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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]:29278701
[Au] Autor:Chen C; Wang YY; Wang YX; Cheng MQ; Yin JB; Zhang X; Hong ZP
[Ad] Endereço:School of Pharmaceutical Sciences & Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, Yunnan, China; Department of Urological Surgery, The 1st Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
[Ti] Título:Gentiopicroside ameliorates bleomycin-induced pulmonary fibrosis in mice via inhibiting inflammatory and fibrotic process.
[So] Source:Biochem Biophys Res Commun;495(4):2396-2403, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pulmonary fibrosis (PF) is a chronic and ultimately fatal interstitial lung disease of various causes. The advent of nintedanib and pirfenidone provides treatment options for PF patients for the first time. However, the adverse effects of the two drugs such as gastrointestinal disorders and hepatic dysfunction often lead to treatment discontinuation. Gentiopicroside (GPS) is a natural secoiridoid glycoside from gentian species of medicinal plants, and has a variety of pharmacological activities, including hepatoprotective and cholagogic, anti-inflammatory, antinociceptive, and smooth muscle relaxing activities. The present study aimed to investigate the therapeutical effects of GPS on bleomycin (BLM)-induced PF in mice. Severe lung inflammation and fibrosis were observed in BLM-treated mice. GPS significantly ameliorated inflammatory and fibrotic responses in lungs of PF mice which were confirmed by histopathological examinations including light microscopy and transmission electron microscopy. Additionally, GPS significantly decreased the levels of inflammatory cytokines including TNF-α and IL-1ß in bronchoalveolar lavage fluid and reduced the content of hydroxyproline in lungs of PF mice. Furthermore, GPS significantly downregulated the expression of TGF-ß1 and CTGF in lungs of PF mice. In vitro, GPS inhibited epithelial-mesenchymal transition of A549 cells stimulated by TGF-ß1, in a dose-dependent manner. Our findings suggest that GPS has the potential as an ideal drug candidate for PF, as it has both anti-inflammatory and anti-fibrotic effects. Alveolar epithelial cells and TGF-ß1 may be the main target cells and molecule of GPS on BLM-induced PF, respectively.
[Mh] Termos MeSH primário: Glucosídeos Iridoides/administração & dosagem
Pulmão/imunologia
Pneumonia/imunologia
Pneumonia/prevenção & controle
Fibrose Pulmonar/imunologia
Fibrose Pulmonar/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/administração & dosagem
Bleomicina
Citocinas/imunologia
Relação Dose-Resposta a Droga
Fatores Imunológicos/imunologia
Pulmão/efeitos dos fármacos
Masculino
Camundongos
Pneumonia/induzido quimicamente
Fibrose Pulmonar/induzido quimicamente
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Immunologic Factors); 0 (Iridoid Glucosides); 0WE09Z21RC (gentiopicroside); 11056-06-7 (Bleomycin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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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]:29225172
[Au] Autor:Nagahara H; Seno T; Yamamoto A; Obayashi H; Inoue T; Kida T; Nakabayashi A; Kukida Y; Fujioka K; Fujii W; Murakami K; Kohno M; Kawahito Y
[Ad] Endereço:Inflammation and Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
[Ti] Título:Role of allograft inflammatory factor-1 in bleomycin-induced lung fibrosis.
[So] Source:Biochem Biophys Res Commun;495(2):1901-1907, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Allograft inflammatory factor-1 (AIF-1) is a protein expressed by macrophages infiltrating the area around the coronary arteries in a rat ectopic cardiac allograft model. We previously reported that AIF-1 is associated with the pathogenesis of rheumatoid arthritis and skin fibrosis in sclerodermatous graft-versus-host disease mice. Here, we used an animal model of bleomycin-induced lung fibrosis to analyze the expression of AIF-1 and examine its function in lung fibrosis. The results showed that AIF-1 was expressed on lung tissues, specifically macrophages, from mice with bleomycin-induced lung fibrosis. Recombinant AIF-1 increased the production of TGF-ß which plays crucial roles in the mechanism of fibrosis by mouse macrophage cell line RAW264.7. Recombinant AIF-1 also increased both the proliferation and migration of lung fibroblasts compared with control group. These results suggest that AIF-1 plays an important role in the mechanism underlying lung fibrosis, and may provide an attractive new therapeutic target.
[Mh] Termos MeSH primário: Bleomicina
Proteínas de Ligação ao Cálcio/imunologia
Fatores Imunológicos/imunologia
Ativação de Macrófagos/imunologia
Macrófagos/imunologia
Proteínas dos Microfilamentos/imunologia
Fibrose Pulmonar/induzido quimicamente
Fibrose Pulmonar/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Macrófagos/patologia
Camundongos
Camundongos Endogâmicos C57BL
Fibrose Pulmonar/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Calcium-Binding Proteins); 0 (Immunologic Factors); 0 (Microfilament Proteins); 11056-06-7 (Bleomycin)
[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:171212
[St] Status:MEDLINE


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[PMID]:29248013
[Au] Autor:Ghalleb M; Bouzaiene H; Slim S; Hadiji A; Hechiche M; Ben Hassouna J; Rahal K
[Ad] Endereço:Surgical Oncology Department, Salah Azaiez Institute of Cancer, Tunis, Tunisia.
[Ti] Título:Fertility-sparing surgery in advanced stage malignant ovarian germ cell tumor: a case report.
[So] Source:J Med Case Rep;11(1):350, 2017 Dec 17.
[Is] ISSN:1752-1947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Malignant ovarian germ cell tumor is a rare type of disease, which generally has a good prognosis due to the high chemosensitivity of this type of tumor. Fertility preservation is an important issue because malignant ovarian germ cell tumor commonly affects young women. Although conservation is the standard for early stage, it becomes more debatable as the disease progresses to more advanced stages. AIM: Report the case of a patient with an International Federation of Gynecology and Obstetrics Stage IIIc malignant ovarian germ cell tumor, who had conservative surgery and chemotherapy with a good fertility outcome. CASE PRESENTATION: A 23-year-old North African woman with a left malignant ovarian germ cell tumor stage IIIc was treated by left adnexectomy and omentectomy followed by chemotherapy. A 15-year follow-up showed no signs of relapse, and she completed three full-term natural pregnancies. CONCLUSIONS: Malignant ovarian germ cell tumor is a rare ovarian tumor with a good prognosis. It is usually associated with a good fertility outcome in early stages. However, due to the rarity of the disease in advanced stages, the fertility outcome for this group of patients is not clear. This lack of data surrounding advanced stages points to the need for a meta-analysis of all published cases.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Preservação da Fertilidade/métodos
Neoplasias Embrionárias de Células Germinativas/cirurgia
Neoplasias Ovarianas/cirurgia
Ovariectomia/métodos
Neoplasias Peritoneais/cirurgia
[Mh] Termos MeSH secundário: Bleomicina/uso terapêutico
Quimioterapia Adjuvante
Cisplatino/uso terapêutico
Etoposídeo/uso terapêutico
Feminino
Seres Humanos
Estadiamento de Neoplasias
Neoplasias Embrionárias de Células Germinativas/patologia
Omento/cirurgia
Neoplasias Ovarianas/patologia
Neoplasias Peritoneais/secundário
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
11056-06-7 (Bleomycin); 6PLQ3CP4P3 (Etoposide); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE
[do] DOI:10.1186/s13256-017-1516-8


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[PMID]:28455433
[Au] Autor:Nie Y; Sun L; Wu Y; Yang Y; Wang J; He H; Hu Y; Chang Y; Liang Q; Zhu J; Ye RD; Christman JW; Qian F
[Ad] Endereço:Engineering Research Center of Cell and Therapeutic Antibody, Ministry of Education, School of Pharmacy, Shanghai Jiao Tong University, Shanghai 200240, People's Republic of China.
[Ti] Título:AKT2 Regulates Pulmonary Inflammation and Fibrosis via Modulating Macrophage Activation.
[So] Source:J Immunol;198(11):4470-4480, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Idiopathic pulmonary fibrosis (IPF) is a highly lethal pathological process that is characterized by inflammation, fibroblast accumulation, and excessive collagen deposition. Although AKT2-mediated signaling pathways modulate inflammatory responses, their role in IPF has not been defined. We report that AKT2 deficiency ( ) protected against bleomycin-induced pulmonary fibrosis and inflammation. Adoptive transfer of wild-type macrophages or administration of IL-13 to mice could restore pulmonary fibrosis. In response to IL-33 treatment, macrophages displayed decreased production of IL-13 and TGF-ß1 and attenuated phosphorylation of FoxO3a compared with macrophages. Furthermore, the expression of IL-13 was increased by small interfering RNA knockdown of FoxO3a or in FoxO3a-deficient macrophages. By evaluating lung sections from pulmonary fibrosis patients, we found that the phosphorylation of AKT2 and FoxO3a was remarkably upregulated. Collectively, these results indicate that AKT2 modulates pulmonary fibrosis through inducing TGF-ß1 and IL-13 production by macrophages, and inhibition of AKT2 may be a potential strategy for treating IPF.
[Mh] Termos MeSH primário: Ativação de Macrófagos
Pneumonia/imunologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Fibrose Pulmonar/imunologia
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Bleomicina/administração & dosagem
Bleomicina/efeitos adversos
Proteína Forkhead Box O3/genética
Proteína Forkhead Box O3/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Interleucina-13/administração & dosagem
Interleucina-13/genética
Interleucina-13/imunologia
Interleucina-33/imunologia
Interleucina-33/farmacologia
Macrófagos/imunologia
Camundongos
Proteínas Proto-Oncogênicas c-akt/deficiência
Proteínas Proto-Oncogênicas c-akt/genética
Fator de Crescimento Transformador beta1/genética
Fator de Crescimento Transformador beta1/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (FOXO3 protein, human); 0 (Forkhead Box Protein O3); 0 (FoxO3 protein, mouse); 0 (Il33 protein, mouse); 0 (Interleukin-13); 0 (Interleukin-33); 0 (Transforming Growth Factor beta1); 11056-06-7 (Bleomycin); EC 2.7.11.1 (AKT2 protein, human); EC 2.7.11.1 (Akt2 protein, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601503


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[PMID]:29175452
[Au] Autor:Kim MS; Kim SH; Jeon D; Kim HY; Lee K
[Ad] Endereço:National Center for Efficacy Evaluation of Respiratory Disease Product, Korea Institute of Toxicology, Jeongeup-si, Jeollabuk-do, 56212, Republic of Korea.
[Ti] Título:Changes in expression of cytokines in polyhexamethylene guanidine-induced lung fibrosis in mice: Comparison of bleomycin-induced lung fibrosis.
[So] Source:Toxicology;393:185-192, 2018 01 15.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Inhalation of polyhexamethylene guanidine (PHMG) causes irreversible pulmonary injury, such as pulmonary fibrosis. However, the mechanism underlying PHMG-induced lung injury is unclear. In this study, we compared the difference in time-dependent lung injury between PHMG- and bleomycin (BLM)-treated mice and determined cytokines involved in inducing lung injury by performing cytokine antibody array analysis. Mice were treated once with 1.8mg/kg BLM or 1.2mg/kg PHMG through intratracheal instillation and were sacrificed on days 7 and 28. Bronchoalveolar lavage fluid (BALF) analysis showed that the number of neutrophils was significantly higher in PHMG-treated mice than in BLM-treated mice on day 7. Histopathological analysis showed inflammatory cell infiltration and fibrosis mainly in the terminal bronchioles and alveoli in the lungs of PHMG- and BLM-treated mice. However, continuous macrophage infiltration in the alveolar space and bronchioloalveolar epithelial hyperplasia (BEH) were only observed in PHMG-treated mice. Cytokine antibody array analysis showed that 15 and eight cytokines were upregulated in PHMG- and BLM-treated mice, respectively, on day 7. On day 28, 13 and five cytokines were upregulated in PHMG and BLM-treated mice, respectively. In addition, the expressed cytokines between days 7 and 28 in BLM-treated mice were clearly different, but were similar in PHMG-treated mice. Consequently, between PHMG- and BLM-treated mice, we observed differences in the expression patterns and types of cytokines. These differences are considered to be a result of the inflammatory processes induced by both substances, which may mainly involve macrophage infiltration. Therefore, continuous induction of the inflammatory response by PHMG may play an important role in the development of pulmonary fibrosis.
[Mh] Termos MeSH primário: Bleomicina
Citocinas/imunologia
Guanidinas
Fibrose Pulmonar/induzido quimicamente
Fibrose Pulmonar/imunologia
[Mh] Termos MeSH secundário: Animais
Líquido da Lavagem Broncoalveolar/citologia
Contagem de Células
Pulmão/efeitos dos fármacos
Pulmão/imunologia
Pulmão/patologia
Macrófagos/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neutrófilos/efeitos dos fármacos
Fibrose Pulmonar/patologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Guanidines); 11056-06-7 (Bleomycin); 31961-54-3 (polyhexamethyleneguanidine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


  8 / 14072 MEDLINE  
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[PMID]:29197869
[Au] Autor:Tai W; Xu Y; Ding J; Wu H; Du M; Qu X; Gao L; Li J; Dong Z
[Ad] Endereço:Department of Clinical Laboratory, Yunnan Molecular Diagnostic Center, The Second affiliated hospital of Kunming Medical University, Kunming, China.
[Ti] Título:Fibrocytes Ameliorate Acute Lung Injury by Decreasing Inflammatory Cytokine and Chemokine Levels and Reducing Neutrophil Accumulation in the Lung.
[So] Source:Cell Physiol Biochem;44(4):1526-1536, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Acute lung injury (ALI) remains a severe disease that threatens human life around the world. To decrease the mortality of ALI and improve ALI treatment efficacy, the development of more ALI treatments is urgently needed. Whether fibrocytes directly participate in ALI has not been studied. Therefore, a mouse model of ALI was induced with lipopolysaccharide (LPS). METHODS: Fibrocytes were harvested from peripheral blood mononuclear cells of bleomycin mice and identified by using flow cytometry to detect the expression of molecular makers. The fibrocytes were injected for the treatment of acute lung injury mice. The curative effects were evaluated by using ELISA to determine the cytokines (including TNF-α, IL-6 and IFN-γ) concentrations in bronchoalveolar lavage fluid (BALF) supernatant. RESULTS: The concentrations of cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (IFN-γ) were increased in mice with ALI induced with LPS. The concentrations of TNF-α, IL-6, and IFN-γ as well as their mRNA and protein expression levels were decreased by administration of fibrocytes. The effect of fibrocytes in ameliorating ALI was time dependent. LPS treatment induced an increase in myeloperoxidase (MPO) activity, whereas the fibrocyte treatment caused inhibition of MPO activity as well as expression of the neutrophil-chemoattractant chemokine macrophage inflammatory protein 2 (MIP-2). CONCLUSION: Taken together, these data suggest that fibrocytes ameliorated ALI by suppressing inflammatory cytokines and chemokines as well as by decreasing the accumulation of neutrophils in the lung.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/patologia
Quimiocinas/metabolismo
Citocinas/metabolismo
Fibroblastos/metabolismo
Neutrófilos/fisiologia
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/etiologia
Animais
Bleomicina/farmacologia
Líquido da Lavagem Broncoalveolar/química
Líquido da Lavagem Broncoalveolar/citologia
Células Cultivadas
Quimiocinas/genética
Citocinas/genética
Modelos Animais de Doenças
Fibroblastos/citologia
Fibroblastos/efeitos dos fármacos
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/efeitos dos fármacos
Lipopolissacarídeos/toxicidade
Pulmão/imunologia
Pulmão/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Neutrófilos/imunologia
Peroxidase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines); 0 (Cytokines); 0 (Lipopolysaccharides); 11056-06-7 (Bleomycin); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE
[do] DOI:10.1159/000485647


  9 / 14072 MEDLINE  
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[PMID]:29277791
[Au] Autor:Bur H; Haapasaari KM; Turpeenniemi-Hujanen T; Kuittinen O; Auvinen P; Marin K; Soini Y; Karihtala P
[Ad] Endereço:Department of Oncology and Radiotherapy, Medical Research Center Oulu, Oulu University Hospital, Oulu, Finland.
[Ti] Título:Strong Prolyl Hydroxylase Domain 1 Expression Predicts Poor Outcome in Radiotherapy-treated Patients with Classical Hodgkin's Lymphoma.
[So] Source:Anticancer Res;38(1):329-336, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hypoxia-inducible factors (HIFs) and prolyl hydroxylase domain (PHD) proteins control cellular oxygen homeostasis and a wide range of other processes. MATERIALS AND METHODS: We immunohistochemically assessed the expression of HIF1α, HIF2α, PHD1, PHD2 and PHD3 in 115 cases of classical Hodgkin's lymphoma, all treated in the first line with doxorubicin, bleomycin, vinblastine and darcabazine (ABVD) chemotherapy. RESULTS: In advanced-stage patients treated with involved-field radiotherapy (IFRT), nuclear HIF1α expression in reactive cellular infiltrate predicted prolonged relapse-free survival (RFS) (p=0.026). Strong cytoplasmic PHD1 expression in Reed-Sternberg cells was associated with poor RFS among patients treated with IFRT and advanced-stage patients treated with ABVD and IFRT (p=0.0028 and p=0.0058, respectively). In Cox regression analysis, PHD1 was a more significant predictor of relapse (risk ratio=18.383; 95% confidence interval(CI)=1.521-222.246; p=0.022) than the International Prognostic Score. CONCLUSION: HIF and PHD expression appear to be novel prognostic biomarkers in classical Hodgkin's lymphoma.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Doença de Hodgkin/patologia
Doença de Hodgkin/radioterapia
Prolil Hidroxilases/biossíntese
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Fatores de Transcrição Hélice-Alça-Hélice Básicos/biossíntese
Bleomicina/uso terapêutico
Hipóxia Celular/fisiologia
Dacarbazina/uso terapêutico
Doxorrubicina/uso terapêutico
Feminino
Doença de Hodgkin/tratamento farmacológico
Doença de Hodgkin/mortalidade
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/biossíntese
Prolina Dioxigenases do Fator Induzível por Hipóxia/biossíntese
Masculino
Meia-Idade
Estudos Retrospectivos
Resultado do Tratamento
Vimblastina/uso terapêutico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Biomarkers, Tumor); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (endothelial PAS domain-containing protein 1); 11056-06-7 (Bleomycin); 5V9KLZ54CY (Vinblastine); 7GR28W0FJI (Dacarbazine); 80168379AG (Doxorubicin); EC 1.14.11.- (Prolyl Hydroxylases); EC 1.14.11.2 (EGLN1 protein, human); EC 1.14.11.29 (EGLN2 protein, human); EC 1.14.11.29 (EGLN3 protein, human); EC 1.14.11.29 (Hypoxia-Inducible Factor-Proline Dioxygenases)
[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


  10 / 14072 MEDLINE  
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[PMID]:28748309
[Au] Autor:Follett SE; Ingersoll AD; Murray SA; Reilly TM; Lehmann TE
[Ad] Endereço:Department of Chemistry, University of Wyoming, 1000 E. University Avenue, Laramie, WY, 82071, USA.
[Ti] Título:Interaction of Zn(II)bleomycin-A and Zn(II)peplomycin with a DNA hairpin containing the 5'-GT-3' binding site in comparison with the 5'-GC-3' binding site studied by NMR spectroscopy.
[So] Source:J Biol Inorg Chem;22(7):1039-1054, 2017 Oct.
[Is] ISSN:1432-1327
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Bleomycins are a group of glycopeptide antibiotics synthesized by Streptomyces verticillus that are widely used for the treatment of various neoplastic diseases. These antibiotics have the ability to chelate a metal center, mainly Fe(II), and cause site-specific DNA cleavage. Bleomycins are differentiated by their C-terminal regions. Although this antibiotic family is a successful course of treatment for some types of cancers, it is known to cause pulmonary fibrosis. Previous studies have identified that bleomycin-related pulmonary toxicity is linked to the C-terminal region of these drugs. This region has been shown to closely interact with DNA. We examined the binding of Zn(II)peplomycin and Zn(II)bleomycin-A to a DNA hairpin of sequence 5'-CCAGTATTTTTACTGG-3', containing the binding site 5'-GT-3', and compared the results with those obtained from our studies of the same MBLMs bound to a DNA hairpin containing the binding site 5'-GC-3'. We provide evidence that the DNA base sequence has a strong impact in the final structure of the drug-target complex.
[Mh] Termos MeSH primário: Antibióticos Antineoplásicos/farmacologia
Bleomicina/farmacologia
DNA/metabolismo
Peplomicina/farmacologia
Zinco/farmacologia
[Mh] Termos MeSH secundário: Antibióticos Antineoplásicos/química
Sítios de Ligação
Bleomicina/análogos & derivados
DNA/química
Seres Humanos
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Ressonância Magnética Nuclear Biomolecular
Peplomicina/análogos & derivados
Zinco/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 11056-06-7 (Bleomycin); 56H9L80NIZ (Peplomycin); 9007-49-2 (DNA); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1007/s00775-017-1482-z



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