12-O-Tetradecanoylphorbol-13-acetate (TPA)-induced dual-specificity phosphatase expression and AML cell survival

Dale G. Schaar; Hao Liu; Shashi Sharma; Yi Ting; John Martin; Curtis Krier; Marie Ciardella; Mona Osman; Lauri Goodell; Daniel A. Notterman; Roger K. Strair

doi:10.1016/j.leukres.2005.02.019

12-O-Tetradecanoylphorbol-13-acetate (TPA)-induced dual-specificity phosphatase expression and AML cell survival

Dale G. Schaar, Hao Liu, Shashi Sharma, Yi Ting, John Martin, Curtis Krier, Marie Ciardella, Mona Osman, Lauri Goodell, Daniel A. Notterman, Roger K. Strair

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

14 Scopus citations

Abstract

12-O-Tetradecanoylphorbol-13-acetate (TPA) is being developed as a therapeutic agent by virtue of its being a potent modulator of signal transduction in pre-clinical models of AML [Strair RK, Schaar D, Goodell L, Aisner J, Chin KV, Eid J, et al. Administration of a phorbol ester to patients with hematological malignancies: preliminary results from a phase I clinical trial of 12-O-tetradecanoylphorbol-13-acetate. Clin Cancer Res 2002;8:2512-8]. In this report, we identify a subset of primary AML samples that undergoes apoptosis after exposure to TPA and demonstrate that TPA-induced cytotoxicity is associated with modulation of the ERK signaling pathway. Analysis of mitogen-activated protein kinase (MAPK) dual-specificity phosphatases (DUSP), as potential regulators of AML cell signaling, indicates that these genes are coordinately regulated and rapidly induced by TPA in primary AML cells. Therefore, TPA-induced primary AML cytotoxicity is associated with modulation of ERK signaling which may be partially mediated by regulation of phosphatase expression.

Original language	English (US)
Pages (from-to)	1171-1179
Number of pages	9
Journal	Leukemia Research
Volume	29
Issue number	10
DOIs	https://doi.org/10.1016/j.leukres.2005.02.019
State	Published - Oct 2005
Externally published	Yes

All Science Journal Classification (ASJC) codes

Hematology
Oncology
Cancer Research

Keywords

12-O-Tetradecanoylphorbol-13-acetate
Acute myelogenous leukemia
Apoptosis
Differentiation
Gene expression
MAPK dual-specificity phosphatases (DUSP)
Mitogen-activated protein kinase (MAPK)

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10.1016/j.leukres.2005.02.019

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@article{bd286f4d6314498297026bdd034f2ce0,

title = "12-O-Tetradecanoylphorbol-13-acetate (TPA)-induced dual-specificity phosphatase expression and AML cell survival",

abstract = "12-O-Tetradecanoylphorbol-13-acetate (TPA) is being developed as a therapeutic agent by virtue of its being a potent modulator of signal transduction in pre-clinical models of AML [Strair RK, Schaar D, Goodell L, Aisner J, Chin KV, Eid J, et al. Administration of a phorbol ester to patients with hematological malignancies: preliminary results from a phase I clinical trial of 12-O-tetradecanoylphorbol-13-acetate. Clin Cancer Res 2002;8:2512-8]. In this report, we identify a subset of primary AML samples that undergoes apoptosis after exposure to TPA and demonstrate that TPA-induced cytotoxicity is associated with modulation of the ERK signaling pathway. Analysis of mitogen-activated protein kinase (MAPK) dual-specificity phosphatases (DUSP), as potential regulators of AML cell signaling, indicates that these genes are coordinately regulated and rapidly induced by TPA in primary AML cells. Therefore, TPA-induced primary AML cytotoxicity is associated with modulation of ERK signaling which may be partially mediated by regulation of phosphatase expression.",

keywords = "12-O-Tetradecanoylphorbol-13-acetate, Acute myelogenous leukemia, Apoptosis, Differentiation, Gene expression, MAPK dual-specificity phosphatases (DUSP), Mitogen-activated protein kinase (MAPK)",

author = "Schaar, \{Dale G.\} and Hao Liu and Shashi Sharma and Yi Ting and John Martin and Curtis Krier and Marie Ciardella and Mona Osman and Lauri Goodell and Notterman, \{Daniel A.\} and Strair, \{Roger K.\}",

note = "Funding Information: This work was supported by grants from the National Cancer Institute and The Leukemia and Lymphoma Society to R.K.S. and from the Foundation of UMDNJ and The Ruth Estrin Goldberg Memorial for Cancer Research to D.G.S. ",

year = "2005",

month = oct,

doi = "10.1016/j.leukres.2005.02.019",

language = "English (US)",

volume = "29",

pages = "1171--1179",

journal = "Leukemia Research",

issn = "0145-2126",

publisher = "Elsevier Ltd",

number = "10",

}

TY - JOUR

T1 - 12-O-Tetradecanoylphorbol-13-acetate (TPA)-induced dual-specificity phosphatase expression and AML cell survival

AU - Schaar, Dale G.

AU - Liu, Hao

AU - Sharma, Shashi

AU - Ting, Yi

AU - Martin, John

AU - Krier, Curtis

AU - Ciardella, Marie

AU - Osman, Mona

AU - Goodell, Lauri

AU - Notterman, Daniel A.

AU - Strair, Roger K.

N1 - Funding Information: This work was supported by grants from the National Cancer Institute and The Leukemia and Lymphoma Society to R.K.S. and from the Foundation of UMDNJ and The Ruth Estrin Goldberg Memorial for Cancer Research to D.G.S.

PY - 2005/10

Y1 - 2005/10

N2 - 12-O-Tetradecanoylphorbol-13-acetate (TPA) is being developed as a therapeutic agent by virtue of its being a potent modulator of signal transduction in pre-clinical models of AML [Strair RK, Schaar D, Goodell L, Aisner J, Chin KV, Eid J, et al. Administration of a phorbol ester to patients with hematological malignancies: preliminary results from a phase I clinical trial of 12-O-tetradecanoylphorbol-13-acetate. Clin Cancer Res 2002;8:2512-8]. In this report, we identify a subset of primary AML samples that undergoes apoptosis after exposure to TPA and demonstrate that TPA-induced cytotoxicity is associated with modulation of the ERK signaling pathway. Analysis of mitogen-activated protein kinase (MAPK) dual-specificity phosphatases (DUSP), as potential regulators of AML cell signaling, indicates that these genes are coordinately regulated and rapidly induced by TPA in primary AML cells. Therefore, TPA-induced primary AML cytotoxicity is associated with modulation of ERK signaling which may be partially mediated by regulation of phosphatase expression.

AB - 12-O-Tetradecanoylphorbol-13-acetate (TPA) is being developed as a therapeutic agent by virtue of its being a potent modulator of signal transduction in pre-clinical models of AML [Strair RK, Schaar D, Goodell L, Aisner J, Chin KV, Eid J, et al. Administration of a phorbol ester to patients with hematological malignancies: preliminary results from a phase I clinical trial of 12-O-tetradecanoylphorbol-13-acetate. Clin Cancer Res 2002;8:2512-8]. In this report, we identify a subset of primary AML samples that undergoes apoptosis after exposure to TPA and demonstrate that TPA-induced cytotoxicity is associated with modulation of the ERK signaling pathway. Analysis of mitogen-activated protein kinase (MAPK) dual-specificity phosphatases (DUSP), as potential regulators of AML cell signaling, indicates that these genes are coordinately regulated and rapidly induced by TPA in primary AML cells. Therefore, TPA-induced primary AML cytotoxicity is associated with modulation of ERK signaling which may be partially mediated by regulation of phosphatase expression.

KW - 12-O-Tetradecanoylphorbol-13-acetate

KW - Acute myelogenous leukemia

KW - Apoptosis

KW - Differentiation

KW - Gene expression

KW - MAPK dual-specificity phosphatases (DUSP)

KW - Mitogen-activated protein kinase (MAPK)

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DO - 10.1016/j.leukres.2005.02.019

M3 - Article

C2 - 16111535

AN - SCOPUS:23844554128

SN - 0145-2126

VL - 29

SP - 1171

EP - 1179

JO - Leukemia Research

JF - Leukemia Research

IS - 10

ER -

12-O-Tetradecanoylphorbol-13-acetate (TPA)-induced dual-specificity phosphatase expression and AML cell survival

Abstract

All Science Journal Classification (ASJC) codes

Keywords

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