PubMed:31262895 JSONTXT

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    PubMed_Structured_Abstracts

    {"project":"PubMed_Structured_Abstracts","denotations":[{"id":"T1","span":{"begin":98,"end":358},"obj":"BACKGROUND"},{"id":"T2","span":{"begin":382,"end":549},"obj":"METHODS"},{"id":"T3","span":{"begin":559,"end":1222},"obj":"RESULTS"},{"id":"T4","span":{"begin":1235,"end":1327},"obj":"CONCLUSIONS"}],"text":"Autophagy Promotes Survival of CHP-212 Neuroblastoma Cells Treated With Casiopeínas®.\nBACKGROUND: Neuroblastoma is the main solid extracranial tumor of childhood. The amplification of N-myc oncogene (MYCN) and 1p deletion are the main molecular alterations. These features are what make treatment impossible, especially in high-risk patients with metastases.\nMATERIALS AND METHODS: Our study investigated the processes undergone by CHP-212 neuroblastoma cells, after being treated with Casiopeínas® (Cas) IIgly, IIIEa, and IIIia for 2, 10, and 24 h.\nRESULTS: At 2 h, all the treatments Ied to apoptosis [defined by the presence of B-cell lymphoma 2 (BCL2), BCL2-associated X protein, cytochrome c, and caspase-3]. In addition, autophagy with specific molecules beclin-1 and microtubule-associated protein 1A/1B-light chain 3 (LC3)-II/LC3-I (ratio \u003e1). Later at 10 h, autophagy-associated proteins were observed, and at 24 h, only survival proteins nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB), and extracellular signal-regulated kinases (ERK)2/ERK1\u003e1 were found. Another relevant finding was the presence of caspase-10 throughout the study, especially in cells treated with CasIIgly and CasIIIEa.\nCONCLUSION: These relationships indicate a possible mechanism of action of Casiopeínas on neuroblastoma."}

    Goldhamster2_Cellosaurus

    {"project":"Goldhamster2_Cellosaurus","denotations":[{"id":"T1","span":{"begin":31,"end":38},"obj":"CVCL_1125|Cancer_cell_line|Homo sapiens"},{"id":"T2","span":{"begin":432,"end":439},"obj":"CVCL_1125|Cancer_cell_line|Homo sapiens"},{"id":"T3","span":{"begin":544,"end":548},"obj":"CVCL_8262|Cancer_cell_line|Homo sapiens"},{"id":"T4","span":{"begin":559,"end":563},"obj":"CVCL_L303|Cancer_cell_line|Rattus norvegicus"},{"id":"T5","span":{"begin":631,"end":632},"obj":"CVCL_6480|Finite_cell_line|Mus musculus"},{"id":"T6","span":{"begin":695,"end":696},"obj":"CVCL_S361|Finite_cell_line|Mus musculus"},{"id":"T7","span":{"begin":861,"end":865},"obj":"CVCL_N538|Hybridoma|Mus musculus"},{"id":"T8","span":{"begin":919,"end":923},"obj":"CVCL_8262|Cancer_cell_line|Homo sapiens"},{"id":"T9","span":{"begin":993,"end":1002},"obj":"CVCL_C410|Hybridoma|Mus musculus"},{"id":"T10","span":{"begin":1003,"end":1004},"obj":"CVCL_6480|Finite_cell_line|Mus musculus"},{"id":"T11","span":{"begin":1012,"end":1014},"obj":"CVCL_W770|Cancer_cell_line|Homo sapiens"},{"id":"T12","span":{"begin":1016,"end":1017},"obj":"CVCL_6480|Finite_cell_line|Mus musculus"},{"id":"T13","span":{"begin":1264,"end":1265},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"}],"text":"Autophagy Promotes Survival of CHP-212 Neuroblastoma Cells Treated With Casiopeínas®.\nBACKGROUND: Neuroblastoma is the main solid extracranial tumor of childhood. The amplification of N-myc oncogene (MYCN) and 1p deletion are the main molecular alterations. These features are what make treatment impossible, especially in high-risk patients with metastases.\nMATERIALS AND METHODS: Our study investigated the processes undergone by CHP-212 neuroblastoma cells, after being treated with Casiopeínas® (Cas) IIgly, IIIEa, and IIIia for 2, 10, and 24 h.\nRESULTS: At 2 h, all the treatments Ied to apoptosis [defined by the presence of B-cell lymphoma 2 (BCL2), BCL2-associated X protein, cytochrome c, and caspase-3]. In addition, autophagy with specific molecules beclin-1 and microtubule-associated protein 1A/1B-light chain 3 (LC3)-II/LC3-I (ratio \u003e1). Later at 10 h, autophagy-associated proteins were observed, and at 24 h, only survival proteins nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB), and extracellular signal-regulated kinases (ERK)2/ERK1\u003e1 were found. Another relevant finding was the presence of caspase-10 throughout the study, especially in cells treated with CasIIgly and CasIIIEa.\nCONCLUSION: These relationships indicate a possible mechanism of action of Casiopeínas on neuroblastoma."}

    GoldHamster

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The amplification of N-myc oncogene (MYCN) and 1p deletion are the main molecular alterations. These features are what make treatment impossible, especially in high-risk patients with metastases.\nMATERIALS AND METHODS: Our study investigated the processes undergone by CHP-212 neuroblastoma cells, after being treated with Casiopeínas® (Cas) IIgly, IIIEa, and IIIia for 2, 10, and 24 h.\nRESULTS: At 2 h, all the treatments Ied to apoptosis [defined by the presence of B-cell lymphoma 2 (BCL2), BCL2-associated X protein, cytochrome c, and caspase-3]. In addition, autophagy with specific molecules beclin-1 and microtubule-associated protein 1A/1B-light chain 3 (LC3)-II/LC3-I (ratio \u003e1). Later at 10 h, autophagy-associated proteins were observed, and at 24 h, only survival proteins nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB), and extracellular signal-regulated kinases (ERK)2/ERK1\u003e1 were found. 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