Activating FLT3 mutations in CD117/KIT+ T-cell acute lymphoblastic leukemias

Elisabeth Paietta; Adolfo A. Ferrando; Donna Neuberg; John M. Bennett; Janis Racevskis; Hillard Lazarus; Gordon Dewald; Jacob M. Rowe; Peter H. Wiernik; Martin S. Tallman; A. Thomas Look

doi:10.1182/blood-2004-01-0168

Activating FLT3 mutations in CD117/KIT⁺ T-cell acute lymphoblastic leukemias

Elisabeth Paietta, Adolfo A. Ferrando, Donna Neuberg, John M. Bennett, Janis Racevskis, Hillard Lazarus, Gordon Dewald, Jacob M. Rowe, Peter H. Wiernik, Martin S. Tallman, A. Thomas Look

Research output: Contribution to journal › Article › peer-review

87 Scopus citations

Abstract

Activating FLT3 mutations are the most common genetic aberrations in acute myeloid leukemia (AML), resulting in the constitutive activation of this receptor tyrosine kinase (RTK), but such mutations are rarely found in acute lymphoblastic leukemia (ALL). Here we describe a unique subset of de novo adult T-cell ALL (T-ALL) cases that coexpress CD117/ KIT and cytoplasmic CD3 (CD117/KIT⁺ ALL). Activating mutations in the FLT3 RTK gene were found in each of 3 CD117/ KIT+ cases that were analyzed, but not in 52 other adult T-ALL samples from the same series that lacked CD117/KIT expression. Our results indicate the need for clinical trials to test the efficacy of drugs that inhibit the FLT3 RTK in this subset of patients with T-ALL.

Original language	English (US)
Pages (from-to)	558-560
Number of pages	3
Journal	Blood
Volume	104
Issue number	2
DOIs	https://doi.org/10.1182/blood-2004-01-0168
State	Published - Jul 15 2004
Externally published	Yes

ASJC Scopus subject areas

Biochemistry
Immunology
Hematology
Cell Biology

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10.1182/blood-2004-01-0168

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title = "Activating FLT3 mutations in CD117/KIT+ T-cell acute lymphoblastic leukemias",

abstract = "Activating FLT3 mutations are the most common genetic aberrations in acute myeloid leukemia (AML), resulting in the constitutive activation of this receptor tyrosine kinase (RTK), but such mutations are rarely found in acute lymphoblastic leukemia (ALL). Here we describe a unique subset of de novo adult T-cell ALL (T-ALL) cases that coexpress CD117/ KIT and cytoplasmic CD3 (CD117/KIT+ ALL). Activating mutations in the FLT3 RTK gene were found in each of 3 CD117/ KIT+ cases that were analyzed, but not in 52 other adult T-ALL samples from the same series that lacked CD117/KIT expression. Our results indicate the need for clinical trials to test the efficacy of drugs that inhibit the FLT3 RTK in this subset of patients with T-ALL.",

author = "Elisabeth Paietta and Ferrando, {Adolfo A.} and Donna Neuberg and Bennett, {John M.} and Janis Racevskis and Hillard Lazarus and Gordon Dewald and Rowe, {Jacob M.} and Wiernik, {Peter H.} and Tallman, {Martin S.} and Look, {A. Thomas}",

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doi = "10.1182/blood-2004-01-0168",

language = "English (US)",

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T1 - Activating FLT3 mutations in CD117/KIT+ T-cell acute lymphoblastic leukemias

AU - Paietta, Elisabeth

AU - Ferrando, Adolfo A.

AU - Neuberg, Donna

AU - Bennett, John M.

AU - Racevskis, Janis

AU - Lazarus, Hillard

AU - Dewald, Gordon

AU - Rowe, Jacob M.

AU - Wiernik, Peter H.

AU - Tallman, Martin S.

AU - Look, A. Thomas

PY - 2004/7/15

Y1 - 2004/7/15

N2 - Activating FLT3 mutations are the most common genetic aberrations in acute myeloid leukemia (AML), resulting in the constitutive activation of this receptor tyrosine kinase (RTK), but such mutations are rarely found in acute lymphoblastic leukemia (ALL). Here we describe a unique subset of de novo adult T-cell ALL (T-ALL) cases that coexpress CD117/ KIT and cytoplasmic CD3 (CD117/KIT+ ALL). Activating mutations in the FLT3 RTK gene were found in each of 3 CD117/ KIT+ cases that were analyzed, but not in 52 other adult T-ALL samples from the same series that lacked CD117/KIT expression. Our results indicate the need for clinical trials to test the efficacy of drugs that inhibit the FLT3 RTK in this subset of patients with T-ALL.

AB - Activating FLT3 mutations are the most common genetic aberrations in acute myeloid leukemia (AML), resulting in the constitutive activation of this receptor tyrosine kinase (RTK), but such mutations are rarely found in acute lymphoblastic leukemia (ALL). Here we describe a unique subset of de novo adult T-cell ALL (T-ALL) cases that coexpress CD117/ KIT and cytoplasmic CD3 (CD117/KIT+ ALL). Activating mutations in the FLT3 RTK gene were found in each of 3 CD117/ KIT+ cases that were analyzed, but not in 52 other adult T-ALL samples from the same series that lacked CD117/KIT expression. Our results indicate the need for clinical trials to test the efficacy of drugs that inhibit the FLT3 RTK in this subset of patients with T-ALL.

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Activating FLT3 mutations in CD117/KIT⁺ T-cell acute lymphoblastic leukemias

Abstract

ASJC Scopus subject areas

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