AMG 900, an aurora kinases inhibitor, enhances the chemosensitivity to topoisomerase II inhibitors and modulates gene expression in H295A adrenocortical tumor cell line (2014)
- Authors:
- USP affiliated authors: SCRIDELI, CARLOS ALBERTO - FMRP ; TONE, LUIZ GONZAGA - FMRP ; ANTONINI, SONIR ROBERTO RAUBER - FMRP ; MARTINELLI JUNIOR, CARLOS EDUARDO - FMRP ; CASTRO, MARGARET DE - FMRP
- Unidade: FMRP
- Subjects: NEOPLASIAS DO CÓRTEX SUPRARRENAL; INIBIDORES DE ENZIMAS
- Language: Inglês
- Imprenta:
- Source:
- Título: Pediatric Blood and Cancer
- ISSN: 1545-5009
- Volume/Número/Paginação/Ano: v. 61, suppl. 2, p. S371, res. EP-532, 2014
- Conference titles: Congress of the International Society of Paediatric Oncology (SIOP)
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ABNT
SCRIDELI, Carlos Alberto et al. AMG 900, an aurora kinases inhibitor, enhances the chemosensitivity to topoisomerase II inhibitors and modulates gene expression in H295A adrenocortical tumor cell line. Pediatric Blood and Cancer. Hoboken: Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo. . Acesso em: 22 fev. 2026. , 2014 -
APA
Scrideli, C. A., Borges, K. S., Andrade, A. F., Silveira, V. S., Antonio, D. A. M., Vasconcelos, E. J. R., et al. (2014). AMG 900, an aurora kinases inhibitor, enhances the chemosensitivity to topoisomerase II inhibitors and modulates gene expression in H295A adrenocortical tumor cell line. Pediatric Blood and Cancer. Hoboken: Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo. -
NLM
Scrideli CA, Borges KS, Andrade AF, Silveira VS, Antonio DAM, Vasconcelos EJR, Antonini SRR, Martinelli Junior CE, Castro M de, Tone LG. AMG 900, an aurora kinases inhibitor, enhances the chemosensitivity to topoisomerase II inhibitors and modulates gene expression in H295A adrenocortical tumor cell line. Pediatric Blood and Cancer. 2014 ; 61 S371.[citado 2026 fev. 22 ] -
Vancouver
Scrideli CA, Borges KS, Andrade AF, Silveira VS, Antonio DAM, Vasconcelos EJR, Antonini SRR, Martinelli Junior CE, Castro M de, Tone LG. AMG 900, an aurora kinases inhibitor, enhances the chemosensitivity to topoisomerase II inhibitors and modulates gene expression in H295A adrenocortical tumor cell line. Pediatric Blood and Cancer. 2014 ; 61 S371.[citado 2026 fev. 22 ] - WNT/beta-catenin pathway dysregulation in childhood adrenocortical tumors harboring the R337H p53 mutation
- Differential microRNAs expressions are associated with relapse and TP53 P.R377H mutation in pediatrics adrenocortical tumors
- High expression of miR-449 in childhood adrenocortical tumors seems to be due to a post-transcriptional event embedded in a tumor suppressive program governed by p53
- Overexpression of MIR‐483‐3P and MIR‐149‐3P is associated with clinical characteristics of pediatric adrenocortical tumors
- R337H P53 mutation and the expression of microRNAs in adrenocortical tumor
- Discriminating pediatric non-neoplastic adrenal tissue, metastatic and non-metastatic pediatric adrenocortical tumors by miRNA signatures
- Abnormal activation of the WNT/B-catenin pathway in childhood adrenocortical tumors is independent of CTNNB1 mutations
- Overexpression of BCL2 and TNFA genes is associated with less aggressive disease in childhood adrenocortical tumors (ACT)
- Wnt/β-catenin pathway deregulation in childhood adrenocortical tumors
- Spindle checkpoint genes expression in childhood adrenocortical tumors (ACT): aurkb is associated with metastatic disease and poor survival
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