Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia

Elise Chapiro; Lisa Russell; Isabelle Radford-Weiss; Christian Bastard; Michel Lessard; Stephanie Struski; Helene Cave; Sandra Fert-Ferrer; Carole Barin; Odile Maarek; Veronique Della-Valle; Jonathan C. Strefford; Roland Berger; Christine J. Harrison; Olivier A. Bernard; Florence Nguyen-Khac

doi:10.1182/blood-2006-03-010835

Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia

Elise Chapiro, Lisa Russell, Isabelle Radford-Weiss, Christian Bastard, Michel Lessard, Stephanie Struski, Helene Cave, Sandra Fert-Ferrer, Carole Barin, Odile Maarek, Veronique Della-Valle, Jonathan C. Strefford, Roland Berger, Christine J. Harrison, Olivier A. Bernard, Florence Nguyen-Khac

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Abstract

Subtle variation in the expression or function of a small group of transcription factors can drive leukemogenesis. The CEBPA protein is known to regulate the balance between cell proliferation and differentiation during early hematopoietic development and myeloid differentiation. In human myeloid leukemia, CEBPA is frequently inactivated by mutation and indirect and posttranslational mechanisms, in keeping with tumor suppressor properties. We report that CEBPA is activated by juxtaposition to the immunoglobulin gene enhancer upon its rearrangement with the immunoglobulin heavy-chain locus in precursor B-cell acute lymphoblastic leukemia harboring t(14;19)(q32;q13). Overexpression of apparently normal CEBPA RNA or protein was observed in 6 patients. These data indicate that CEBPA may exhibit oncogenic as well as tumor suppressor properties in human leukemogenesis.

Original language	English
Pages (from-to)	3560-3563
Number of pages	4
Journal	Blood
Volume	108
Issue number	10
DOIs	https://doi.org/10.1182/blood-2006-03-010835
Publication status	Published - 15 Nov 2006

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Chapiro, E., Russell, L., Radford-Weiss, I., Bastard, C., Lessard, M., Struski, S., Cave, H., Fert-Ferrer, S., Barin, C., Maarek, O., Della-Valle, V., Strefford, J. C., Berger, R., Harrison, C. J., Bernard, O. A., & Nguyen-Khac, F. (2006). Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia. Blood, 108(10), 3560-3563. https://doi.org/10.1182/blood-2006-03-010835

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title = "Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia",

abstract = "Subtle variation in the expression or function of a small group of transcription factors can drive leukemogenesis. The CEBPA protein is known to regulate the balance between cell proliferation and differentiation during early hematopoietic development and myeloid differentiation. In human myeloid leukemia, CEBPA is frequently inactivated by mutation and indirect and posttranslational mechanisms, in keeping with tumor suppressor properties. We report that CEBPA is activated by juxtaposition to the immunoglobulin gene enhancer upon its rearrangement with the immunoglobulin heavy-chain locus in precursor B-cell acute lymphoblastic leukemia harboring t(14;19)(q32;q13). Overexpression of apparently normal CEBPA RNA or protein was observed in 6 patients. These data indicate that CEBPA may exhibit oncogenic as well as tumor suppressor properties in human leukemogenesis.",

author = "Elise Chapiro and Lisa Russell and Isabelle Radford-Weiss and Christian Bastard and Michel Lessard and Stephanie Struski and Helene Cave and Sandra Fert-Ferrer and Carole Barin and Odile Maarek and Veronique Della-Valle and Strefford, {Jonathan C.} and Roland Berger and Harrison, {Christine J.} and Bernard, {Olivier A.} and Florence Nguyen-Khac",

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doi = "10.1182/blood-2006-03-010835",

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Chapiro, E, Russell, L, Radford-Weiss, I, Bastard, C, Lessard, M, Struski, S, Cave, H, Fert-Ferrer, S, Barin, C, Maarek, O, Della-Valle, V, Strefford, JC, Berger, R, Harrison, CJ, Bernard, OA & Nguyen-Khac, F 2006, 'Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia', Blood, vol. 108, no. 10, pp. 3560-3563. https://doi.org/10.1182/blood-2006-03-010835

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T1 - Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia

AU - Chapiro, Elise

AU - Russell, Lisa

AU - Radford-Weiss, Isabelle

AU - Bastard, Christian

AU - Lessard, Michel

AU - Struski, Stephanie

AU - Cave, Helene

AU - Fert-Ferrer, Sandra

AU - Barin, Carole

AU - Maarek, Odile

AU - Della-Valle, Veronique

AU - Strefford, Jonathan C.

AU - Berger, Roland

AU - Harrison, Christine J.

AU - Bernard, Olivier A.

AU - Nguyen-Khac, Florence

PY - 2006/11/15

Y1 - 2006/11/15

N2 - Subtle variation in the expression or function of a small group of transcription factors can drive leukemogenesis. The CEBPA protein is known to regulate the balance between cell proliferation and differentiation during early hematopoietic development and myeloid differentiation. In human myeloid leukemia, CEBPA is frequently inactivated by mutation and indirect and posttranslational mechanisms, in keeping with tumor suppressor properties. We report that CEBPA is activated by juxtaposition to the immunoglobulin gene enhancer upon its rearrangement with the immunoglobulin heavy-chain locus in precursor B-cell acute lymphoblastic leukemia harboring t(14;19)(q32;q13). Overexpression of apparently normal CEBPA RNA or protein was observed in 6 patients. These data indicate that CEBPA may exhibit oncogenic as well as tumor suppressor properties in human leukemogenesis.

AB - Subtle variation in the expression or function of a small group of transcription factors can drive leukemogenesis. The CEBPA protein is known to regulate the balance between cell proliferation and differentiation during early hematopoietic development and myeloid differentiation. In human myeloid leukemia, CEBPA is frequently inactivated by mutation and indirect and posttranslational mechanisms, in keeping with tumor suppressor properties. We report that CEBPA is activated by juxtaposition to the immunoglobulin gene enhancer upon its rearrangement with the immunoglobulin heavy-chain locus in precursor B-cell acute lymphoblastic leukemia harboring t(14;19)(q32;q13). Overexpression of apparently normal CEBPA RNA or protein was observed in 6 patients. These data indicate that CEBPA may exhibit oncogenic as well as tumor suppressor properties in human leukemogenesis.

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U2 - 10.1182/blood-2006-03-010835

DO - 10.1182/blood-2006-03-010835

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AN - SCOPUS:33751196596

SN - 0006-4971

VL - 108

SP - 3560

EP - 3563

JO - Blood

JF - Blood

IS - 10

ER -

Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia

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