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[PMID]:28697868
[Au] Autor:Bavcar S; de Vos J; Kessler M; de Fornel P; Buracco P; Murphy S; Hirschberger J; Argyle DJ
[Ad] Endereço:Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Edinburgh EH25 9RE, United Kingdom. Electronic address: spela.bavcar@ed.ac.uk.
[Ti] Título:Combination toceranib and lomustine shows frequent high grade toxicities when used for treatment of non-resectable or recurrent mast cell tumours in dogs: A European multicentre study.
[So] Source:Vet J;224:1-6, 2017 Jun.
[Is] ISSN:1532-2971
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mast cell tumours (MCTs) in dogs can present in a variety of forms. Non-resectable, recurrent or metastatic MCTs usually carry a poor prognosis and present a therapeutic challenge. Both toceranib and lomustine have shown single agent activity against MCTs in dogs. In this study, 10 dogs with advanced MCTs were enrolled prospectively and treated with toceranib (median dose 2.7mg/kg orally every other day), lomustine (median dose 60mg/m orally every 3 weeks) and prednisolone (1mg/kg orally every other day, alternating with toceranib). Severe adverse events (SAEs), requiring alterations in the protocol, occurred in all dogs. The objective response rate was 50%. Three dogs died or were euthanased due to SAEs and therefore enrolment of new dogs was discontinued prematurely. A long term response (>1year) was observed in two dogs. Modifications of the protocol are required for future prospective studies.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Doenças do Cão/tratamento farmacológico
Indóis/administração & dosagem
Lomustina/administração & dosagem
Mastócitos/patologia
Pirróis/administração & dosagem
Neoplasias Cutâneas/veterinária
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Alquilantes
Doenças do Cão/patologia
Cães
Europa (Continente)
Indóis/efeitos adversos
Lomustina/efeitos adversos
Recidiva Local de Neoplasia/tratamento farmacológico
Recidiva Local de Neoplasia/veterinária
Prednisolona/administração & dosagem
Estudos Prospectivos
Pirróis/efeitos adversos
Receptores Proteína Tirosina Quinases/antagonistas & inibidores
Neoplasias Cutâneas/tratamento farmacológico
Neoplasias Cutâneas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Indoles); 0 (Pyrroles); 24F9PF7J3R (toceranib phosphate); 7BRF0Z81KG (Lomustine); 9PHQ9Y1OLM (Prednisolone); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE


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[PMID]:28248186
[Au] Autor:Vincenti S; Findji F
[Ad] Endereço:VRCC Veterinary Referrals, Laindon, United Kingdom.
[Ti] Título:Influence of treatment on the outcome of dogs with incompletely excised grade-2 mast cell tumors.
[Ti] Título:Einfluss der Behandlung auf das Ergebnis von Hunden mit unvollständing entfernten Grad-2 Mastzelltumoren..
[So] Source:Schweiz Arch Tierheilkd;159(3):171-177, 2017 Mar.
[Is] ISSN:0036-7281
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: In this study we compared the outcomes of dogs with incompletely-excised grade-2 mast cell tumors (incompletely- excised grade-2 MCTs) either adjuvantly treated or not. Dogs with a grade-2 mast cell tumour (MCT) excised either incompletely or with narrow (.
[Mh] Termos MeSH primário: Doenças do Cão/terapia
Mastocitose/veterinária
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Terapia Combinada
Cães
Seguimentos
Lomustina/uso terapêutico
Mastocitose/mortalidade
Mastocitose/terapia
Reoperação
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 7BRF0Z81KG (Lomustine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE
[do] DOI:10.17236/sat00109


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[PMID]:28222789
[Au] Autor:Laprais A; Olivry T
[Ad] Endereço:Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA.
[Ti] Título:Is CCNU (lomustine) valuable for treatment of cutaneous epitheliotropic lymphoma in dogs? A critically appraised topic.
[So] Source:BMC Vet Res;13(1):61, 2017 Feb 21.
[Is] ISSN:1746-6148
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: CCNU and other treatment protocols are commonly offered to owners for the treatment of dogs diagnosed with cutaneous (epitheliotropic) T-cell lymphoma (CTCL). Chemotherapy protocols provide variable benefits; they have different side-effects, and they typically require monitoring to detect drug toxicity at a non-negligible cost to the owner. At this time, even though CCNU is most often recommended to treat dogs with CTCL, there is no clear consensus on the benefit of this drug. Knowing which chemotherapy protocol yields the highest rate of complete remission and longest survival times would help veterinarians and pet owners select treatment options based on the best evidence available. Our objective was to review the literature to compare the complete remission rates and survival times of CCNU-based protocols to those of other interventions. We critically assessed the data included in articles reporting treatment outcome in at least five dogs with CTCL. Single case reports and case series with less than five patients were not reviewed to avoid anecdotal evidence of lower quality. RESULTS: The search for, and review and analysis of, the best evidence available as of February 8, 2017, suggests that CCNU and pegylated liposomal doxorubicin appear to yield the highest rate of complete remission in approximately one-third of dogs with CTCL. Other treatment protocols did not report usable information on remission rates. Without any treatment, the mean/median survival time in dogs with CTCL varied between 3 and 5 months. With CCNU protocols, the median survival time was 6 months and the one with retinoids (isotretinoin and/or etretinate), PEG L-asparaginase or prednisolone monotherapy was 11, 9 and 4 months, respectively; all these durations were obtained from small numbers of dogs, however. CONCLUSIONS: CCNU leads to a complete remission of signs in approximately one-third of dogs with CTCL, but such remissions are of short duration. The median survival time after CCNU appears longer than that without treatment, but other drugs appear to provide a better long-term prognosis. Further studies are required to investigate the effect of CCNU, alone or in combination, on remission rates, survival times and impact on quality of life.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/uso terapêutico
Doenças do Cão/tratamento farmacológico
Lomustina/uso terapêutico
Linfoma Cutâneo de Células T/veterinária
[Mh] Termos MeSH secundário: Animais
Cães
Linfoma Cutâneo de Células T/tratamento farmacológico
Indução de Remissão
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 7BRF0Z81KG (Lomustine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170306
[Lr] Data última revisão:
170306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE
[do] DOI:10.1186/s12917-017-0978-7


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[PMID]:28117638
[Au] Autor:KuKanich B; Warner M; Hahn K
[Ti] Título:Analysis of lomustine drug content in FDA-approved and compounded lomustine capsules.
[So] Source:J Am Vet Med Assoc;250(3):322-326, 2017 Feb 01.
[Is] ISSN:1943-569X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE To determine the lomustine content (potency) in compounded and FDA-approved lomustine capsules. DESIGN Evaluation study. SAMPLE 2 formulations of lomustine capsules (low dose [7 to 11 mg] and high dose [40 to 48 mg]; 5 capsules/dose/source) from 3 compounders and from 1 manufacturer of FDA-approved capsules. PROCEDURES Lomustine content was measured by use of a validated high-pressure liquid chromatography method. An a priori acceptable range of 90% to 110% of the stated lomustine content was selected on the basis of US Pharmacopeia guidelines. RESULTS The measured amount of lomustine in all compounded capsules was less than the stated content (range, 59% to 95%) and was frequently outside the acceptable range (failure rate, 2/5 to 5/5). Coefficients of variation for lomustine content ranged from 4.1% to 16.7% for compounded low-dose capsules and from 1.1% to 10.8% for compounded high-dose capsules. The measured amount of lomustine in all FDA-approved capsules was slightly above the stated content (range, 104% to 110%) and consistently within the acceptable range. Coefficients of variation for lomustine content were 0.5% for low-dose and 2.3% for high-dose FDA-approved capsules. CONCLUSIONS AND CLINICAL RELEVANCE Compounded lomustine frequently did not contain the stated content of active drug and had a wider range of lomustine content variability than did the FDA-approved product. The sample size was small, and larger studies are needed to confirm these findings; however, we recommend that compounded veterinary formulations of lomustine not be used when appropriate doses can be achieved with FDA-approved capsules or combinations of FDA-approved capsules.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/química
Composição de Medicamentos
Lomustina/química
United States Food and Drug Administration
[Mh] Termos MeSH secundário: Antineoplásicos Alquilantes/normas
Cápsulas/química
Cápsulas/normas
Lomustina/normas
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Capsules); 7BRF0Z81KG (Lomustine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE
[do] DOI:10.2460/javma.250.3.322


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[PMID]:27766591
[Au] Autor:Staberg M; Michaelsen SR; Rasmussen RD; Villingshøj M; Poulsen HS; Hamerlik P
[Ad] Endereço:Department of Radiation Biology, The Finsen Center, Rigshospitalet, Copenhagen, Denmark. mikkel.staberg@regionh.dk.
[Ti] Título:Inhibition of histone deacetylases sensitizes glioblastoma cells to lomustine.
[So] Source:Cell Oncol (Dordr);40(1):21-32, 2017 Feb.
[Is] ISSN:2211-3436
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Glioblastoma (GBM) ranks among the deadliest solid cancers worldwide and its prognosis has remained dismal, despite the use of aggressive chemo-irradiation treatment regimens. Limited drug delivery into the brain parenchyma and frequent resistance to currently available therapies are problems that call for a prompt development of novel therapeutic strategies. While only displaying modest efficacies as mono-therapy in pre-clinical settings, histone deacetylase inhibitors (HDACi) have shown promising sensitizing effects to a number of cytotoxic agents. Here, we sought to investigate the sensitizing effect of the HDACi trichostatin A (TSA) to the alkylating agent lomustine (CCNU), which is used in the clinic for the treatment of GBM. METHODS: Twelve primary GBM cell cultures grown as neurospheres were used in this study, as well as one established GBM-derived cell line (U87 MG). Histone deacetylase (HDAC) expression levels were determined using quantitative real-time PCR and Western blotting. The efficacy of either CCNU alone or its combination with TSA was assessed using various assays, i.e., cell viability assays (MTT), cell cycle assays (flow cytometry, FACS), double-strand DNA break (DSB) quantification assays (microscopy/immunofluorescence) and expression profiling assays of proteins involved in apoptosis and cell stress (Western blotting and protein array). RESULTS: We found that the HDAC1, 3 and 6 expression levels were significantly increased in GBM samples compared to non-neoplastic brain control samples. Additionally, we found that pre-treatment of GBM cells with TSA resulted in an enhancement of their sensitivity to CCNU, possibly via the accumulation of DSBs, decreased cell proliferation and viability rates, and an increased apoptotic rate. CONCLUSION: From our data we conclude that the combined administration of TSA and CCNU eradicates GBM cells with a higher efficacy than either drug alone, thereby opening a novel avenue for the treatment of GBM.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Neoplasias Encefálicas/enzimologia
Glioblastoma/enzimologia
Inibidores de Histona Desacetilases/administração & dosagem
Ácidos Hidroxâmicos/administração & dosagem
Lomustina/administração & dosagem
[Mh] Termos MeSH secundário: Antineoplásicos Alquilantes/administração & dosagem
Western Blotting
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Citometria de Fluxo
Imunofluorescência
Seres Humanos
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 3X2S926L3Z (trichostatin A); 7BRF0Z81KG (Lomustine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161022
[St] Status:MEDLINE
[do] DOI:10.1007/s13402-016-0301-9


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[PMID]:28033329
[Au] Autor:Steidl E; Pilatus U; Hattingen E; Steinbach JP; Zanella F; Ronellenfitsch MW; Bähr O
[Ad] Endereço:Dr. Senckenberg Institute of Neurooncology, Center for Neurology and Neurosurgery, Johann Wolfgang Goethe-University, Frankfurt/Main, Germany.
[Ti] Título:Myoinositol as a Biomarker in Recurrent Glioblastoma Treated with Bevacizumab: A 1H-Magnetic Resonance Spectroscopy Study.
[So] Source:PLoS One;11(12):e0168113, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Antiangiogenic treatment of glioblastomas with Bevacizumab lacks predictive markers. Myoinositol (MI) is an organic osmolyte, with intracellular concentration changes depending on the extracellular osmolality. Since Bevacizumab markedly reduces tumor edema and influences the tumor microenvironment, we investigated whether the MI concentration in the tumor changes during therapy. METHODS: We used 1H-magnetic resonance spectroscopy to measure the MI concentrations in the tumor and contralateral control tissue of 39 prospectively recruited patients with recurrent glioblastomas before and 8-12 weeks after starting therapy. 30 patients received Bevacizumab and 9 patients were treated with CCNU/VM26 as control. We performed a survival analysis to evaluate MI as a predictive biomarker for Bevacizumab therapy. RESULTS: MI concentrations increased significantly during Bevacizumab therapy in tumor (p < .001) and control tissue (p = .001), but not during CCNU/VM26 treatment. For the Bevacizumab cohort, higher MI concentrations in the control tissue at baseline (p = .021) and higher differences between control and tumor tissue (delta MI, p = .011) were associated with longer survival. A Kaplan-Meier analysis showed a median OS of 164 days for patients with a deltaMI < 1,817 mmol/l and 275 days for patients with a deltaMI > 1,817 mmol/l. No differences were observed for the relative changes or the post treatment concentrations. Additionally calculated creatine concentrations showed no differences in between subgroups or between pre and post treatment measurements. CONCLUSION: Our data suggest that recurrent glioblastoma shows a strong metabolic reaction to Bevacizumab. Further, our results support the hypothesis that MI might be a marker for early tumor cell invasion. Pre-therapeutic MI concentrations are predictive of overall survival in patients with recurrent glioblastoma treated with Bevacizumab.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/uso terapêutico
Bevacizumab/uso terapêutico
Biomarcadores Tumorais/metabolismo
Glioblastoma/tratamento farmacológico
Inositol/metabolismo
Espectroscopia de Ressonância Magnética/métodos
[Mh] Termos MeSH secundário: Adulto
Idoso
Antineoplásicos/uso terapêutico
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/mortalidade
Neoplasias Encefálicas/patologia
Feminino
Glioblastoma/mortalidade
Glioblastoma/patologia
Seres Humanos
Hidrogênio/química
Lomustina/uso terapêutico
Imagem por Ressonância Magnética/métodos
Masculino
Meia-Idade
Estudos Prospectivos
Análise de Sobrevida
Teniposídeo/uso terapêutico
Microambiente Tumoral/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores
Fator A de Crescimento do Endotélio Vascular/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Antineoplastic Agents); 0 (Biomarkers, Tumor); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 2S9ZZM9Q9V (Bevacizumab); 4L6452S749 (Inositol); 7BRF0Z81KG (Lomustine); 7YNJ3PO35Z (Hydrogen); 957E6438QA (Teniposide)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170706
[Lr] Data última revisão:
170706
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161230
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0168113


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[PMID]:27474153
[Au] Autor:Berte N; Piée-Staffa A; Piecha N; Wang M; Borgmann K; Kaina B; Nikolova T
[Ad] Endereço:Institute of Toxicology, University Medical Center Mainz, Mainz, Germany.
[Ti] Título:Targeting Homologous Recombination by Pharmacological Inhibitors Enhances the Killing Response of Glioblastoma Cells Treated with Alkylating Drugs.
[So] Source:Mol Cancer Ther;15(11):2665-2678, 2016 Nov.
[Is] ISSN:1538-8514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Malignant gliomas exhibit a high level of intrinsic and acquired drug resistance and have a dismal prognosis. First- and second-line therapeutics for glioblastomas are alkylating agents, including the chloroethylating nitrosoureas (CNU) lomustine, nimustine, fotemustine, and carmustine. These agents target the tumor DNA, forming O -chloroethylguanine adducts and secondary DNA interstrand cross-links (ICL). These cross-links are supposed to be converted into DNA double-strand breaks, which trigger cell death pathways. Here, we show that lomustine (CCNU) with moderately toxic doses induces ICLs in glioblastoma cells, inhibits DNA replication fork movement, and provokes the formation of DSBs and chromosomal aberrations. Since homologous recombination (HR) is involved in the repair of DSBs formed in response to CNUs, we elucidated whether pharmacologic inhibitors of HR might have impact on these endpoints and enhance the killing effect. We show that the Rad51 inhibitors RI-1 and B02 greatly ameliorate DSBs, chromosomal changes, and the level of apoptosis and necrosis. We also show that an inhibitor of MRE11, mirin, which blocks the formation of the MRN complex and thus the recognition of DSBs, has a sensitizing effect on these endpoints as well. In a glioma xenograft model, the Rad51 inhibitor RI-1 clearly enhanced the effect of CCNU on tumor growth. The data suggest that pharmacologic inhibition of HR, for example by RI-1, is a reasonable strategy for enhancing the anticancer effect of CNUs. Mol Cancer Ther; 15(11); 2665-78. ©2016 AACR.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Recombinação Homóloga/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Apoptose/genética
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Aberrações Cromossômicas/efeitos dos fármacos
Dano ao DNA
Metilases de Modificação do DNA/metabolismo
Reparo do DNA
Enzimas Reparadoras do DNA/metabolismo
Replicação do DNA/efeitos dos fármacos
Proteínas de Ligação a DNA/metabolismo
Modelos Animais de Doenças
Glioblastoma/tratamento farmacológico
Glioblastoma/genética
Glioblastoma/metabolismo
Seres Humanos
Lomustina/farmacologia
Proteína Homóloga a MRE11
Camundongos
Rad51 Recombinase/metabolismo
Proteínas Supressoras de Tumor/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (DNA-Binding Proteins); 0 (MRE11A protein, human); 0 (Tumor Suppressor Proteins); 7BRF0Z81KG (Lomustine); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 2.7.7.- (Rad51 Recombinase); EC 3.1.- (MRE11 Homologue Protein); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160731
[St] Status:MEDLINE


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[PMID]:27430318
[Au] Autor:Nakamoto Y; Yamada A; Uchida K; Matsunaga S; Ozawa T
[Ad] Endereço:Kyoto Animal Referral Medical Center, 208-4, Shinarami, Tai, Kumiyama-cho, Kuze-gun, Kyoto 613-0036, Japan.
[Ti] Título:Case of a miniature dachshund with a primitive neuroectodermal tumor confined to the forebrain region treated with a combination of surgery and chemotherapy.
[So] Source:J Vet Med Sci;78(11):1703-1707, 2016 Dec 01.
[Is] ISSN:1347-7439
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:A miniature dachshund aged 9 years and 7 months with a history of polyuria/polydipsia and depression was referred. General physical and neurological examinations revealed no obvious abnormalities. MRI of the brain revealed a large space-occupying lesion in the left frontal lobe. This was surgically removed and pathologically diagnosed as a primitive neuroectodermal tumor (PNET). Although the clinical signs had been improved, follow-up MRI revealed recurrence of the tumor. Lomustine was administered, but 1 year after surgery, the dog exhibited cluster seizures and died. This is the first reported case of a dog with PNET confined to the forebrain region treated by surgical resection in combination with chemotherapy, as observed by repeated follow-up MRI.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/uso terapêutico
Neoplasias Encefálicas/veterinária
Doenças do Cão/tratamento farmacológico
Doenças do Cão/cirurgia
Lomustina/uso terapêutico
Tumores Neuroectodérmicos Primitivos/veterinária
[Mh] Termos MeSH secundário: Animais
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/cirurgia
Terapia Combinada/veterinária
Cães
Feminino
Lobo Frontal/patologia
Imagem por Ressonância Magnética/veterinária
Recidiva Local de Neoplasia/veterinária
Tumores Neuroectodérmicos Primitivos/tratamento farmacológico
Tumores Neuroectodérmicos Primitivos/cirurgia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 7BRF0Z81KG (Lomustine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160720
[St] Status:MEDLINE


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[PMID]:27402390
[Au] Autor:Combs SE; Schmidt-Graf F; Meyer B
[Ad] Endereço:Institut für Innovative Radiotherapie (iRT) Department of Radiation Sciences (DRS), Helmholtz Zentrum München, Ingolstädter Landstraße 1, 85764, Oberschleißheim, Deutschland. stephanie.combs@tum.de.
[Ti] Título:[Not Available].
[Ti] Título:Bessere Prognose von Low-grade-Gliomen durch Kombination von Bestrahlung, Procarbazin, CCNU und Vincristin..
[So] Source:Strahlenther Onkol;192(9):672-4, 2016 Sep.
[Is] ISSN:1439-099X
[Cp] País de publicação:Germany
[La] Idioma:ger
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Astrocitoma/mortalidade
Astrocitoma/terapia
Neoplasias Encefálicas/mortalidade
Neoplasias Encefálicas/terapia
Quimiorradioterapia/mortalidade
Quimiorradioterapia/estatística & dados numéricos
[Mh] Termos MeSH secundário: Astrocitoma/patologia
Neoplasias Encefálicas/patologia
Intervalo Livre de Doença
Feminino
Seguimentos
Seres Humanos
Lomustina/administração & dosagem
Masculino
Gradação de Tumores
Prevalência
Procarbazina/administração & dosagem
Prognóstico
Medição de Risco
Análise de Sobrevida
Resultado do Tratamento
Estados Unidos/epidemiologia
Vincristina/administração & dosagem
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
35S93Y190K (Procarbazine); 5J49Q6B70F (Vincristine); 7BRF0Z81KG (Lomustine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160713
[St] Status:MEDLINE
[do] DOI:10.1007/s00066-016-1016-6


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Registro de Ensaios Clínicos
[PMID]:27370396
[Au] Autor:Wick W; Roth P; Hartmann C; Hau P; Nakamura M; Stockhammer F; Sabel MC; Wick A; Koeppen S; Ketter R; Vajkoczy P; Eyupoglu I; Kalff R; Pietsch T; Happold C; Galldiks N; Schmidt-Graf F; Bamberg M; Reifenberger G; Platten M; von Deimling A; Meisner C; Wiestler B; Weller M; Neurooncology Working Group (NOA) of the German Cancer Society
[Ad] Endereço:Department of Neurology Clinic, University of Heidelberg, Heidelberg, Germany (W.W., A.W., M.P., B.W.); Clinical Cooperation Unit (CCU Neurooncology), German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany (W.W., B.W.); Department of Neurology, University Hospital
[Ti] Título:Long-term analysis of the NOA-04 randomized phase III trial of sequential radiochemotherapy of anaplastic glioma with PCV or temozolomide.
[So] Source:Neuro Oncol;18(11):1529-1537, 2016 Nov.
[Is] ISSN:1523-5866
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Optimal treatment and precise classification for anaplastic glioma are needed. METHODS: The objective for long-term follow-up of NOA-04 is to optimize the treatment sequence for patients with anaplastic gliomas. Patients were randomized 2:1:1 to receive the standard radiotherapy (RT) (arm A), procarbazine, lomustine and vincristine (PCV) (arm B1), or temozolomide (TMZ) (arm B2). RESULTS: Primary endpoint was time-to-treatment-failure (TTF), defined as progression after 2 lines of therapy or any time before if no further therapy was administered. Exploratory analyses examined associations of molecular marker status with TTF, progression-free survival (PFS), and overall survival (OS). At 9.5 (95% CI: 8.6-10.2) years, no difference between arms (A vs B1/B2) was observed: median TTF (4.6 [3.4-5.1] y vs 4.4 [3.3-5.3) y), PFS (2.5 [1.3-3.5] y vs 2.7 [1.9-3.2] y), and OS (8 [5.5-10.3] y vs 6.5 [5.4-8.3] y). Oligodendroglial versus astrocytic histology-but more so the subgroups according to CpG island methylator phenotype (CIMP) and 1p/19q co-deletion status-revealed a strong prognostic value of CIMP with (CIMP ) versus without 1p/19 co-deletion (CIMP ) versus CIMP . but no differential efficacy of RT versus chemotherapy for any of the endpoints. PFS was better for PCV- than for TMZ-treated patients with CIMP tumors (HR B1 vs B2 0.39 [0.17-0.92], P = .031). In CIMP . tumors, hypermethylation of the O6-methyl-guanyl-DNA methyltransferase promoter (MGMT) provided a risk reduction for PFS with chemotherapy. CONCLUSIONS: There is no differential activity of primary chemotherapy versus RT in any subgroup of anaplastic glioma. Molecular diagnosis is superior to histology. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00717210.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/radioterapia
Quimiorradioterapia/métodos
Dacarbazina/análogos & derivados
Glioma/tratamento farmacológico
Glioma/radioterapia
[Mh] Termos MeSH secundário: Adulto
Idoso
Antineoplásicos Alquilantes/uso terapêutico
Antineoplásicos Fitogênicos/uso terapêutico
Neoplasias Encefálicas/diagnóstico
Dacarbazina/uso terapêutico
Intervalo Livre de Doença
Feminino
Glioma/diagnóstico
Seres Humanos
Lomustina/uso terapêutico
Masculino
Meia-Idade
Procarbazina/uso terapêutico
Resultado do Tratamento
Vincristina/uso terapêutico
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Antineoplastic Agents, Alkylating); 0 (Antineoplastic Agents, Phytogenic); 35S93Y190K (Procarbazine); 5J49Q6B70F (Vincristine); 7BRF0Z81KG (Lomustine); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160703
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE



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