Sorafenib for refractory FMS-like tyrosine kinase receptor-3 (FLT3/ITD+) acute myeloid leukemia after allogenic stem cell transplantation.

Federica Sora'; Patrizia Chiusolo; Elisabetta Metafuni; Silvia Bellesi; Sabrina Giammarco; Luca Laurenti; Giuseppe Ausoni; Gina Zini Tanzi; Jolanta Alina Bajer; Mario Balducci; Giuseppe Leone; Simona Sica

doi:10.1016/j.leukres.2010.10.025

Sorafenib for refractory FMS-like tyrosine kinase receptor-3 (FLT3/ITD+) acute myeloid leukemia after allogenic stem cell transplantation.

Federica Sora', Patrizia Chiusolo, Elisabetta Metafuni, Silvia Bellesi, Sabrina Giammarco, Luca Laurenti, Giuseppe Ausoni, Gina Zini Tanzi, Jolanta Alina Bajer, Mario Balducci, Giuseppe Leone, Simona Sica

Risultato della ricerca: Contributo in rivista › Articolo in rivista

Abstract

Mutations of FLT3 in AML is an entity characterized by a significant poor prognosis and are described in about 30% of AML in adults. Usually patients with this subtype of AML carrying either internal tandem duplication (ITD) or mutation at codon 835 are referred for allogeneic stem cell transplantation (ASCT) but a proportion of them would eventually relapse. The introduction of targeted therapy against FLT3 + AML is yielding conflicting results and many trials are running with new molecules. We used sorafenib, a multi-targeted tyrosine kinase inhibitor FDA approved for the treatment of advanced renal cell and hepatocellular carcinoma, on a compassionate basis in two patients with FLT3 + AML relapsing after ASCT.

Lingua originale	English
pagine (da-a)	422-423
Numero di pagine	2
Rivista	Leukemia Research
Volume	35
DOI	https://doi.org/10.1016/j.leukres.2010.10.025
Stato di pubblicazione	Pubblicato - 2011

Keywords

sorafenib

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10.1016/j.leukres.2010.10.025

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Sora', F., Chiusolo, P., Metafuni, E., Bellesi, S., Giammarco, S., Laurenti, L., Ausoni, G., Zini Tanzi, G., Bajer, J. A., Balducci, M., Leone, G., & Sica, S. (2011). Sorafenib for refractory FMS-like tyrosine kinase receptor-3 (FLT3/ITD+) acute myeloid leukemia after allogenic stem cell transplantation. Leukemia Research, 35, 422-423. https://doi.org/10.1016/j.leukres.2010.10.025

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title = "Sorafenib for refractory FMS-like tyrosine kinase receptor-3 (FLT3/ITD+) acute myeloid leukemia after allogenic stem cell transplantation.",

abstract = "Mutations of FLT3 in AML is an entity characterized by a significant poor prognosis and are described in about 30% of AML in adults. Usually patients with this subtype of AML carrying either internal tandem duplication (ITD) or mutation at codon 835 are referred for allogeneic stem cell transplantation (ASCT) but a proportion of them would eventually relapse. The introduction of targeted therapy against FLT3 + AML is yielding conflicting results and many trials are running with new molecules. We used sorafenib, a multi-targeted tyrosine kinase inhibitor FDA approved for the treatment of advanced renal cell and hepatocellular carcinoma, on a compassionate basis in two patients with FLT3 + AML relapsing after ASCT.",

keywords = "sorafenib, sorafenib",

author = "Federica Sora' and Patrizia Chiusolo and Elisabetta Metafuni and Silvia Bellesi and Sabrina Giammarco and Luca Laurenti and Giuseppe Ausoni and {Zini Tanzi}, Gina and Bajer, {Jolanta Alina} and Mario Balducci and Giuseppe Leone and Simona Sica",

year = "2011",

doi = "10.1016/j.leukres.2010.10.025",

language = "English",

volume = "35",

pages = "422--423",

journal = "Leukemia Research",

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Sora', F , Chiusolo, P, Metafuni, E, Bellesi, S, Giammarco, S, Laurenti, L, Ausoni, G, Zini Tanzi, G, Bajer, JA, Balducci, M, Leone, G & Sica, S 2011, 'Sorafenib for refractory FMS-like tyrosine kinase receptor-3 (FLT3/ITD+) acute myeloid leukemia after allogenic stem cell transplantation.', Leukemia Research, vol. 35, pagg. 422-423. https://doi.org/10.1016/j.leukres.2010.10.025

TY - JOUR

T1 - Sorafenib for refractory FMS-like tyrosine kinase receptor-3 (FLT3/ITD+) acute myeloid leukemia after allogenic stem cell transplantation.

AU - Sora', Federica

AU - Chiusolo, Patrizia

AU - Metafuni, Elisabetta

AU - Bellesi, Silvia

AU - Giammarco, Sabrina

AU - Laurenti, Luca

AU - Ausoni, Giuseppe

AU - Zini Tanzi, Gina

AU - Bajer, Jolanta Alina

AU - Balducci, Mario

AU - Leone, Giuseppe

AU - Sica, Simona

PY - 2011

Y1 - 2011

N2 - Mutations of FLT3 in AML is an entity characterized by a significant poor prognosis and are described in about 30% of AML in adults. Usually patients with this subtype of AML carrying either internal tandem duplication (ITD) or mutation at codon 835 are referred for allogeneic stem cell transplantation (ASCT) but a proportion of them would eventually relapse. The introduction of targeted therapy against FLT3 + AML is yielding conflicting results and many trials are running with new molecules. We used sorafenib, a multi-targeted tyrosine kinase inhibitor FDA approved for the treatment of advanced renal cell and hepatocellular carcinoma, on a compassionate basis in two patients with FLT3 + AML relapsing after ASCT.

AB - Mutations of FLT3 in AML is an entity characterized by a significant poor prognosis and are described in about 30% of AML in adults. Usually patients with this subtype of AML carrying either internal tandem duplication (ITD) or mutation at codon 835 are referred for allogeneic stem cell transplantation (ASCT) but a proportion of them would eventually relapse. The introduction of targeted therapy against FLT3 + AML is yielding conflicting results and many trials are running with new molecules. We used sorafenib, a multi-targeted tyrosine kinase inhibitor FDA approved for the treatment of advanced renal cell and hepatocellular carcinoma, on a compassionate basis in two patients with FLT3 + AML relapsing after ASCT.

KW - sorafenib

UR - http://hdl.handle.net/10807/62678

U2 - 10.1016/j.leukres.2010.10.025

DO - 10.1016/j.leukres.2010.10.025

M3 - Article

SN - 0145-2126

VL - 35

SP - 422

EP - 423

JO - Leukemia Research

JF - Leukemia Research

ER -

Sorafenib for refractory FMS-like tyrosine kinase receptor-3 (FLT3/ITD+) acute myeloid leukemia after allogenic stem cell transplantation.

Abstract

Keywords

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