NT157, an IGF1R-IRS1/2 inhibitor, exhibits antineoplastic effects in pre-clinical models of chronic myeloid leukemia (2021)
- Authors:
- Ribeiro, Renata Scopim
- Machado Neto, João Agostinho
- Eide, Christopher A.
- Silva, Juan Luiz Coelho da
- Fenerich, Bruna Alves
- Fernandes, Jaqueline Cristina
- Scheucher, Priscila Santos
- Stevens, Samantha L. Savage
- Campos, Paula de Melo
- Saad, Sara T. Olalla
- Palma, Leonardo de Carvalho
- Pontes, Lorena Lobo de Figueiredo
- Simões, Belinda Pinto
- Rego, Eduardo Magalhães
- Tognon, Cristina E.
- Druker, Brian J.
- Traina, Fabiola
- USP affiliated authors: MACHADO NETO, JOÃO AGOSTINHO - ICB ; SCHEUCHER, PRISCILA SANTOS - FMRP ; PONTES, LORENA LÔBO DE FIGUEIREDO - FMRP ; SIMOES, BELINDA PINTO - FMRP ; REGO, EDUARDO MAGALHÃES - FM ; TRAINA, FABÍOLA - FMRP ; SILVA, JUAN LUIZ COELHO DA - FMRP ; FENERICH, BRUNA ALVES - FMRP ; FERNANDES, JAQUELINE CRISTINA - FMRP
- Unidades: ICB; FMRP; FM
- DOI: 10.1007/s10637-020-01028-8
- Subjects: FARMACOLOGIA; LEUCEMIA MIELOIDE; INSULINA; ANTINEOPLÁSICOS; PROTEÍNAS QUINASES; CÉLULAS SANGUÍNEAS; PROLIFERAÇÃO CELULAR; APOPTOSE; ONCOGENES
- Agências de fomento:
- Language: Inglês
- Imprenta:
- Source:
- Título: Investigational New Drugs
- ISSN: 1573-0646
- Volume/Número/Paginação/Ano: v. 39, n. 3, p. 736-746, 2021
- Este periódico é de assinatura
- Este artigo NÃO é de acesso aberto
- Cor do Acesso Aberto: closed
-
ABNT
RIBEIRO, Renata Scopim et al. NT157, an IGF1R-IRS1/2 inhibitor, exhibits antineoplastic effects in pre-clinical models of chronic myeloid leukemia. Investigational New Drugs, v. 39, n. 3, p. 736-746, 2021Tradução . . Disponível em: https://doi.org/10.1007/s10637-020-01028-8. Acesso em: 11 nov. 2024. -
APA
Ribeiro, R. S., Machado Neto, J. A., Eide, C. A., Silva, J. L. C. da, Fenerich, B. A., Fernandes, J. C., et al. (2021). NT157, an IGF1R-IRS1/2 inhibitor, exhibits antineoplastic effects in pre-clinical models of chronic myeloid leukemia. Investigational New Drugs, 39( 3), 736-746. doi:10.1007/s10637-020-01028-8 -
NLM
Ribeiro RS, Machado Neto JA, Eide CA, Silva JLC da, Fenerich BA, Fernandes JC, Scheucher PS, Stevens SLS, Campos P de M, Saad STO, Palma L de C, Pontes LL de F, Simões BP, Rego EM, Tognon CE, Druker BJ, Traina F. NT157, an IGF1R-IRS1/2 inhibitor, exhibits antineoplastic effects in pre-clinical models of chronic myeloid leukemia [Internet]. Investigational New Drugs. 2021 ; 39( 3): 736-746.[citado 2024 nov. 11 ] Available from: https://doi.org/10.1007/s10637-020-01028-8 -
Vancouver
Ribeiro RS, Machado Neto JA, Eide CA, Silva JLC da, Fenerich BA, Fernandes JC, Scheucher PS, Stevens SLS, Campos P de M, Saad STO, Palma L de C, Pontes LL de F, Simões BP, Rego EM, Tognon CE, Druker BJ, Traina F. NT157, an IGF1R-IRS1/2 inhibitor, exhibits antineoplastic effects in pre-clinical models of chronic myeloid leukemia [Internet]. Investigational New Drugs. 2021 ; 39( 3): 736-746.[citado 2024 nov. 11 ] Available from: https://doi.org/10.1007/s10637-020-01028-8 - IGF1R/IRS1 targeting has cytotoxic activity and inhibits PI3K/AKT/mTOR and MAPK signaling in acute lymphoblastic leukemia cells
- Differential cytotoxic activity of pharmacological inhibitors of IGF1R-related pathways in JAK2(V617F) driven cells
- NT157 has antineoplastic effects and inhibits IRS1/2 and STAT3/5 in JAK2V617F-positive myeloproliferative neoplasm cells
- Paclitaxel induces Stathmin 1 phosphorylation, microtubule stability and apoptosis in acute lymphoblastic leukemia cells
- Autophagy inhibition potentiates ruxolitinib-induced apoptosis in JAK2V617F cells
- Differential cytotoxic activity of pharmacological inhibitors of IGF1R-related pathways in JAK2V617F driven cells
- A inibição farmacológica de IRS1/2 induz apoptose em células BCR-ABL1 T315I
- IGF signaling predicts outcomes and is a promising target therapy for acute myeloid leukemia
- A ativação da via IGF1R prediz prognóstico e representa uma estratégia terapêutica em leucemia mieloide aguda
- Metformin reduces tumor burden and splenomegaly in JAK2V617F murine models
Informações sobre o DOI: 10.1007/s10637-020-01028-8 (Fonte: oaDOI API)
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