-apoptotic gene BIM as a critical target of AP-1, which is upregulated following TMZ and ACNU. Importantly, shRNA mediated downregulation of BIM in the malignant glioma cell lines LN-229 and U87MG led to an attenuated cleavage of caspase-9 and, consequently, reduced the level of apoptosis following TMZ and ACNU treatment. Overall, we identified JNK/c-Jun activation and BIM induction as a late pro-apoptotic response of glioma cells treated with alkylating anticancer drugs.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/metabolismo
Apoptose
Dacarbazina/análogos & derivados
Glioblastoma/patologia
MAP Quinase Quinase 4/metabolismo
Proteínas de Membrana/metabolismo
Nimustina/farmacologia
Proteínas Proto-Oncogênicas c-jun/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos Alquilantes/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Proteína 11 Semelhante a Bcl-2
Linhagem Celular Tumoral/efeitos dos fármacos
Núcleo Celular/metabolismo
Ensaio Cometa
Dacarbazina/farmacologia
Regulação Neoplásica da Expressão Gênica
Glioblastoma/metabolismo
Seres Humanos
Sistema de Sinalização das MAP Quinases
Fosforilação
Estrutura Terciária de Proteína
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Apoptosis Regulatory Proteins); 0 (BCL2L11 protein, human); 0 (Bcl-2-Like Protein 11); 0 (Membrane Proteins); 0 (Proto-Oncogene Proteins); 0 (Proto-Oncogene Proteins c-jun); 0 (RNA, Small Interfering); 0S726V972K (Nimustine); 7GR28W0FJI (Dacarbazine); EC 2.7.12.2 (MAP Kinase Kinase 4); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150930
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.5274


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[PMID]:26391598
[Au] Autor:Agarwal S; Ray B; Mehrotra R
[Ad] Endereço:Academy of Scientific & Innovative Research (AcSIR), CSIR-National Physical Laboratory Campus, New Delhi 110012, India; Quantum Phenomenon and Applications, CSIR-National Physical Laboratory, Dr. K. S. Krishnan Marg, New Delhi 110012, India.
[Ti] Título:SERS as an advanced tool for investigating chloroethyl nitrosourea derivatives complexation with DNA.
[So] Source:Int J Biol Macromol;81:891-7, 2015 Nov.
[Is] ISSN:1879-0003
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We report surface-enhanced Raman spectroscopic (SERS) studies on free calf thymus DNA and its complexes with anti-tumor chloroethyl nitrosourea derivatives; semustine and nimustine. Since, first incident of SERS in 1974, it has rapidly established into an analytical tool, which can be used for the trace detection and characterization of analytes. Here, we depict yet another application of SERS in the field of drug-DNA interaction and thereby, its promising role in rational designing of new chemotherapeutic agents. Vibrational spectral analysis has been performed in an attempt to delineate the anti-cancer action mechanism of above mentioned nitrosourea derivatives. Strong SERS bands associated with the complexation of DNA with semustine and nimustine have been observed, which reveal binding of nitrosourea derivatives with heterocyclic nitrogenous base pair of DNA duplex. Formation of dG-dC interstrand cross-link in DNA double helices is also suggested by the SERS spectral outcomes of CENUs-DNA adduct. Results, demonstrated here, reflect recent progress in the newly developing field of drug-DNA interaction analysis via SERS.
[Mh] Termos MeSH primário: DNA/química
Nimustina/química
Semustina/química
Análise Espectral Raman/métodos
[Mh] Termos MeSH secundário: Animais
Bovinos
Coloides
Nanopartículas Metálicas/química
Prata/química
Espectrofotometria Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Colloids); 0S726V972K (Nimustine); 13909-09-6 (Semustine); 3M4G523W1G (Silver); 9007-49-2 (DNA); 91080-16-9 (calf thymus DNA)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150923
[St] Status:MEDLINE



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