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[PMID]:29330228
[Au] Autor:McCormack A; Dekkers OM; Petersenn S; Popovic V; Trouillas J; Raverot G; Burman P; ESE survey collaborators
[Ad] Endereço:St Vincent's Hospital and Garvan Institute of Medical ResearchSydney, Australia.
[Ti] Título:Treatment of aggressive pituitary tumours and carcinomas: results of a European Society of Endocrinology (ESE) survey 2016.
[So] Source:Eur J Endocrinol;178(3):265-276, 2018 03.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To collect outcome data in a large cohort of patients with aggressive pituitary tumours (APT)/carcinomas (PC) and specifically report effects of temozolomide (TMZ) treatment. DESIGN: Electronic survey to ESE members Dec 2015-Nov 2016. RESULTS: Reports on 166 patients (40 PC, 125 APT, 1 unclassified) were obtained. Median age at diagnosis was 43 (range 4-79) years. 69% of the tumours were clinically functioning, and the most frequent immunohistochemical subtype were corticotroph tumours (45%). Ki-67 index did not distinguish APT from PC, median 7% and 10% respectively. TMZ was first-line chemotherapy in 157 patients. At the end of the treatment (median 9 cycles), radiological evaluation showed complete response (CR) in 6%, partial response (PR) in 31%, stable disease (SD) in 33% and progressive disease in 30%. Response was more frequent in patients receiving concomitant radiotherapy and TMZ. CR was seen only in patients with low MGMT expression. Clinically functioning tumours were more likely to respond than non-functioning tumours, independent of MGMT status. Of patients with CR, PR and SD, 25, 40 and 48% respectively progressed after a median of 12-month follow-up. Other oncological drugs given as primary treatment and to TMZ failures resulted in PR in 20%. CONCLUSION: This survey confirms that TMZ is established as first-line chemotherapeutic treatment of APT/PC. Clinically functioning tumours, low MGMT and concurrent radiotherapy were associated with a better response. The limited long-term effect of TMZ and the poor efficacy of other drugs highlight the need to identify additional effective therapies.
[Mh] Termos MeSH primário: Adenoma/terapia
Antineoplásicos Alquilantes/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Carcinoma/terapia
Irradiação Craniana
Dacarbazina/análogos & derivados
Procedimentos Neurocirúrgicos
Neoplasias Hipofisárias/terapia
[Mh] Termos MeSH secundário: Adenoma/metabolismo
Adenoma/patologia
Adolescente
Adulto
Idoso
Bevacizumab/administração & dosagem
Capecitabina/administração & dosagem
Carcinoma/metabolismo
Carcinoma/patologia
Carmustina/administração & dosagem
Criança
Pré-Escolar
Metilases de Modificação do DNA/metabolismo
Enzimas Reparadoras do DNA/metabolismo
Dacarbazina/administração & dosagem
Dacarbazina/uso terapêutico
Endocrinologia
Europa (Continente)
Feminino
Seres Humanos
Antígeno Ki-67/metabolismo
Masculino
Meia-Idade
Invasividade Neoplásica
Neoplasias Hipofisárias/metabolismo
Neoplasias Hipofisárias/patologia
Sociedades Médicas
Inquéritos e Questionários
Talidomida/administração & dosagem
Proteínas Supressoras de Tumor/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Ki-67 Antigen); 0 (Tumor Suppressor Proteins); 2S9ZZM9Q9V (Bevacizumab); 4Z8R6ORS6L (Thalidomide); 6804DJ8Z9U (Capecitabine); 7GR28W0FJI (Dacarbazine); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 6.5.1.- (DNA Repair Enzymes); U68WG3173Y (Carmustine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0933


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[PMID]:29224502
[Au] Autor:Connors JM; Jurczak W; Straus DJ; Ansell SM; Kim WS; Gallamini A; Younes A; Alekseev S; Illés Á; Picardi M; Lech-Maranda E; Oki Y; Feldman T; Smolewski P; Savage KJ; Bartlett NL; Walewski J; Chen R; Ramchandren R; Zinzani PL; Cunningham D; Rosta A; Josephson NC; Song E; Sachs J; Liu R; Jolin HA; Huebner D; Radford J; ECHELON-1 Study Group
[Ad] Endereço:From the University of British Columbia and the Department of Medical Oncology, British Columbia Cancer Agency Centre for Lymphoid Cancer, Vancouver, Canada (J.M.C., K.J.S.); the Department of Hematology, Jagiellonian University, Krakow (W.J.), the Department of Hematology, Institute of Hematology a
[Ti] Título:Brentuximab Vedotin with Chemotherapy for Stage III or IV Hodgkin's Lymphoma.
[So] Source:N Engl J Med;378(4):331-344, 2018 01 25.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Brentuximab vedotin is an anti-CD30 antibody-drug conjugate that has been approved for relapsed and refractory Hodgkin's lymphoma. METHODS: We conducted an open-label, multicenter, randomized phase 3 trial involving patients with previously untreated stage III or IV classic Hodgkin's lymphoma, in which 664 were assigned to receive brentuximab vedotin, doxorubicin, vinblastine, and dacarbazine (A+AVD) and 670 were assigned to receive doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD). The primary end point was modified progression-free survival (the time to progression, death, or noncomplete response and use of subsequent anticancer therapy) as adjudicated by an independent review committee. The key secondary end point was overall survival. RESULTS: At a median follow-up of 24.6 months, 2-year modified progression-free survival rates in the A+AVD and ABVD groups were 82.1% (95% confidence interval [CI], 78.8 to 85.0) and 77.2% (95% CI, 73.7 to 80.4), respectively, a difference of 4.9 percentage points (hazard ratio for an event of progression, death, or modified progression, 0.77; 95% CI, 0.60 to 0.98; P=0.04). There were 28 deaths with A+AVD and 39 with ABVD (hazard ratio for interim overall survival, 0.73 [95% CI, 0.45 to 1.18]; P=0.20) [corrected]. All secondary efficacy end points trended in favor of A+AVD. Neutropenia occurred in 58% of the patients receiving A+AVD and in 45% of those receiving ABVD; in the A+AVD group, the rate of febrile neutropenia was lower among the 83 patients who received primary prophylaxis with granulocyte colony-stimulating factor than among those who did not (11% vs. 21%). Peripheral neuropathy occurred in 67% of patients in the A+AVD group and in 43% of patients in the ABVD group; 67% of patients in the A+AVD group who had peripheral neuropathy had resolution or improvement at the last follow-up visit. Pulmonary toxicity of grade 3 or higher was reported in less than 1% of patients receiving A+AVD and in 3% of those receiving ABVD. Among the deaths that occurred during treatment, 7 of 9 in the A+AVD group were associated with neutropenia and 11 of 13 in the ABVD group were associated with pulmonary-related toxicity. CONCLUSIONS: A+AVD had superior efficacy to ABVD in the treatment of patients with advanced-stage Hodgkin's lymphoma, with a 4.9 percentage-point lower combined risk of progression, death, or noncomplete response and use of subsequent anticancer therapy at 2 years. (Funded by Millennium Pharmaceuticals and Seattle Genetics; ECHELON-1 ClinicalTrials.gov number, NCT01712490 ; EudraCT number, 2011-005450-60 .).
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Doença de Hodgkin/tratamento farmacológico
Imunoconjugados/administração & dosagem
Fatores Imunológicos/administração & dosagem
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Bleomicina/administração & dosagem
Dacarbazina/administração & dosagem
Intervalo Livre de Doença
Doxorrubicina/administração & dosagem
Feminino
Seguimentos
Doença de Hodgkin/mortalidade
Seres Humanos
Imunoconjugados/efeitos adversos
Fatores Imunológicos/efeitos adversos
Masculino
Meia-Idade
Estadiamento de Neoplasias
Neutropenia/induzido quimicamente
Taxa de Sobrevida
Vimblastina/administração & dosagem
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Immunoconjugates); 0 (Immunologic Factors); 11056-06-7 (Bleomycin); 5V9KLZ54CY (Vinblastine); 7GR28W0FJI (Dacarbazine); 7XL5ISS668 (brentuximab vedotin); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171212
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1708984


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[PMID]:29260225
[Au] Autor:Stupp R; Taillibert S; Kanner A; Read W; Steinberg DM; Lhermitte B; Toms S; Idbaih A; Ahluwalia MS; Fink K; Di Meco F; Lieberman F; Zhu JJ; Stragliotto G; Tran DD; Brem S; Hottinger AF; Kirson ED; Lavy-Shahaf G; Weinberg U; Kim CY; Paek SH; Nicholas G; Burna J; Hirte H; Weller M; Palti Y; Hegi ME; Ram Z
[Ad] Endereço:Lou and Jean MalnatiBrain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University Feinberg School of Medicine, Chicago, Illinois.
[Ti] Título:Effect of Tumor-Treating Fields Plus Maintenance Temozolomide vs Maintenance Temozolomide Alone on Survival in Patients With Glioblastoma: A Randomized Clinical Trial.
[So] Source:JAMA;318(23):2306-2316, 2017 12 19.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Tumor-treating fields (TTFields) is an antimitotic treatment modality that interferes with glioblastoma cell division and organelle assembly by delivering low-intensity alternating electric fields to the tumor. Objective: To investigate whether TTFields improves progression-free and overall survival of patients with glioblastoma, a fatal disease that commonly recurs at the initial tumor site or in the central nervous system. Design, Setting, and Participants: In this randomized, open-label trial, 695 patients with glioblastoma whose tumor was resected or biopsied and had completed concomitant radiochemotherapy (median time from diagnosis to randomization, 3.8 months) were enrolled at 83 centers (July 2009-2014) and followed up through December 2016. A preliminary report from this trial was published in 2015; this report describes the final analysis. Interventions: Patients were randomized 2:1 to TTFields plus maintenance temozolomide chemotherapy (n = 466) or temozolomide alone (n = 229). The TTFields, consisting of low-intensity, 200 kHz frequency, alternating electric fields, was delivered (≥ 18 hours/d) via 4 transducer arrays on the shaved scalp and connected to a portable device. Temozolomide was administered to both groups (150-200 mg/m2) for 5 days per 28-day cycle (6-12 cycles). Main Outcomes and Measures: Progression-free survival (tested at α = .046). The secondary end point was overall survival (tested hierarchically at α = .048). Analyses were performed for the intent-to-treat population. Adverse events were compared by group. Results: Of the 695 randomized patients (median age, 56 years; IQR, 48-63; 473 men [68%]), 637 (92%) completed the trial. Median progression-free survival from randomization was 6.7 months in the TTFields-temozolomide group and 4.0 months in the temozolomide-alone group (HR, 0.63; 95% CI, 0.52-0.76; P < .001). Median overall survival was 20.9 months in the TTFields-temozolomide group vs 16.0 months in the temozolomide-alone group (HR, 0.63; 95% CI, 0.53-0.76; P < .001). Systemic adverse event frequency was 48% in the TTFields-temozolomide group and 44% in the temozolomide-alone group. Mild to moderate skin toxicity underneath the transducer arrays occurred in 52% of patients who received TTFields-temozolomide vs no patients who received temozolomide alone. Conclusions and Relevance: In the final analysis of this randomized clinical trial of patients with glioblastoma who had received standard radiochemotherapy, the addition of TTFields to maintenance temozolomide chemotherapy vs maintenance temozolomide alone, resulted in statistically significant improvement in progression-free survival and overall survival. These results are consistent with the previous interim analysis. Trial Registration: clinicaltrials.gov Identifier: NCT00916409.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/uso terapêutico
Dacarbazina/análogos & derivados
Terapia por Estimulação Elétrica
Glioblastoma/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Antineoplásicos Alquilantes/efeitos adversos
Quimiorradioterapia
Dacarbazina/efeitos adversos
Dacarbazina/uso terapêutico
Intervalo Livre de Doença
Feminino
Seguimentos
Glioblastoma/radioterapia
Glioblastoma/cirurgia
Seres Humanos
Quimioterapia de Manutenção
Masculino
Meia-Idade
Mitose
Análise de Sobrevida
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171221
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.18718


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[PMID]:29352318
[Au] Autor:William D; Walther M; Schneider B; Linnebacher M; Classen CF
[Ad] Endereço:University Children's and Adolescents' Hospital, University Medicine of Rostock, Rostock, Germany.
[Ti] Título:Temozolomide-induced increase of tumorigenicity can be diminished by targeting of mitochondria in in vitro models of patient individual glioblastoma.
[So] Source:PLoS One;13(1):e0191511, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma multiforme (GBM) is a highly heterogeneous and aggressive brain tumor with a dismal prognosis. Development of resistance towards cytostatic drugs like the GBM standard drug temozolomide is a severe problem in GBM treatment. One potential source of GBM relapse could be so called cancer stem like cells (CSCs). These represent an undifferentiated subpopulation of cells with high potential for tumor initiation. Furthermore, it has been shown that differentiated GBM cells can regain CSC properties when exposed to continuous temozolomide treatment in vitro. In this study, treatment of several primary GBM cell lines with clinically relevant doses of temozolomide increased their tumorigenicity as determined by colony formation assays in soft agar. Increased tumorigenicity is a known property of CSCs. Hence, therapy options that specifically target CSCs are under investigation. CSCs appear to be particularly dependent on mitochondria biogenesis which may represent a useful target for CSC elimination. Toxicity towards mitochondria is a known side effect of several antibiotics. Thus, addition of antibiotics like doxycycline may represent a useful tool to inhibit CSCs in GBM. Here, we show that combining temozolomide treatment of primary GBM cells with doxycycline could counteract the increase of tumorigenicity induced by temozolomide treatment.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/efeitos adversos
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/patologia
Dacarbazina/análogos & derivados
Glioblastoma/tratamento farmacológico
Glioblastoma/patologia
[Mh] Termos MeSH secundário: Antibacterianos/administração & dosagem
Antineoplásicos Alquilantes/administração & dosagem
Biomarcadores Tumorais/metabolismo
Neoplasias Encefálicas/metabolismo
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Metilases de Modificação do DNA/genética
Enzimas Reparadoras do DNA/genética
Dacarbazina/administração & dosagem
Dacarbazina/efeitos adversos
Doxiciclina/administração & dosagem
Resistência a Medicamentos Antineoplásicos
Fucosiltransferases/metabolismo
Glioblastoma/metabolismo
Seres Humanos
Antígeno Lewis X/metabolismo
Mitocôndrias/efeitos dos fármacos
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/patologia
Nestina/metabolismo
Ensaio Tumoral de Célula-Tronco
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Antineoplastic Agents, Alkylating); 0 (Biomarkers, Tumor); 0 (Lewis X Antigen); 0 (NES protein, human); 0 (Nestin); 0 (Tumor Suppressor Proteins); 7GR28W0FJI (Dacarbazine); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 2.4.1.- (FUT4 protein, human); EC 2.4.1.- (Fucosyltransferases); EC 6.5.1.- (DNA Repair Enzymes); N12000U13O (Doxycycline); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191511


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[PMID]:29248133
[Au] Autor:Mikkilineni L; Whitaker-Menezes D; Domingo-Vidal M; Sprandio J; Avena P; Cotzia P; Dulau-Florea A; Gong J; Uppal G; Zhan T; Leiby B; Lin Z; Pro B; Sotgia F; Lisanti MP; Martinez-Outschoorn U
[Ad] Endereço:Department of Medical Oncology, National Cancer Institute, Bethesda, MD.
[Ti] Título:Hodgkin lymphoma: A complex metabolic ecosystem with glycolytic reprogramming of the tumor microenvironment.
[So] Source:Semin Oncol;44(3):218-225, 2017 06.
[Is] ISSN:1532-8708
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Twenty percent of patients with classical Hodgkin Lymphoma (cHL) have aggressive disease defined as relapsed or refractory disease to initial therapy. At present we cannot identify these patients pre-treatment. The microenvironment is very important in cHL because non-cancer cells constitute the majority of the cells in these tumors. Non-cancer intra-tumoral cells, such as tumor-associated macrophages (TAMs) have been shown to promote tumor growth in cHL via crosstalk with the cancer cells. Metabolic heterogeneity is defined as high mitochondrial metabolism in some tumor cells and glycolysis in others. We hypothesized that there are metabolic differences between cancer cells and non-cancer tumor cells, such as TAMs and tumor-infiltrating lymphocytes in cHL and that greater metabolic differences between cancer cells and TAMs are associated with poor outcomes. METHODS: A case-control study was conducted with 22 tissue samples of cHL at diagnosis from a single institution. The case samples were from 11 patients with aggressive cHL who had relapsed after standard treatment with adriamycin, bleomycin, vinblastine, and dacarbazine (ABVD) or were refractory to this treatment. The control samples were from 11 patients with cHL who achieved a remission and never relapsed after ABVD. Reactive non-cancerous lymph nodes from four subjects served as additional controls. Samples were stained by immunohistochemistry for three metabolic markers: translocase of the outer mitochondrial membrane 20 (TOMM20), monocarboxylate transporter 1 (MCT1), and monocarboxylate transporter 4 (MCT4). TOMM20 is a marker of mitochondrial oxidative phosphorylation (OXPHOS) metabolism. Monocarboxylate transporter 1 (MCT1) is the main importer of lactate into cells and is a marker of OXPHOS. Monocarboxylate transporter 4 (MCT4) is the main lactate exporter out of cells and is a marker of glycolysis. The immunoreactivity for TOMM20, MCT1, and MCT4 was scored based on staining intensity and percentage of positive cells, as follows: 0 for no detectable staining in > 50% of cells; 1+ for faint to moderate staining in > 50% of cells, and 2+ for high or strong staining in > 50% of cells. RESULTS: TOMM20, MCT1, and MCT4 expression was significantly different in Hodgkin and Reed Sternberg (HRS) cells, which are the cancerous cells in cHL compared with TAMs and tumor-associated lymphocytes. HRS have high expression of TOMM20 and MCT1, while TAMs have absent expression of TOMM20 and MCT1 in all but two cases. Tumor-infiltrating lymphocytes have low TOMM20 expression and absent MCT1 expression. Conversely, high MCT4 expression was found in TAMs, but absent in HRS cells in all but one case. Tumor-infiltrating lymphocytes had absent MCT4 expression. Reactive lymph nodes in contrast to cHL tumors had low TOMM20, MCT1, and MCT4 expression in lymphocytes and macrophages. High TOMM20 and MCT1 expression in cancer cells with high MCT4 expression in TAMs is a signature of high metabolic heterogeneity between cancer cells and the tumor microenvironment. A high metabolic heterogeneity signature was associated with relapsed or refractory cHL with a hazard ratio of 5.87 (1.16-29.71; two-sided P < .05) compared with the low metabolic heterogeneity signature. CONCLUSION: Aggressive cHL exhibits features of metabolic heterogeneity with high mitochondrial metabolism in cancer cells and high glycolysis in TAMs, which is not seen in reactive lymph nodes. Future studies will need to confirm the value of these markers as prognostic and predictive biomarkers in clinical practice. Treatment intensity may be tailored in the future to the metabolic profile of the tumor microenvironment and drugs that target metabolic heterogeneity may be valuable in this disease.
[Mh] Termos MeSH primário: Glicólise
Doença de Hodgkin/metabolismo
Proteínas de Membrana Transportadoras/metabolismo
Mitocôndrias/metabolismo
Transportadores de Ácidos Monocarboxílicos/metabolismo
Recidiva Local de Neoplasia/metabolismo
Fosforilação Oxidativa
Receptores de Superfície Celular/metabolismo
Células de Reed-Sternberg/metabolismo
Simportadores/metabolismo
Microambiente Tumoral
[Mh] Termos MeSH secundário: Adulto
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Bleomicina/administração & dosagem
Estudos de Casos e Controles
Dacarbazina/administração & dosagem
Doxorrubicina/administração & dosagem
Feminino
Doença de Hodgkin/tratamento farmacológico
Seres Humanos
Imuno-Histoquímica
Linfócitos do Interstício Tumoral/metabolismo
Macrófagos/metabolismo
Masculino
Meia-Idade
Proteínas Musculares/metabolismo
Indução de Remissão
Vimblastina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Membrane Transport Proteins); 0 (Monocarboxylic Acid Transporters); 0 (Muscle Proteins); 0 (Receptors, Cell Surface); 0 (SLC16A4 protein, human); 0 (Symporters); 0 (TOMM20 protein, human); 0 (monocarboxylate transport protein 1); 11056-06-7 (Bleomycin); 5V9KLZ54CY (Vinblastine); 7GR28W0FJI (Dacarbazine); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE


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[PMID]:29443778
[Au] Autor:He X; Chen Z; Dong Y; Tong D
[Ad] Endereço:Department of Radiology.
[Ti] Título:A primitive neuroectodermal tumor in an adult: Case report of a unique location and MRI characteristics.
[So] Source:Medicine (Baltimore);97(7):e9933, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Central nervous system primitive neuroectodermal tumors (CNS PNETs) mostly occur in children and present as cerebellar medulloblastoma. A few cases of PNETs occur in the cerebral hemisphere. The presence of a PNET in ventricles is extremely rare. The prognosis of CNS PNET is extremely poor, and the 5-year survival rate does not exceed 35%. In the present study, we describe the first case of a PNET in the ventricles with good prognosis. PATIENT CONCERNS: The case of a 36-year-old man is reported, who presented with a progressively worsening headache for 2 months. DIAGNOSES: Magnetic resonance imaging (MRI) revealed multiple tubercula on the walls of the lateral and third ventricles. Histopathologic analysis revealed a hypercellular tumor with small round cells containing hyperchromatic nuclei and a high nucleus:cytoplasm ratio. The analysis was consistent with PNET. INTERVENTIONS: Radiation therapy covering the entire craniospinal axis was administered, with Temozolomide for synchronous auxiliary treatment. OUTCOMES: The patient was follow-up for a year and showed no signs of recurrence. LESSONS: We present the first CNS PNET located in the ventricles with good prognosis. In this case, radiotherapy with Temozolomide auxiliary treatment presented good efficacy and safety to treat PNET. Additional studies on biomarkers may be useful in predicting personalized therapeutic response.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/diagnóstico por imagem
Ventrículos Cerebrais/diagnóstico por imagem
Imagem por Ressonância Magnética
Tumores Neuroectodérmicos Primitivos/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adulto
Antineoplásicos Alquilantes/uso terapêutico
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/radioterapia
Quimioterapia Adjuvante
Dacarbazina/análogos & derivados
Dacarbazina/uso terapêutico
Seres Humanos
Masculino
Tumores Neuroectodérmicos Primitivos/tratamento farmacológico
Tumores Neuroectodérmicos Primitivos/radioterapia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009933


  7 / 6584 MEDLINE  
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[PMID]:29381964
[Au] Autor:Chen C; Yin S; Zhang S; Wang M; Hu Y; Zhou P; Jiang S
[Ad] Endereço:Department of Neurosurgery, West China Hospital of Sichuan University, Chengdu, Sichuan Province.
[Ti] Título:Treatment of aggressive prolactinoma with temozolomide: A case report and review of literature up to date.
[So] Source:Medicine (Baltimore);96(47):e8733, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Aggressive pituitary adenomas and pituitary carcinomas are rare and demand multiple treatment strategies. Temozolomide, an orally active alkylating chemotherapeutic agent, has recently been recommended as a salvage medication for refractory pituitary adenomas or carcinomas. PATIENT CONCERNS: A 17-year-old male presenting with aggressive prolactinoma that continued to progress despite surgery, gamma knife, and dopamine agonists. DIAGNOSES: The diagnosis of refractory aggressive prolactinoma was made on the basis of clinical findings and the lack of efficacy of conventional treatment. INTERVENTIONS: The patient received the most frequently recommended regimen of temozolomide treatment for 22 cycles. OUTCOMES: Temozolomide resulted in a remarkable shrinkage of tumor mass and inhibition of prolactin secretion and this patient's clinical condition improved progressively. LESSONS: Temozolomide can be used as a salvage treatment to refractory pituitary tumors and o(6)-methylguanine-DNA methyltransferase (MGMT) status is a significant predictor to the effectiveness of temozolomide based on the existing literature.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/uso terapêutico
Dacarbazina/análogos & derivados
Neoplasias Hipofisárias/tratamento farmacológico
Prolactinoma/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Dacarbazina/uso terapêutico
Seres Humanos
Masculino
Prolactina/secreção
Terapia de Salvação
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 7GR28W0FJI (Dacarbazine); 9002-62-4 (Prolactin); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008733


  8 / 6584 MEDLINE  
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[PMID]:29248726
[Au] Autor:Immanuel SRC; Ghanate AD; Parmar DS; Marriage F; Panchagnula V; Day PJ; Raghunathan A
[Ad] Endereço:Division of Evolution and Genomic Sciences, The Manchester Institute of Biotechnology, University of Manchester, United Kingdom; Chemical Engineering Division, CSIR-National Chemical Laboratory, Pune, India; Academy of Scientific & Innovative Research (AcSIR), CSIR-National Chemical Laboratory,
[Ti] Título:Integrative analysis of rewired central metabolism in temozolomide resistant cells.
[So] Source:Biochem Biophys Res Commun;495(2):2010-2016, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An authenticated U87MG clonal glioblastoma cell line was investigated to identify a sub-population of neurospheroidal (NSP) cells within the main epithelial population (U87MG). The NSP cells sorted using Fluorescence Assisted Cell Sorting (FACS) showed varied morphology, 30% lower growth rates, 40% higher IC values for temozolomide drug and could differentiate into the glial cell type (NDx). Metabolite profiling using HR-LCMS identified glucose, glutamine and serine in both populations and tryptophan only in U87MG as growth limiting substrates. Glycine, alanine, glutamate and proline were secreted by U87MG, however proline and glycine were re-utilized in NSP. Exo-metabolite profiling and phenotypic microarrays identified differential metabolism of primary carbon sources glucose and derived pyruvate for U87MG; glutamine and derived glutamate metabolism in NSP. Differential mRNA abundance of AKT1, PTEN, PIK3CA controlling metabolism, drug efflux, nutrient transport and epigenetic control MDM2 are potentially critical in shaping DNA methylation effects of temozolomide. Our study provides a new insight into the combined effect of these factors leading to temozolomide resistance in NSP.
[Mh] Termos MeSH primário: Aminoácidos/metabolismo
Dacarbazina/análogos & derivados
Glioblastoma/tratamento farmacológico
Glioblastoma/metabolismo
Glucose/metabolismo
Análise do Fluxo Metabólico/métodos
Ácido Pirúvico/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos Alquilantes/administração & dosagem
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Dacarbazina/administração & dosagem
Relação Dose-Resposta a Droga
Glioblastoma/patologia
Seres Humanos
Integração de Sistemas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amino Acids); 0 (Antineoplastic Agents, Alkylating); 7GR28W0FJI (Dacarbazine); 8558G7RUTR (Pyruvic Acid); IY9XDZ35W2 (Glucose); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE


  9 / 6584 MEDLINE  
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[PMID]:29381948
[Au] Autor:Qin Y; Zhang HB; Ke CS; Huang J; Wu B; Wan C; Yang CS; Yang KY
[Ad] Endereço:Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei.
[Ti] Título:Primary extraskeletal myxoid chondrosarcoma in cerebellum: A case report with literature review.
[So] Source:Medicine (Baltimore);96(47):e8684, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Extraskeletal myxoid chondrosarcoma (EMC) is a rare malignant neoplasm of which intracranial EMC is the rarest. PATIENT CONCERNS: We present an unusual case report of a 41-year-old woman who was sent to the emergency department for a sudden headache and other symptoms related to increased intracranial pressure. INTERVENTIONS: Emergent CT revealed an occupying lesion in the left cerebellum with surrounding edema. A complete surgical excision of the lesion through a transcortical approach was performed. After the operation, this patient received adjuvant radiotherapy and temozolomide treatment. DIAGNOSES: Pathology diagnosis was an intracranial EMC. OUTCOMES: The patient survives with no tumor recurrence as of the last follow-up. Progression-free survival exceeded 20 months. LESSONS: We have reviewed the literature and here summarize the diagnosis and treatment options for intracranial EMC. Diagnosis and treatment options of this rare disease are discussed.
[Mh] Termos MeSH primário: Neoplasias Cerebelares
Cerebelo
Condrossarcoma
Dacarbazina/análogos & derivados
Neoplasias de Tecido Conjuntivo e de Tecidos Moles
Procedimentos Neurocirúrgicos/métodos
[Mh] Termos MeSH secundário: Adulto
Antineoplásicos Alquilantes/administração & dosagem
Neoplasias Cerebelares/complicações
Neoplasias Cerebelares/patologia
Neoplasias Cerebelares/fisiopatologia
Neoplasias Cerebelares/cirurgia
Cerebelo/diagnóstico por imagem
Cerebelo/cirurgia
Quimiorradioterapia Adjuvante/métodos
Condrossarcoma/complicações
Condrossarcoma/patologia
Condrossarcoma/fisiopatologia
Condrossarcoma/cirurgia
Dacarbazina/administração & dosagem
Feminino
Seres Humanos
Hipertensão Intracraniana/diagnóstico
Hipertensão Intracraniana/etiologia
Neoplasias de Tecido Conjuntivo e de Tecidos Moles/complicações
Neoplasias de Tecido Conjuntivo e de Tecidos Moles/patologia
Neoplasias de Tecido Conjuntivo e de Tecidos Moles/fisiopatologia
Neoplasias de Tecido Conjuntivo e de Tecidos Moles/cirurgia
Tomografia Computadorizada por Raios X/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008684


  10 / 6584 MEDLINE  
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[PMID]:28470120
[Au] Autor:Slat EA; Sponagel J; Marpegan L; Simon T; Kfoury N; Kim A; Binz A; Herzog ED; Rubin JB
[Ad] Endereço:Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri, USA.
[Ti] Título:Cell-intrinsic, Bmal1-dependent Circadian Regulation of Temozolomide Sensitivity in Glioblastoma.
[So] Source:J Biol Rhythms;32(2):121-129, 2017 Apr.
[Is] ISSN:1552-4531
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The safety and efficacy of chemotherapeutics can vary as a function of the time of their delivery during the day. This study aimed to improve the treatment of glioblastoma (GBM), the most common brain cancer, by testing whether the efficacy of the DNA alkylator temozolomide (TMZ) varies with the time of its administration. We found cell-intrinsic, daily rhythms in both human and mouse GBM cells. Circadian time of treatment affected TMZ sensitivity of murine GBM tumor cells in vitro. The maximum TMZ-induced DNA damage response, activation of apoptosis, and growth inhibition occurred near the daily peak in expression of the core clock gene Bmal1. Deletion of Bmal1 (Arntl) abolished circadian rhythms in gene expression and TMZ-induced activation of apoptosis and growth inhibition. These data indicate that tumor cell-intrinsic circadian rhythms are common to GBM tumors and can regulate TMZ cytotoxicity. Optimization of GBM treatment by timing TMZ administration to daily rhythms should be evaluated in prospective clinical trials.
[Mh] Termos MeSH primário: Fatores de Transcrição ARNTL/genética
Antineoplásicos Alquilantes/farmacologia
Ritmo Circadiano/efeitos dos fármacos
Dacarbazina/análogos & derivados
Regulação Neoplásica da Expressão Gênica
[Mh] Termos MeSH secundário: Fatores de Transcrição ARNTL/deficiência
Fatores de Transcrição ARNTL/metabolismo
Animais
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular
Reparo do DNA/efeitos dos fármacos
Dacarbazina/farmacologia
Esquema de Medicação
Glioblastoma/tratamento farmacológico
Seres Humanos
Camundongos
Proteínas Circadianas Period/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ARNTL Transcription Factors); 0 (ARNTL protein, human); 0 (Antineoplastic Agents, Alkylating); 0 (Arntl protein, mouse); 0 (Per2 protein, mouse); 0 (Period Circadian Proteins); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180126
[Lr] Data última revisão:
180126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1177/0748730417696788



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