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  1 / 15121 MEDLINE  
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[PMID]:29364966
[Au] Autor:Maleki Vareki S; Salim KY; Danter WR; Koropatnick J
[Ad] Endereço:Cancer Research Laboratory Program, Lawson Health Research Institute, London, Ontario, Canada.
[Ti] Título:Novel anti-cancer drug COTI-2 synergizes with therapeutic agents and does not induce resistance or exhibit cross-resistance in human cancer cell lines.
[So] Source:PLoS One;13(1):e0191766, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Emerging drug-resistance and drug-associated toxicities are two major factors limiting successful cancer therapy. Combinations of chemotherapeutic drugs have been used in the clinic to improve patient outcome. However, cancer cells can acquire resistance to drugs, alone or in combination. Resistant tumors can also exhibit cross-resistance to other chemotherapeutic agents, resulting in sub-optimal treatment and/or treatment failure. Therefore, developing novel oncology drugs that induce no or little acquired resistance and with a favorable safety profile is essential. We show here that combining COTI-2, a novel clinical stage agent, with multiple chemotherapeutic and targeted agents enhances the activity of these drugs in vitro and in vivo. Importantly, no overt toxicity was observed in the combination treatment groups in vivo. Furthermore, unlike the tested chemotherapeutic drugs, cancer cells did not develop resistance to COTI-2. Finally, some chemo-resistant tumor cell lines only showed mild cross-resistance to COTI-2 while most remained sensitive to it.
[Mh] Termos MeSH primário: Aminoquinolinas/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Tiossemicarbazonas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular Tumoral
Cisplatino/administração & dosagem
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Resistência a Medicamentos Antineoplásicos
Neoplasias Pulmonares/patologia
Camundongos
Paclitaxel/administração & dosagem
Vimblastina/administração & dosagem
Vimblastina/análogos & derivados
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (COTI-2 compound); 0 (Thiosemicarbazones); 0W860991D6 (Deoxycytidine); 5V9KLZ54CY (Vinblastine); B76N6SBZ8R (gemcitabine); P88XT4IS4D (Paclitaxel); Q20Q21Q62J (Cisplatin); Q6C979R91Y (vinorelbine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191766


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[PMID]:28745824
[Au] Autor:Ma D; Wang J; Hao X; Wang Y; Hu X; Xing P; Li J
[Ad] Endereço:Department of Medical Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
[Ti] Título:Gemcitabine combined with cisplatin as adjuvant chemotherapy for non-small cell lung cancer: A retrospective analysis.
[So] Source:Thorac Cancer;8(5):482-488, 2017 Sep.
[Is] ISSN:1759-7714
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This study was conducted to evaluate the value of gemcitabine combined with cisplatin as adjuvant chemotherapy for radical resection of non-small cell lung cancer. METHODS: Data of 100 patients who had undergone radical resection of non-small cell lung cancer and were treated with cisplatin/gemcitabine as adjuvant chemotherapy between June 2007 and December 2010 at the Chinese Academy of Medical Sciences were reviewed. RESULTS: The median age was 59 years (range 36-73); 82% of the patients were male. Forty-two percent had adenocarcinoma and 55% had squamous cell carcinoma. Most patients had pathologic IIB (29%) and IIIA (44%) stage disease. Eighty-five percent of patients completed four cycles of chemotherapy, with 76% completing the planned full dose. The main reason for a reduced gemcitabine dose in 13 patients was grade 3/4 neutropenia or thrombocytopenia. The median dose and dose intensity were 8377.1 mg/m and 708 mg/(m /week) for gemcitabine and 293.38 mg/m and 25.24 mg/(m /week) for cisplatin, respectively. During follow-up the median disease-free survival was 33.8 months (95% confidence interval [CI] 15.938-51.676). Patients with squamous cell carcinoma (hazard ratio [HR] 0.404, 95% CI 0.241-0.676; P = 0.001) and pathologic stage I (HR 4.379, 95% CI 1.721-11.142; P = 0.002) achieved better disease-free survival. The survival rates at one, two, and five years were 94%, 77%, and 55%, while the survival rates without recurrence were 64%, 53%, and 39%, respectively. CONCLUSION: As an adjuvant chemotherapy regimen, gemcitabine with cisplatin is well tolerated. Patients with squamous cell carcinomas or pathologic stage I achieve better results.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Cisplatino/administração & dosagem
Desoxicitidina/análogos & derivados
Neoplasias Pulmonares/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Carcinoma Pulmonar de Células não Pequenas/patologia
Carcinoma Pulmonar de Células não Pequenas/cirurgia
Quimioterapia Adjuvante
Cisplatino/uso terapêutico
Desoxicitidina/administração & dosagem
Desoxicitidina/uso terapêutico
Feminino
Seres Humanos
Neoplasias Pulmonares/patologia
Neoplasias Pulmonares/cirurgia
Masculino
Meia-Idade
Estadiamento de Neoplasias
Estudos Retrospectivos
Análise de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0W860991D6 (Deoxycytidine); B76N6SBZ8R (gemcitabine); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1111/1759-7714.12472


  3 / 15121 MEDLINE  
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[PMID]:29480952
[Au] Autor:Loveday BPT; Knox JJ; Dawson LA; Metser U; Brade A; Horgan AM; Gallinger S; Greig PD; Moulton CA
[Ad] Endereço:Department of Surgery, Toronto General Hospital, Ontario, Canada.
[Ti] Título:Neoadjuvant hyperfractionated chemoradiation and liver transplantation for unresectable perihilar cholangiocarcinoma in Canada.
[So] Source:J Surg Oncol;117(2):213-219, 2018 Feb.
[Is] ISSN:1096-9098
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND OBJECTIVES: Neoadjuvant chemoradiation and liver transplantation may be offered for unresectable perihilar cholangiocarcinoma (pCCA). This study aimed to determine the dropout rate and survival of patients who entered a national tri-modality protocol. METHOD: Patients enrolled Jan 2009-Aug 2015 were included. Enrolment criteria: ≤65 years, brush biopsy-proven unresectable pCCA <3.5 cm diameter. Conformal radiotherapy was given concurrently with Capecitabine. Following surgical staging, patients received maintenance Cisplatin and Gemcitabine until transplant or progression. Time to event analyses were performed from start of neoadjuvant therapy. RESULTS: Of 43 patients screened, 18 started treatment; median age 53.9 (26.7-62.8) years, tumour diameter 2.7 (2.0-3.4) cm. 11/18 dropped out due to metastatic disease identified during chemoradiation (n = 2), surgical staging (n = 6), or maintenance chemotherapy (n = 3). Six patients underwent transplantation. Median follow up was 17.6 (4.9-57.7) months and overall survival 16.4 months. One and two year survival was 70.6% and 35.3%, respectively. One and 2 year post transplant survival was 83.3% and 55.6%. Median progression free survival was 11.5 months. CONCLUSION: Neoadjuvant chemoradiation and liver transplantation for unresectable early stage pCCA is feasible, although with high rates of dropout and disease progression. Further research is required to determine factors to help select patients for treatment.
[Mh] Termos MeSH primário: Neoplasias dos Ductos Biliares/terapia
Quimiorradioterapia
Tumor de Klatskin/terapia
Transplante de Fígado
Terapia Neoadjuvante
[Mh] Termos MeSH secundário: Adulto
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias dos Ductos Biliares/patologia
Cisplatino/administração & dosagem
Terapia Combinada
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Feminino
Seguimentos
Seres Humanos
Tumor de Klatskin/patologia
Masculino
Meia-Idade
Prognóstico
Estudos Prospectivos
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0W860991D6 (Deoxycytidine); B76N6SBZ8R (gemcitabine); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE
[do] DOI:10.1002/jso.24833


  4 / 15121 MEDLINE  
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[PMID]:28460461
[Au] Autor:Nilofar Danishmalik S; Lee SH; Sin JI
[Ad] Endereço:BK21 Plus Graduate Program and Department of Microbiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon-do 200-701, Korea.
[Ti] Título:Tumor regression is mediated via the induction of HER263-71- specific CD8+ CTL activity in a 4T1.2/HER2 tumor model: no involvement of CD80 in tumor control.
[So] Source:Oncotarget;8(16):26771-26788, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the CT26/HER2 and 4T1.2/HER2 tumor models, CT26/HER2 cells form tumors that continue to grow, whereas 4T1.2/HER2 cells form tumors that eventually regress. Here, we investigated the differences in the behaviors of these two cell lines. When immune cells from 4T1.2/HER2 tumor-bearing animals were stimulated with HER2 class I peptides, they displayed a 2-fold increase in IFN-γ levels, in response to the peptides, HER263-71 and HER2342-350. In contrast, extremely high levels of antigen-non-specific IFN-γ production were observed with immune cells and sera from CT26/HER2 tumor-bearing mice. However, IFN-γ had no effect on tumor progression in the CT26/HER2 model, as determined by an IFN-γ knockout assay. 4T1.2/HER2 tumor-bearing mice displayed CTL activity in response to HER263-71 but not to HER2342-350, whereas no such induction was observed in CT26/HER2 tumor-bearing mice. When 4T1.2/HER2 cell-challenged mice were depleted of CD8+ T cells, they lost their tumor-regressing activity, suggesting an antitumor role of HER263-71-specific CD8+ CTLs in the control of this tumor type. CT26/HER2 cells also expressed CD80. However, CD80-transfected 4T1.2/HER2 and CD80-non-expressing CT26/HER2 cells failed to alter their tumorigenicity, suggesting no role of CD80 in tumor control. Despite increased levels of myeloid-derived suppressor cells in the tumor, they were not associated with tumor progression in the CT26/HER2 model, as determined by a cell depletion assay. Overall, these data show that, contrary to CT26/HER2 tumors, 4T1.2/HER2 tumors regress via the induction of HER263-71-specific CD8+ CTLs and that CD80 is not associated with the regression of these tumors.
[Mh] Termos MeSH primário: Neoplasias/imunologia
Neoplasias/metabolismo
Receptor ErbB-2/imunologia
Especificidade do Receptor de Antígeno de Linfócitos T/imunologia
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos de Neoplasias/imunologia
Biomarcadores
Linhagem Celular Tumoral
Desoxicitidina/análogos & derivados
Desoxicitidina/farmacologia
Modelos Animais de Doenças
Feminino
Imunoglobulina G/imunologia
Interferon gama/genética
Interferon gama/metabolismo
Camundongos
Camundongos Knockout
Neoplasias/patologia
Subpopulações de Linfócitos T/efeitos dos fármacos
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Linfócitos T Citotóxicos/efeitos dos fármacos
Células Th1/imunologia
Células Th1/metabolismo
Carga Tumoral/efeitos dos fármacos
Carga Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Biomarkers); 0 (Immunoglobulin G); 0W860991D6 (Deoxycytidine); 82115-62-6 (Interferon-gamma); B76N6SBZ8R (gemcitabine); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15816


  5 / 15121 MEDLINE  
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[PMID]:29352306
[Au] Autor:Peraldo-Neia C; Cavalloni G; Fenocchio E; Cagnazzo C; Gammaitoni L; Cereda S; Nasti G; Satolli MA; Aprile G; Reni M; Avallone A; Spadi R; Venesio T; Martin V; Doglioni C; Frattini M; Aglietta M; Leone F
[Ad] Endereço:Medical Oncology, Fondazione del Piemonte per l'Oncologia (FPO), IRCCS-Institute of Candiolo, Candiolo, Italy.
[Ti] Título:Prognostic and predictive role of EGFR pathway alterations in biliary cancer patients treated with chemotherapy and anti-EGFR.
[So] Source:PLoS One;13(1):e0191593, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The association of anti-EGFR to gemcitabine and oxaliplatin (GEMOX) chemotherapy did not improve survival in biliary tract carcinoma (BTC) patients. Multiple mechanisms might be involved in the resistance to anti-EGFR. Here, we explored the mutation profile of EGFR extracellular domain (ECD), of tyrosine kinase domain (TKD), and its amplification status. EGFR mutational status of exons 12, 18-21 was analyzed in 57 tumors by Sanger sequencing. EGFR amplification was evaluated in 37 tumors by Fluorescent In Situ Hybridization (FISH). Kaplan-Meier curves were calculated using the log-rank test. Six patients had mutations in exon 12 of EGFR ECD and 7 in EGFR TKD. Neither EGFR ECD nor TKD mutations affected progression free survival (PFS) or overall survival (OS) in the entire population. In the panitumumab plus GEMOX (P-GEMOX) arm, ECD mutated patients had a worse OS, while EGFR TKD mutated patients had a trend towards shorter PFS and OS. Overall, the presence of mutations in EGFR or in its transducers did not affect PFS or OS, while the extrahepatic cholangiocarcinoma (ECC) mutated patients had a worse prognosis compared to WT. Nineteen out of 37 tumors were EGFR amplified, but the amplification did not correlate with survival. ECC EGFR amplified patients had improved OS, whereas the amplification significantly correlated with poor PFS (p = 0.03) in gallbladder carcinoma patients. The high molecular heterogeneity is a predominant feature of BTC: the alterations found in this work seem to have a prognostic impact rather than a predictive role towards anti-EGFR therapy.
[Mh] Termos MeSH primário: Neoplasias do Sistema Biliar/tratamento farmacológico
Neoplasias do Sistema Biliar/genética
Genes erbB-1
Mutação
Receptor do Fator de Crescimento Epidérmico/genética
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/administração & dosagem
Anticorpos Monoclonais/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias dos Ductos Biliares/tratamento farmacológico
Neoplasias dos Ductos Biliares/genética
Neoplasias dos Ductos Biliares/metabolismo
Neoplasias do Sistema Biliar/metabolismo
Colangiocarcinoma/tratamento farmacológico
Colangiocarcinoma/genética
Colangiocarcinoma/metabolismo
Análise Mutacional de DNA
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Desoxicitidina/uso terapêutico
Neoplasias da Vesícula Biliar/tratamento farmacológico
Neoplasias da Vesícula Biliar/genética
Neoplasias da Vesícula Biliar/metabolismo
Amplificação de Genes
Seres Humanos
Hibridização in Situ Fluorescente
Estimativa de Kaplan-Meier
Compostos Organoplatínicos/administração & dosagem
Compostos Organoplatínicos/uso terapêutico
Prognóstico
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Organoplatinum Compounds); 04ZR38536J (oxaliplatin); 0W860991D6 (Deoxycytidine); 6A901E312A (panitumumab); B76N6SBZ8R (gemcitabine); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[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.0191593


  6 / 15121 MEDLINE  
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[PMID]:28449702
[Au] Autor:Verma V; Bhirud AR; Denniston KA; Bennion NR; Lin C
[Ad] Endereço:Department of Radiation Oncology, University of Nebraska Medical Center, 987521 Nebraska Medical Center, Ground Floor, Clarkson Tower, Omaha, NE, 68198, USA.
[Ti] Título:Quantification of renal function following stereotactic body radiotherapy for pancreatic cancer: secondary dosimetric analysis of a prospective clinical trial.
[So] Source:Radiat Oncol;12(1):71, 2017 Apr 27.
[Is] ISSN:1748-717X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This is the first known study examining renal function following stereotactic body radiotherapy (SBRT) for pancreatic head adenocarcinoma. METHODS: Thirty-eight borderline-resectable/unresectable patients, part of an ongoing prospective trial, underwent 3 cycles of gemcitabine/5-fluorouracil followed by SBRT (5 daily fractions of 5/6/7/8 Gy) and concurrent nelfinavir. Thereafter, in resectable cases, surgery was performed within 4-8 weeks. The last available pre-SBRT creatinine was recorded, along with the highest post-SBRT value. Glomerular filtration rate (GFR) was calculated by the commonly-utilized Modification of Diet in Renal Disease formula. GFR decline was defined as the post-SBRT nadir GFR minus the pre-SBRT GFR. Correlations with the V5-V30, and mean/maximum kidney doses was performed. Statistics included Pearson correlation, Mann-Whitney, and Fisher's exact tests. RESULTS: The median total kidney volume was 355 cm . Median dosimetric values were as follows: V5 (209 cm ), V10 (103 cm ), V15 (9 cm ), V20 (0 cm ), V25 (0 cm ); and mean (6.7 Gy) & maximum kidney dose (18.3 Gy). Median GFR change was -23 (range, -105 to 25) mL/min/1.73 cm . Of all dosimetric parameters, only V5 was significantly associated with changes in GFR (Pearson r = -0.40, p = 0.012). In patients with V5 < 210 cm , median GFR change was -11.8 mL/min/1.73 cm , as compared with -37.1 mL/min/1.73 cm change in those with V5 ≥ 210 cm (p = 0.02). A GFR change < -23 mL/min/1.73 cm was observed in 6/20 (30%) patients with V5 < 210 cm , versus 15/18 (83%) of those with V5 ≥ 210 cm . Patients with V5 ≥ 210 cm were over ten times as likely to have GFR change < -23 mL/min/1.73 cm (p = 0.003). Using linear regression, GFR change ≈ -0.1748 × V5(cm ) + 8.63. CONCLUSIONS: In the first known analysis of renal function after pancreatic SBRT, evaluating patients on a prospective study, V5 ≥ 210 cm was associated with a post-SBRT GFR decline of >23 mL/min/1.73 cm . If V5 is kept <210 cm , median GFR decline was only 11.8 mL/min/1.73 cm . Further validation is needed to ascertain definite dose-volume parameters and examine late renal decline.
[Mh] Termos MeSH primário: Adenocarcinoma/cirurgia
Nefropatias/etiologia
Neoplasias Pancreáticas/cirurgia
Radiocirurgia/efeitos adversos
[Mh] Termos MeSH secundário: Adenocarcinoma/tratamento farmacológico
Adenocarcinoma/patologia
Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Ensaios Clínicos como Assunto
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Feminino
Fluoruracila/administração & dosagem
Seguimentos
Seres Humanos
Nefropatias/patologia
Masculino
Meia-Idade
Neoplasias Pancreáticas/tratamento farmacológico
Neoplasias Pancreáticas/patologia
Prognóstico
Estudos Prospectivos
Estudos Retrospectivos
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0W860991D6 (Deoxycytidine); B76N6SBZ8R (gemcitabine); U3P01618RT (Fluorouracil)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1186/s13014-017-0798-8


  7 / 15121 MEDLINE  
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[PMID]:29381963
[Au] Autor:Liang L; Wang L; Zhu P; Xia Y; Qiao Y; Hui K; Hu C; Ren Y; Jiang X
[Ad] Endereço:Department of Radiation Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University.
[Ti] Título:Apatinib concurrent gemcitabine for controlling malignant ascites in advanced pancreatic cancer patient: A case report.
[So] Source:Medicine (Baltimore);96(47):e8725, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Malignant ascites (MA) is one of the poor prognostic factors for advanced pancreatic cancer and can bring about serious symptoms. The improvement of quality of life for patients is priority. However, there is no standard method for the treatment for pancreatic cancer-mediated MA. Apatinib is a novel and highly selective tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2. There are no reports of concurrent apatinib with gemcitabine in patients with pancreatic cancer-mediated MA. PATIENT CONCERNS: Herein, we presented a 64-year-old man patient who visited hospital due to abdominal pain for 1 month. DIAGNOSES: He was initially diagnosed with pancreatic cancer and his first symptom was MA. INTERVENTIONS: After failing in tube drainage and gemcitabine therapy, the patient received gemcitabine combined apatinib orally and after administrated 1 month, the MA was evaluated as nearly clear response according to the RECIST 1.1 standard, and without further need of paracentesis. The CEA and CA199 reached the lowest level after administrating for 2.5 months during the treatment process. OUTCOMES: 10.5 months following apatinib administration, the patient achieved a progression-free survival for more than 11 months. Hypertension (grade IV), hand-foot syndrome (grade I) and proteinuria (grade II) were observed. LESSONS: It indicated that apatinib concurrent gemcitabine may be a superior choice for pancreatic cancer-mediated MA. Further clinical trials required to confirm its efficacy and safety.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Ascite/tratamento farmacológico
Ascite/etiologia
Desoxicitidina/análogos & derivados
Neoplasias Pancreáticas/complicações
Piridinas/uso terapêutico
[Mh] Termos MeSH secundário: Antineoplásicos/administração & dosagem
Desoxicitidina/administração & dosagem
Desoxicitidina/uso terapêutico
Quimioterapia Combinada
Seres Humanos
Masculino
Meia-Idade
Proteínas Tirosina Quinases/antagonistas & inibidores
Piridinas/administração & dosagem
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Pyridines); 0W860991D6 (Deoxycytidine); 5S371K6132 (apatinib); B76N6SBZ8R (gemcitabine); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2)
[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.0000000000008725


  8 / 15121 MEDLINE  
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[PMID]:28470260
[Au] Autor:Han Y; Zhang Z; Smith GS; Do C
[Ad] Endereço:Biology and Soft Matter Division, Neutron Sciences Directorate, Oak Ridge National Laboratory, Oak Ridge, TN 37831, USA. doc1@ornl.gov.
[Ti] Título:Effect of nucleoside analogue antimetabolites on the structure of PEO-PPO-PEO micelles investigated by SANS.
[So] Source:Phys Chem Chem Phys;19(24):15686-15692, 2017 Jun 21.
[Is] ISSN:1463-9084
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The effect of three nucleoside analogue antimetabolites (5-fluorouracil, floxuridine, and gemcitabine) on the structure of Pluronic L62 copolymer micelles was investigated using small-angle neutron scattering. These antimetabolites used for cancer chemotherapy have analogous molecular structures but different molecular sizes and aqueous solubilities. It was found that the addition of the three antimetabolites slightly reduced the micellar size and aggregation number, and the micellar anisotropy. The added antimetabolites also changed the internal molecular distribution of the micelles as measured by the scattering length densities, resulting in enhanced hydration of the hydrophobic core region of the micelle. The strength of the effect was found to correlate with the molecular properties of the model drugs, i.e. a larger molecular size and a higher aqueous solubility lead to enhanced hydration of the micellar core.
[Mh] Termos MeSH primário: Antimetabólitos/química
Micelas
Difração de Nêutrons
Polietilenoglicóis/química
Propilenoglicóis/química
Espalhamento a Baixo Ângulo
[Mh] Termos MeSH secundário: Desoxicitidina/análogos & derivados
Desoxicitidina/química
Floxuridina/química
Fluoruracila/química
Poloxâmero/química
Temperatura de Transição
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites); 0 (Micelles); 0 (PEO-PPO-PEO); 0 (Propylene Glycols); 039LU44I5M (Floxuridine); 059QF0KO0R (Water); 0W860991D6 (Deoxycytidine); 106392-12-5 (Poloxamer); 30IQX730WE (Polyethylene Glycols); B76N6SBZ8R (gemcitabine); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1039/c7cp02028g


  9 / 15121 MEDLINE  
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[PMID]:27771389
[Au] Autor:Welch SR; Guerrero LW; Chakrabarti AK; McMullan LK; Flint M; Bluemling GR; Painter GR; Nichol ST; Spiropoulou CF; Albariño CG
[Ad] Endereço:Viral Special Pathogens Branch, Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, MG G-14, Atlanta, GA, 30329, USA.
[Ti] Título:Lassa and Ebola virus inhibitors identified using minigenome and recombinant virus reporter systems.
[So] Source:Antiviral Res;136:9-18, 2016 12.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Lassa virus (LASV) and Ebola virus (EBOV) infections are important global health issues resulting in significant morbidity and mortality. While several promising drug and vaccine trials for EBOV are ongoing, options for LASV infection are currently limited to ribavirin treatment. A major factor impeding the development of antiviral compounds to treat these infections is the need to manipulate the virus under BSL-4 containment, limiting research to a few institutes worldwide. Here we describe the development of a novel LASV minigenome assay based on the ambisense LASV S segment genome, with authentic terminal untranslated regions flanking a ZsGreen (ZsG) fluorescent reporter protein and a Gaussia princeps luciferase (gLuc) reporter gene. This assay, along with a similar previously established EBOV minigenome, was optimized for high-throughput screening (HTS) of potential antiviral compounds under BSL-2 containment. In addition, we rescued a recombinant LASV expressing ZsG, which, in conjunction with a recombinant EBOV reporter virus, was used to confirm any potential antiviral hits in vitro. Combining an initial screen to identify potential antiviral compounds at BSL-2 containment before progressing to HTS with infectious virus will reduce the amount of expensive and technically challenging BSL-4 containment research. Using these assays, we identified 6-azauridine as having anti-LASV activity, and demonstrated its anti-EBOV activity in human cells. We further identified 2'-deoxy-2'-fluorocytidine as having potent anti-LASV activity, with an EC value 10 times lower than that of ribavirin.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Ebolavirus/efeitos dos fármacos
Ebolavirus/genética
Vírus Lassa/efeitos dos fármacos
Vírus Lassa/genética
[Mh] Termos MeSH secundário: Antivirais/química
Azauridina/farmacologia
Desoxicitidina/análogos & derivados
Desoxicitidina/farmacologia
Descoberta de Drogas/métodos
Genes Reporter
Genoma Viral
Proteínas de Fluorescência Verde/genética
Doença pelo Vírus Ebola
Ensaios de Triagem em Larga Escala/métodos
Seres Humanos
Febre Lassa
Luciferases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Antiviral Agents); 0W860991D6 (Deoxycytidine); 147336-22-9 (Green Fluorescent Proteins); 7BVB29RCPR (Azauridine); EC 1.13.12.- (Luciferases); LCY080JPY9 (2'-fluoro-2'-deoxycytidine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  10 / 15121 MEDLINE  
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[PMID]:29277822
[Au] Autor:Bruckner HW; Gurell D; Hirschfeld A
[Ad] Endereço:MZB Foundation for Cancer Research, New York, NY, U.S.A. bruckneroncology@gmail.com.
[Ti] Título:Bevacizumab Added to Moderate-dose Chemotherapy for Refractory Uterine Cancer.
[So] Source:Anticancer Res;38(1):547-552, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Bevacizumab (bev), when added to a moderate dose combination of previously failed cytotoxins, as a third- and fourth-line therapy for refractory gastric, cholangiocarcinoma, and ovarian cancers, produced high-quality responses. The regimen was based on preclinical models designed in order to simultaneously partner both bev and each of the cytotoxins with 4-5 synergistic drugs. PATIENTS AND METHODS: Eligible patients (n=9) had high-grade endometrial tumors and had failed standard chemotherapy. Bev (10 mg/kg every 2 weeks) and cyclophosphamide (150-250 mg/m ), were added to a combination of gemcitabine, fluorouracil, leucovorin, irinotecan and a platinum analogue -first without and then with docetaxel- each at approximately 1/2 to 1/3 of their standard dosage. Dose modification aimed at a repeated absolute neutrophil count (ANC) of 750-1,500 µl or platelets of 125,000-75,000 µl. Safety measures included stop-go use (intermittent, as needed, brief withholding of bev with resumption when again tolerated), of bev, and both prospective and ongoing dose modification in order to protect the bowels. RESULTS: Induction treatment was free of life-threatening complications. Nine consecutive patients, 3 under second- and 6 under multi-line treatment, had 9 objective responses and 8 produced long clinical benefits, 2 of which were complete responses. Seven responses created opportunities for personalized added treatment and research. Absolute median survival was 21.5 months for the 8 patients with platinum-resistant tumors. One patient was unable to tolerate a first standard adjuvant dose of paclitaxel. After rapid peritoneal progression of disease, treatment has produced 52+ months of unmaintained complete remission. CONCLUSION: Bev, in the combination that was used in this study, meets response, survival, and toxicity criteria for further testing against second- or multi-line chemotherapy-resistant tumors and also when a standard treatment is not safe.
[Mh] Termos MeSH primário: Antineoplásicos Imunológicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Bevacizumab/uso terapêutico
Neoplasias dos Ductos Biliares/tratamento farmacológico
Colangiocarcinoma/tratamento farmacológico
Neoplasias do Endométrio/tratamento farmacológico
Neoplasias Ovarianas/tratamento farmacológico
[Mh] Termos MeSH secundário: Adenocarcinoma/tratamento farmacológico
Camptotecina/análogos & derivados
Camptotecina/uso terapêutico
Cisplatino/uso terapêutico
Desoxicitidina/análogos & derivados
Desoxicitidina/uso terapêutico
Feminino
Fluoruracila/uso terapêutico
Seres Humanos
Quimioterapia de Indução/métodos
Leucovorina/uso terapêutico
Meia-Idade
Estudos Retrospectivos
Taxoides/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Immunological); 0 (Taxoids); 0W860991D6 (Deoxycytidine); 15H5577CQD (docetaxel); 2S9ZZM9Q9V (Bevacizumab); 7673326042 (irinotecan); B76N6SBZ8R (gemcitabine); Q20Q21Q62J (Cisplatin); Q573I9DVLP (Leucovorin); U3P01618RT (Fluorouracil); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE



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