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[PMID]:29288428
[Au] Autor:Scappaticci GB; Marini BL; Nachar VR; Uebel JR; Vulaj V; Crouch A; Bixby DL; Talpaz M; Perissinotti AJ
[Ad] Endereço:Department of Pharmacy Services and Clinical Sciences, Michigan Medicine and University of Michigan College of Pharmacy, 1500 East Medical Center Drive, Ann Arbor, MI, 48109, USA.
[Ti] Título:Outcomes of previously untreated elderly patients with AML: a propensity score-matched comparison of clofarabine vs. FLAG.
[So] Source:Ann Hematol;97(4):573-584, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The 5-year overall survival (OS) in patients ≥ 60 years old with acute myeloid leukemia (AML) remains < 10%. Clofarabine-based induction (CLO) provides an alternative to low-intensity therapy (LIT) and palliative care for this population, but supporting data are conflicted. Recently, our institution adopted the FLAG regimen (fludarabine, cytarabine, and granulocyte colony-stimulating factor) based on data reporting similar outcomes to CLO in elderly patients with AML unable to tolerate anthracycline-based induction. We retrospectively analyzed the efficacy and safety of patients ≥ 60 years old with AML treated with FLAG or CLO over the past 10 years. We performed a propensity score match that provided 32 patients in each group. Patients treated with FLAG had a higher CR/CRi rate (65.6 vs. 37.5%, P = 0.045) and OS (7.9 vs. 2.8 months, P = 0.085) compared to CLO. Furthermore, FLAG was better tolerated with significantly less grade 3/4 toxicities and a shorter duration of neutropenia (18.5 vs. 30 days, P = 0.002). Finally, we performed a cost analysis that estimated savings to be $30,000-45,000 per induction with FLAG. Our study supports the use of FLAG both financially and as an effective, well-tolerated high-dose treatment regimen for elderly patients with AML. No cases of cerebellar neurotoxicity occurred.
[Mh] Termos MeSH primário: Nucleotídeos de Adenina/uso terapêutico
Envelhecimento
Antimetabólitos Antineoplásicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Arabinonucleosídeos/uso terapêutico
Quimioterapia de Indução
Leucemia Mieloide Aguda/tratamento farmacológico
Vidarabina/análogos & derivados
[Mh] Termos MeSH secundário: Nucleotídeos de Adenina/efeitos adversos
Nucleotídeos de Adenina/economia
Idoso
Idoso de 80 Anos ou mais
Antimetabólitos Antineoplásicos/efeitos adversos
Antimetabólitos Antineoplásicos/economia
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Protocolos de Quimioterapia Combinada Antineoplásica/economia
Arabinonucleosídeos/efeitos adversos
Arabinonucleosídeos/economia
Estudos de Casos e Controles
Doença Hepática Induzida por Substâncias e Drogas/economia
Doença Hepática Induzida por Substâncias e Drogas/epidemiologia
Doença Hepática Induzida por Substâncias e Drogas/mortalidade
Doença Hepática Induzida por Substâncias e Drogas/terapia
Estudos de Coortes
Terapia Combinada/economia
Redução de Custos
Custos e Análise de Custo
Citarabina/efeitos adversos
Citarabina/economia
Citarabina/uso terapêutico
Fator Estimulador de Colônias de Granulócitos/efeitos adversos
Fator Estimulador de Colônias de Granulócitos/economia
Fator Estimulador de Colônias de Granulócitos/uso terapêutico
Custos Hospitalares
Seres Humanos
Incidência
Quimioterapia de Indução/efeitos adversos
Quimioterapia de Indução/economia
Tempo de Internação
Leucemia Mieloide Aguda/economia
Leucemia Mieloide Aguda/mortalidade
Michigan/epidemiologia
Meia-Idade
Neutropenia/induzido quimicamente
Neutropenia/economia
Neutropenia/mortalidade
Neutropenia/terapia
Pontuação de Propensão
Estudos Retrospectivos
Análise de Sobrevida
Centros de Atenção Terciária
Vidarabina/efeitos adversos
Vidarabina/economia
Vidarabina/uso terapêutico
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenine Nucleotides); 0 (Antimetabolites, Antineoplastic); 0 (Arabinonucleosides); 04079A1RDZ (Cytarabine); 143011-72-7 (Granulocyte Colony-Stimulating Factor); 762RDY0Y2H (clofarabine); FA2DM6879K (Vidarabine)
[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:171231
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3217-1


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[PMID]:29249005
[Au] Autor:Trevisani F; Brandi G; Garuti F; Barbera MA; Tortora R; Casadei Gardini A; Granito A; Tovoli F; De Lorenzo S; Inghilesi AL; Foschi FG; Bernardi M; Marra F; Sacco R; Di Costanzo GG
[Ad] Endereço:Department of Medical and Surgical Sciences, Medical Semeiotics, University of Bologna, via Albertoni 15, 40138, Bologna, Italy. franco.trevisani@unibo.it.
[Ti] Título:Metronomic capecitabine as second-line treatment for hepatocellular carcinoma after sorafenib discontinuation.
[So] Source:J Cancer Res Clin Oncol;144(2):403-414, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Metronomic capecitabine (MC) is a well-tolerated systemic treatment showing promising results in one retrospective study, as second-line therapy after sorafenib failure, in patients with hepatocellular carcinoma (HCC). METHODS: 117 patients undergoing MC were compared to 112 patients, eligible for this treatment, but undergoing best supportive care (BSC) after sorafenib discontinuation for toxicity or HCC progression. The two groups were compared for demographic and clinical features. A multivariate regression analysis was conducted to detect independent prognostic factors. To balance confounding factors between the two groups, a propensity score model based on independent prognosticators (performance status, neoplastic thrombosis, causes of sorafenib discontinuation and pre-sorafenib treatment) was performed. RESULTS: Patients undergoing MC showed better performance status, lower tumor burden, lower prevalence of portal vein thrombosis, and better cancer stage. Median (95% CI) post-sorafenib survival (PSS) was longer in MC than in BSC patients [9.5 (7.5-11.6) vs 5.0 (4.2-5.7) months (p < 0.001)]. Neoplastic thrombosis, cause of sorafenib discontinuation, pre-sorafenib treatment and MC were independent prognosticators. The benefit of capecitabine was confirmed in patients after matching with propensity score [PSS: 9.9 (6.8-12.9) vs. 5.8 (4.8-6.8) months, (p = 0.001)]. MC lowered the mortality risk by about 40%. MC achieved better results in patients who stopped sorafenib for adverse events than in those who progressed during it [PSS: 17.3 (10.5-24.1) vs. 7.8 (5.2-10.1) months, (p = 0.035)]. Treatment toxicity was low and easily manageable with dose modulation. CONCLUSIONS: MC may be an efficient and safe second-line systemic therapy for HCC patients who discontinued sorafenib for toxicity or tumor progression.
[Mh] Termos MeSH primário: Capecitabina/administração & dosagem
Carcinoma Hepatocelular/tratamento farmacológico
Neoplasias Hepáticas/tratamento farmacológico
Niacinamida/análogos & derivados
Compostos de Fenilureia/administração & dosagem
[Mh] Termos MeSH secundário: Administração Metronômica
Idoso
Antimetabólitos Antineoplásicos/administração & dosagem
Feminino
Seres Humanos
Masculino
Niacinamida/administração & dosagem
Niacinamida/efeitos adversos
Compostos de Fenilureia/efeitos adversos
Inibidores de Proteínas Quinases/administração & dosagem
Inibidores de Proteínas Quinases/efeitos adversos
Estudos Retrospectivos
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (Phenylurea Compounds); 0 (Protein Kinase Inhibitors); 25X51I8RD4 (Niacinamide); 6804DJ8Z9U (Capecitabine); 9ZOQ3TZI87 (sorafenib)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2556-6


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[PMID]:29200853
[Au] Autor:Briot T; Roger E; Lautram N; Verger A; Clavreul A; Lagarce F
[Ad] Endereço:Micro & Nanomédecines Translationelles - MINT, UNIV Angers, INSERM 1066, CNRS 6021, Université Bretagne Loire, MINT IBS-CHU.
[Ti] Título:Development and in vitro evaluations of new decitabine nanocarriers for the treatment of acute myeloid leukemia.
[So] Source:Int J Nanomedicine;12:8427-8442, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Decitabine is a hydrophilic drug that acts by hypomethylating DNA. Decitabine is used in Europe for the treatment of acute myeloid leukemia (AML) in patients aged ≥65 years. However, it can only be administered intravenously due to very low oral bioavailability and a large distribution volume. Oral administration would allow outpatient treatment, improving quality of life and reducing treatment costs. The present study proposes to develop lipid nanocapsules (LNCs), originally designed for lipophilic drugs, to encapsulate decitabine. Two different formulations of LNCs were designed: LNCs based on a high proportion of Transcutol HP (THP-LNCs) and LNCs associated with a mixture of Transcutol HP and Tween 80 (THP-T80-LNCs). The second formulation had a diameter of 26.5±0.5 nm, high encapsulation efficiency (>85%), and a drug payload of 472±64 µg/mL. Decitabine-loaded THP-T80-LNC cytotoxicity was evaluated on two AML cell lines depending on their decitabine resistance: HEL (not resistant) and HL-60 (resistant). The permeability of decitabine-loaded THP-T80-LNCs was also evaluated on Caco-2 cell monolayers. Decitabine cytotoxicity against HEL and HL-60 was higher when decitabine was loaded in THP-T80-LNCs than when free. Apparent permeability on Caco-2 cell monolayers was also increased, suggesting a potentially useful formulation to increase the oral bioavailability of decitabine.
[Mh] Termos MeSH primário: Azacitidina/análogos & derivados
Portadores de Fármacos/química
Leucemia Mieloide Aguda/tratamento farmacológico
Nanocápsulas/administração & dosagem
[Mh] Termos MeSH secundário: Administração Oral
Antimetabólitos Antineoplásicos/administração & dosagem
Antimetabólitos Antineoplásicos/farmacocinética
Azacitidina/administração & dosagem
Azacitidina/farmacocinética
Disponibilidade Biológica
Células CACO-2
Linhagem Celular Tumoral
Portadores de Fármacos/administração & dosagem
Liberação Controlada de Fármacos
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Estabilidade de Medicamentos
Etilenoglicóis/química
Seres Humanos
Lipídeos/química
Nanocápsulas/química
Polissorbatos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (Drug Carriers); 0 (Ethylene Glycols); 0 (Lipids); 0 (Nanocapsules); 0 (Polysorbates); 776B62CQ27 (decitabine); A1A1I8X02B (carbitol); M801H13NRU (Azacitidine)
[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:171205
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S147659


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[PMID]:29311456
[Au] Autor:Uchiyama M; Ueno M; Takamatsu Y; Matsuo K; Imakyure O; Kamimura H
[Ad] Endereço:Department of Pharmacy, Fukuoka University Hospital.
[Ti] Título:[A Survey of the Adverse Effects and Influence of Concomitant Drugs for Methotrexate Intrathecal Administration].
[So] Source:Yakugaku Zasshi;138(1):111-115, 2018.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:In general, the intraventricular administration of cytotoxic antitumor drugs provides a high drug concentration in the cerebrospinal fluid with a reduced risk of systemic adverse reactions. Methotrexate (MTX) high-dose therapy requires close monitoring when performed in combination with trimethoprim-sulfamethoxazole (ST) therapy and proton pump inhibitor (PPI) and nonsteroidal anti-inflammatory drug administration for excretion delay and toxicity enhancement. While the frequency of systemic side effects is thought to be low with intrathecal administration, such effects do rarely but occasionally occur. We must consider drug interactions with combination therapy as a potential factor inducing such effects. We examined the patients who received MTX intrathecal administration at Fukuoka University Hospital from January 2013 to December 2014 with respect to the onset of side effects and combination therapy. MTX intrathecal administration was performed a total of 79 times in 27 patients. In five of these 27 patients, MTX intrathecal administration was performed twice a week, and hematotoxicity and non-hematotoxicity developed in two patients in whom ST was also administered. On the other hand, even if ST and/or PPI was administered, no side effects were observed in the patients administered levofolinate.
[Mh] Termos MeSH primário: Antibacterianos/administração & dosagem
Antibacterianos/efeitos adversos
Antimetabólitos Antineoplásicos/administração & dosagem
Antimetabólitos Antineoplásicos/efeitos adversos
Metotrexato/administração & dosagem
Metotrexato/efeitos adversos
Combinação Trimetoprima e Sulfametoxazol/administração & dosagem
Combinação Trimetoprima e Sulfametoxazol/efeitos adversos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Anti-Inflamatórios não Esteroides/administração & dosagem
Anti-Inflamatórios não Esteroides/efeitos adversos
Esquema de Medicação
Interações Medicamentosas
Quimioterapia Combinada
Feminino
Seres Humanos
Injeções Espinhais
Masculino
Meia-Idade
Inibidores da Bomba de Prótons/administração & dosagem
Inibidores da Bomba de Prótons/efeitos adversos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antimetabolites, Antineoplastic); 0 (Proton Pump Inhibitors); 8064-90-2 (Trimethoprim, Sulfamethoxazole Drug Combination); YL5FZ2Y5U1 (Methotrexate)
[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:180110
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.17-00122


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[PMID]:28456772
[Au] Autor:Sano T; Utsumi D; Amagase K; Matsumoto K; Tominaga M; Higuchi K; Takeuchi T; Kato S
[Ad] Endereço:Division of Pathological Sciences, Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Yamashina, Kyoto, Japan. beatatsuo0507@gmail.com.
[Ti] Título:Lafutidine, a histamine H2 receptor antagonist with mucosal protective properties, attenuates 5-fluorouracil-induced intestinal mucositis in mice through activation of extrinsic primary afferent neurons.
[So] Source:J Physiol Pharmacol;68(1):79-90, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Intestinal mucositis accompanied by severe diarrhea is one of the most common side effects during cancer chemotherapy. Lafutidine, a histamine H2 receptor antagonist with mucosal protective properties via sensory afferent neurons, is used for the treatment of upper gastrointestinal diseases. The present study investigated the effects of lafutidine on 5-fluorouracil (5-FU)-induced intestinal mucositis induced in mice. Male C57BL/6 wild-type (WT), sensory deafferented mice, and transient receptor potential vanilloid subfamily 1 knockout (TRPV1KO) mice were used. Animals were administered 5-FU once daily, while lafutidine and famotidine were administered twice daily for 6 days. Repeated administration of 5-FU caused severe intestinal mucositis, characterized by shortening of villi and destruction of crypts and was accompanied by diarrhea and body weight loss. Daily administration of lafutidine reduced the severity of intestinal mucositis, diarrhea and body weight loss in a dose-dependent manner, while famotidine had no effect on intestinal mucositis. The preventive effects of lafutidine were completely abolished in sensory deafferented and TRPV1-KO mice. Lafutidine significantly suppressed 5-FU-increased MPO activity and inflammatory cytokine expression on day 6, but not apoptosis induction in intestinal crypts on day 1. Lafutidine induced Alcian Blue and PAS-positive mucus production in the small intestine. These findings suggest that lafutidine attenuates 5-FU-induced intestinal mucositis, most likely by increasing mucus production via activation of sensory afferent neurons. Furthermore, intact TRPV1 signaling is essential for the activation of sensory afferent neurons induced by lafutidine. Therefore, lafutidine is more useful than other common antacids for the treatment of intestinal mucositis during cancer chemotherapy.
[Mh] Termos MeSH primário: Acetamidas/uso terapêutico
Diarreia/tratamento farmacológico
Antagonistas dos Receptores Histamínicos H2/uso terapêutico
Mucosite/tratamento farmacológico
Piperidinas/uso terapêutico
Piridinas/uso terapêutico
[Mh] Termos MeSH secundário: Acetamidas/farmacologia
Animais
Antimetabólitos Antineoplásicos
Diarreia/metabolismo
Diarreia/patologia
Famotidina/uso terapêutico
Fluoruracila
Antagonistas dos Receptores Histamínicos H2/farmacologia
Interleucina-1beta/genética
Intestinos/efeitos dos fármacos
Intestinos/metabolismo
Intestinos/patologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Mucosite/induzido quimicamente
Mucosite/patologia
Peroxidase/metabolismo
Piperidinas/farmacologia
Piridinas/farmacologia
RNA Mensageiro/metabolismo
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetamides); 0 (Antimetabolites, Antineoplastic); 0 (Histamine H2 Antagonists); 0 (IL1B protein, mouse); 0 (Interleukin-1beta); 0 (Piperidines); 0 (Pyridines); 0 (RNA, Messenger); 0 (Tumor Necrosis Factor-alpha); 49S4O7ADLC (lafutidine); 5QZO15J2Z8 (Famotidine); EC 1.11.1.7 (Peroxidase); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29275107
[Au] Autor:Moghimipour E; Rezaei M; Ramezani Z; Kouchak M; Amini M; Angali KA; Dorkoosh FA; Handali S
[Ad] Endereço:Nanotechnology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Cellular and Molecular Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
[Ti] Título:Transferrin targeted liposomal 5-fluorouracil induced apoptosis via mitochondria signaling pathway in cancer cells.
[So] Source:Life Sci;194:104-110, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to prepare transferrin (Tf) targeted liposomal 5-Fluorouracil (5FU) to improve the safety and efficacy of the drug. Liposomes were prepared using thin layer method. Morphology of liposomes was characterized by transmission electron microscopy (TEM) and their particle size was also determined. The in vitro cytotoxicity was investigated via MTT assay on HT-29 (as cancer cell) and fibroblast (as normal cell). Moreover, cytotoxicity mechanism of targeted liposomes was determined through the production of reactive oxygen species (ROS), mitochondrial membrane potential (∆Ψ ) and release of cytochrome c. Results showed that encapsulation efficiency (EE%) was 58.66±0.58 and average size of liposomes was 107nm. Also, nano-particles were spherical as shown by TEM. MTT assay on HT-29 cells revealed the higher cytotoxic activity of targeted liposomes in comparison to free drug and non-targeted liposome. In contrast, comparing with cancer cells, targeted liposomes had no cytotoxic effect on normal cells. In addition, targeted liposomes induced apoptosis through activation of mitochondrial apoptosis pathways, as evidenced by decreased mitochondrial membrane potential and release of cytochrome c. Results of the study indicated that targeted liposomes would provide a potential strategy to treat colon cancer by inducing apoptosis via mitochondria signaling pathway with reducing dose of the drug and resulting fewer side-effects.
[Mh] Termos MeSH primário: Antimetabólitos Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Neoplasias do Colo/tratamento farmacológico
Fluoruracila/farmacologia
Transdução de Sinais/efeitos dos fármacos
Transferrina/metabolismo
[Mh] Termos MeSH secundário: Antimetabólitos Antineoplásicos/administração & dosagem
Linhagem Celular
Neoplasias do Colo/metabolismo
Sistemas de Liberação de Medicamentos
Fluoruracila/administração & dosagem
Células HT29
Seres Humanos
Lipossomos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (Liposomes); 0 (Reactive Oxygen Species); 0 (Transferrin); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171225
[St] Status:MEDLINE


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[PMID]:29374697
[Au] Autor:Osada S; Gotoh A; Yokoi R; Tsuchiya H; Sakuratani T; Sasaki Y; Okumura N; Hayashi H; Mukai T
[Ad] Endereço:Hepato-Biliary Pancreas Center, Gifu Municipal Hospital, Gifu, Japan sting_7237@yahoo.co.jp.
[Ti] Título:Effective Timing of Surgical Resection of Colorectal Cancer Liver Metastases During Chemotherapy.
[So] Source:Anticancer Res;38(2):737-743, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The aim of the present study was to further develop our previous study on c-Met expression in colorectal cancer and epithelial-mesenchymal transition (EMT) induced by hepatocyte growth factor (HGF), to investigate EMT in the process of liver metastases, and evaluate the effects of chemotherapy on EMT cells as a therapeutic strategy for colorectal liver metastasis. MATERIALS AND METHODS: CT26 colon cancer cells were treated with 5-FU and oxaliplatin with or without HGF. The signaling pathway was evaluated by western blotting analysis, and drug resistance was evaluated by the MTT (3-(4,5-dimethyl-2-tetrazolyl)-2,5-diphenyl-2H tetrazolium bromide) assay. RESULTS: Under pretreatment with HGF for 96 h, 5 µM and 10 µM of 5-FU mediated significant growth inhibition by 72.5±3.9% and 76.2±2.4%, respectively, compared to HGF alone, and by 105.1±2.8% and 103.5±2.9%, respectively, without HGF. The expression of E2F1 was decreased significantly to 50.5±3.8% after 24 hours by HGF with a reduction of both cyclin D1 to 52.1±7.0% and E to 73.7±3.8%. Thymidylate synthase was also decreased in a time-dependent manner to 80.6±2.0% after 24 h and to 52.7±1.5% after 96 h. CONCLUSION: The presence of HGF was found to increase the 5-FU-induced death signal, JNK pathway, and inhibition of cell growth. As its mechanism, HGF was shown to decrease E2F-1 by reducing cyclin D or E by cell-cycle activation, resulting in inactivation of thymidylate synthase. The chemotherapeutic effect of 5-FU was increased in HGF- but not TGF-ß-induced EMT.
[Mh] Termos MeSH primário: Neoplasias Colorretais/tratamento farmacológico
Neoplasias Colorretais/patologia
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Neoplasias Hepáticas/secundário
[Mh] Termos MeSH secundário: Animais
Antimetabólitos Antineoplásicos/farmacologia
Caderinas/metabolismo
Linhagem Celular Tumoral
Neoplasias Colorretais/metabolismo
Fator de Transcrição E2F1/metabolismo
Fluoruracila/farmacologia
Fator de Crescimento de Hepatócito/farmacologia
Seres Humanos
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Hepáticas/cirurgia
Camundongos
Compostos Organoplatínicos/farmacologia
Transdução de Sinais/efeitos dos fármacos
Timidilato Sintase/metabolismo
Fatores de Tempo
Fator de Crescimento Transformador beta/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (Cadherins); 0 (E-cadherin protein, mouse); 0 (E2F1 Transcription Factor); 0 (E2f1 protein, mouse); 0 (Organoplatinum Compounds); 0 (Transforming Growth Factor beta); 04ZR38536J (oxaliplatin); 67256-21-7 (Hepatocyte Growth Factor); EC 2.1.1.45 (Thymidylate Synthase); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  8 / 18489 MEDLINE  
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[PMID]:29262503
[Au] Autor:Wang Y; Han ZX; Zhang JC
[Ad] Endereço:Department of Oncology, Xuzhou Central Hospital of Southeast University, Xuzhou 221000, China.
[Ti] Título:[Effects of bone marrow stromal cells on the chemotherapeutic sensitivity of acute lymphoblastic leukemia cells].
[So] Source:Zhonghua Zhong Liu Za Zhi;39(12):885-890, 2017 Dec 23.
[Is] ISSN:0253-3766
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the influences of bone marrow stromal cells, components of extracellular matrix and cytokine secreted by stromal cells on the chemotherapeutic sensitivity of acute lymphoblastic leukemia cells to cytosine arabinoside (Ara-C). The co-culture model of acute lymphoblastic leukemia cell Sup-B15 and bone marrow stromal cell OP9 was constructed. Sup-B15 cells were cultured alone or co-cultured with OP9 cells, inactivated OP9 cells, the conditional medium (CM) of co-cultured OP9 cells and Sup-B15 cells, the CM of OP9 cells alone or Sup-B15 cells alone, respectively. The effects of different concentrations of Ara-C on the proliferation of each Sup-B1 cell group mentioned above were detected by cell counting kit-8 (CCK-8) method. The effects of different concentrations of Ara-C on the apoptosis of each group were detected by flow cytometry (FCM). The expressions of Bcl-2 protein in each group were detected by western blot. The results of CCK-8 test showed that the inhibitory efficiency of Ara-C was in a dose-dependent manner. With different concentrations of Ara-C treatment for 48 hours, the half maximal inhibitory concentrations (IC(50)) of Sup-B15 and OP9 co-cultured group, Sup-B15 and inactivated OP9 co-cultured group were 0.510 and 0.339 µg/ml, respectively, significantly higher than 0.091 µg/ml of Sup-B15 cultured alone group ( <0.05). The IC(50) of CM of Sup-B15 and OP9 co-cultured group was 0.204 µg/ml, significantly higher than 0.087 µg/ml of the CM of OP9 cultured alone group ( <0.05) and 0.097 µg/ml of the CM of Sup-B15 cultured alone group ( <0.05). The results of flow cytometry showed that with 0.10 µg/ml Ara-C treatment for 24 hours, the early apoptotic cell percentages of Sup-B15 and OP9 co-cultured group, Sup-B15 and inactivated OP9 co-cultured group and Sup-B15 cultured alone group were (6.67±2.19) %, (8.95±3.04) % and (20.46±2.63) %, respectively. The early apoptotic cell percentages of Sup-B15 and OP9 co-cultured group, Sup-B15 and inactivated OP9 co-cultured group were significantly lower than that of Sup-B15 cultured alone group ( <0.05). The early apoptotic cell percentages of the CM of Sup-B15 and OP9 co-cultured group, the CM of OP9 cultured alone group and the CM of Sup-B15 cultured alone group were (11.16±2.97)%, (22.08±2.71)% and (19.25±1.57)%, respectively, the former two of which were significantly lower than the last one ( <0.05). The results of western blot showed that the relative expression levels of Bcl-2 protein of Sup-B15 cultured alone group, Sup-B15 and OP9 co-cultured group, Sup-B15 and inactivated OP9 co-cultured group, the CM of Sup-B15 and OP9 co-cultured group, the CM of OP9 cultured alone group and the CM of Sup-B15 cultured alone group were 1.00±0.00, 1.53±0.03, 1.38±0.01, 1.26±0.05, 1.03±0.01 and 0.98±0.02, respectively. The expression levels of bcl-2 protein of three combined groups were significantly higher than that of Sup-B15 cultured alone group ( <0.05). while no statistically significant difference was observed between the CM of OP9 cultured alone group and the CM of Sup-B15 cultured alone group ( >0.05). Bone marrow stromal cell OP9, the components of bone marrow extracellular matrix and cytokine secreted by stromal cells are involved in the induction of the chemotherapeutic resistance of Sup-B15 cells to Ara-C.
[Mh] Termos MeSH primário: Antimetabólitos Antineoplásicos/farmacologia
Células da Medula Óssea/secreção
Citarabina/farmacologia
Citocinas/fisiologia
Citocinas/secreção
Resistência a Medicamentos Antineoplásicos
Células Mesenquimais Estromais/secreção
Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia
[Mh] Termos MeSH secundário: Apoptose
Contagem de Células
Linhagem Celular Tumoral
Técnicas de Cocultura
Meios de Cultivo Condicionados
Seres Humanos
Proteínas Proto-Oncogênicas c-bcl-2
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (BCL2 protein, human); 0 (Culture Media, Conditioned); 0 (Cytokines); 0 (Proto-Oncogene Proteins c-bcl-2); 04079A1RDZ (Cytarabine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0253-3766.2017.12.002


  9 / 18489 MEDLINE  
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[PMID]:29325248
[Au] Autor:Yin WJ; Zhu X; Yang HY; Sun WY; Wu MJ
[Ad] Endereço:Department of Pathology, Zhejiang Cancer Hospital, Hangzhou 310022, China.
[Ti] Título:[Survival of patients with primary central nervous system diffuse large B-cell lymphoma: impact of gene aberrations and protein overexpression of bcl-2 and C-MYC, and selection of chemotherapy regimens].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(1):32-38, 2018 Jan 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the impact of clinicopathological features, gene rearrangements and protein expression of bcl-6, bcl-2, C-MYC and chemotherapy regime on the prognosis of patients with primary central nervous system diffuse large B-cell lymphoma (PCNS-DLBCL). Thirty-three cases of PCNS-DLBCL diagnosed from January 2006 to December 2016 at Zhejiang Cancer Hospital were collected. The expression of CD10, bcl-6, bcl-2, MUM1 and MYC were detected by immunohistochemical staining (IHC). The presence of EB virus was detected by in situ hybridization(EBER). Copy number variation (ICN) and translocation status of bcl-6, bcl-2 and C-MYC genes were detected by fluorescence in situ hybridization (FISH). The relationship between the above indexes and the prognosis was analyzed by univariate, bivariate survival analysis and multiple Cox hazard regression analysis. The study included 33 patients of PCNS-DLBCL, without evidence of primary or secondary immunodeficient disease. Male to female ratio was 1.36∶1.00, and the average age was 56 years. Twenty cases had single lesion while 13 had multiple lesions. Deep brain involvement was seen in 12 cases. All patients underwent partial or total tumor resection. Five patients received whole brain post-surgery radiotherapy, nine patients received high-dose methotrexate (HD-MTX) based chemotherapy, and 12 patients received whole-brain radiotherapy combined with HD-MTX based chemotherapy. Severn patients received no further treatment and rituximab was used in 8 patients. According to the Hans model, 27 cases were classified as non-GCB subtypes (81.8%). Bcl-2 was positive in 25 cases (75.8%, 25/33) and highly expressed in 8 (24.2%). MYC was positive in 12 cases (36.4%) and double expression of bcl-2 and MYC was seen in 6 cases. EBER positive rate was 10.0%(3/30), all of which had multiple lesions. Two bcl-6 gene translocations and 3 amplifications were found in 28 patients. Two translocations, 3 ICN or with both bcl-2 gene translocation and ICN were found in 30 patients. Four ICNs of C-MYC gene were found in 28 patients. Elevated protein in cerebrospinal fluid (CSF) was found in 13 patients. LDH increased in 10 cases. Follow-up period was 2-90 months with the average survival time of (23.0±3.7) months and two-year survival rate of 39.0%. Univariate survival analysis showed that overexpression of bcl-2 protein (≥70%) and MYC protein (≥40%), bcl-2 gene abnormality (including copy number increase and translocation), C-MYC gene copy number increased were adverse factors for survival. C-MYC/ bcl-2 gene double hit was seen in 2 cases. Bivariate survival analysis found that of bcl-2/MYC protein double expression and bcl-2 and C-MYC genes double aberration were significantly associated with adverse outcomes. Cox multivariate risk regression analysis found that gender, cerebrospinal fluid protein increasing, and ICN of C-MYC gene were independent poor prognostic factors. DH-MTX based comprehensive chemotherapy was associated with better prognosis. Double hit at genomic level (copy number variations and gene rearrangements) and double protein expression of bcl-2 and C-MYC in PCNS-DLBCL are significantly associated with an adverse outcome. DH-MTX based comprehensive treatment may prolong the patient survival.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias do Sistema Nervoso Central/mortalidade
Rearranjo Gênico
Linfoma Difuso de Grandes Células B/mortalidade
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
[Mh] Termos MeSH secundário: Antimetabólitos Antineoplásicos/uso terapêutico
Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/mortalidade
Neoplasias Encefálicas/patologia
Neoplasias Encefálicas/terapia
Neoplasias do Sistema Nervoso Central/genética
Neoplasias do Sistema Nervoso Central/metabolismo
Neoplasias do Sistema Nervoso Central/terapia
Variações do Número de Cópias de DNA
Feminino
Dosagem de Genes
Genes bcl-2
Genes myc
Herpesvirus Humano 4/isolamento & purificação
Seres Humanos
Hibridização in Situ Fluorescente
Fatores Reguladores de Interferon/metabolismo
Linfoma Difuso de Grandes Células B/genética
Linfoma Difuso de Grandes Células B/metabolismo
Linfoma Difuso de Grandes Células B/terapia
Masculino
Metotrexato/uso terapêutico
Meia-Idade
Neprilisina/metabolismo
Prognóstico
Proteínas Proto-Oncogênicas c-bcl-6/genética
Proteínas Proto-Oncogênicas c-bcl-6/metabolismo
Análise de Sobrevida
Taxa de Sobrevida
Translocação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (BCL2 protein, human); 0 (Interferon Regulatory Factors); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Proto-Oncogene Proteins c-bcl-6); 0 (Proto-Oncogene Proteins c-myc); 0 (interferon regulatory factor-4); EC 3.4.24.11 (Neprilysin); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.01.007


  10 / 18489 MEDLINE  
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[PMID]:27777774
[Au] Autor:Van Der Kraak L; Goel G; Ramanan K; Kaltenmeier C; Zhang L; Normolle DP; Freeman GJ; Tang D; Nason KS; Davison JM; Luketich JD; Dhupar R; Lotze MT
[Ad] Endereço:Department of Cardiothoracic Surgery, University of Pittsburgh, Pittsburgh, PA USA.
[Ti] Título:5-Fluorouracil upregulates cell surface B7-H1 (PD-L1) expression in gastrointestinal cancers.
[So] Source:J Immunother Cancer;4:65, 2016.
[Is] ISSN:2051-1426
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Resistance to chemotherapy is a major obstacle in the effective treatment of cancer patients. B7-homolog 1, also known as programmed death ligand-1 (PD-L1), is an immunoregulatory protein that is overexpressed in several human cancers. Interaction of B7-H1 with programmed death 1 (PD-1) prevents T-cell activation and proliferation, sequestering the T-cell receptor from the cell membrane, inducing T-cell apoptosis, thereby leading to cancer immunoresistance. B7-H1 upregulation contributes to chemoresistance in several types of cancer, but little is known with respect to changes associated with 5-fluorouracil (5-FU) or gastrointestinal cancers. METHODS: HCT 116 p53 , HCT 116 p53 colorectal cancer (CRC) and OE33 esophageal adenocarcinoma (EAC) cells were treated with increasing doses of 5-FU (0.5 uM, 5 uM, 50 uM, 500 uM) or interferon gamma (IFN-γ, 10 ng/mL) in culture for 24 h and B7-H1 expression was quantified using flow cytometry and western blot analysis. We also evaluated B7-H1 expression, by immunohistochemistry, in tissue collected prior to and following neoadjuvant therapy in 10 EAC patients. RESULTS: B7-H1 expression in human HCT 116 p53 and HCT 116 p53 CRC cells lines, while low at baseline, can be induced by treatment with 5-FU. OE33 baseline B7-H1 expression exceeded CRC cell maximal expression and could be further increased in a dose dependent manner following 5-FU treatment in the absence of immune cells. We further demonstrate tumor B7-H1 expression in esophageal adenocarcinoma patient-derived pre-treatment biopsies. While B7-H1 expression was not enhanced in post-treatment esophagectomy specimens, this may be due to the limits of immunohistochemical quantification. CONCLUSIONS: B7-H1/PD-L1 expression can be increased following treatment with 5-FU in gastrointestinal cancer cell lines, suggesting alternative mechanisms to classic immune-mediated upregulation. This suggests that combining 5-FU treatment with PD-1/B7-H1 blockade may improve treatment in patients with gastrointestinal adenocarcinoma.
[Mh] Termos MeSH primário: Antimetabólitos Antineoplásicos/farmacologia
Antígeno B7-H1/metabolismo
Membrana Celular/metabolismo
Fluoruracila/farmacologia
Neoplasias Gastrointestinais/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/metabolismo
Adenocarcinoma/patologia
Antígeno B7-H1/genética
Esôfago de Barrett/genética
Esôfago de Barrett/metabolismo
Esôfago de Barrett/patologia
Biópsia
Linhagem Celular Tumoral
Neoplasias Esofágicas/genética
Neoplasias Esofágicas/metabolismo
Neoplasias Esofágicas/patologia
Citometria de Fluxo
Neoplasias Gastrointestinais/tratamento farmacológico
Neoplasias Gastrointestinais/genética
Neoplasias Gastrointestinais/patologia
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Técnicas de Inativação de Genes
Seres Humanos
Imuno-Histoquímica
Interferon gama/farmacologia
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (B7-H1 Antigen); 0 (CD274 protein, human); 0 (Tumor Suppressor Protein p53); 82115-62-6 (Interferon-gamma); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1186/s40425-016-0163-8



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