Glycogen synthase kinase−3β inhibitors suppress leukemia cell growth

Song, Emma; Palladinetti, Patricia; Klamer, Guy; Ko, Kap-Hyoun; Lindeman, Robert; O’Brien, Tracey; Dolnikov, Alla

doi:10.1016/j.exphem.2010.06.001

Cited by 38 publications

(31 citation statements)

References 36 publications

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“…GSK-3β has been reported as a candidate target in leukemia and other malignancies (13)(14)(15)(16)(17)(18). In this manuscript, we report a role for GSK-3α in human AML.…”

Section: Introductionmentioning

confidence: 73%

The intersection of genetic and chemical genomic screens identifies GSK-3α as a target in human acute myeloid leukemia

Banerji¹,

Frumm²,

Ross³

et al. 2012

J. Clin. Invest.

102

112

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Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long-term survival of patients with AML has changed little over the past decade, necessitating the identification and validation of new AML targets. Integration of genomic approaches with small-molecule and genetically based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. Here, we identified a role for glycogen synthase kinase 3α (GSK-3α) in AML by performing 2 independent small-molecule library screens and an shRNA screen for perturbations that induced a differentiation expression signature in AML cells. GSK-3 is a serine-threonine kinase involved in diverse cellular processes, including differentiation, signal transduction, cell cycle regulation, and proliferation. We demonstrated that specific loss of GSK-3α induced differentiation in AML by multiple measurements, including induction of gene expression signatures, morphological changes, and cell surface markers consistent with myeloid maturation. GSK-3α-specific suppression also led to impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in methylcellulose, and anti-AML activity in vivo. Although the role of GSK-3β has been well studied in cancer development, these studies support a role for GSK-3α in AML.

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“…GSK-3β has been reported as a candidate target in leukemia and other malignancies (13)(14)(15)(16)(17)(18). In this manuscript, we report a role for GSK-3α in human AML.…”

Section: Introductionmentioning

confidence: 73%

The intersection of genetic and chemical genomic screens identifies GSK-3α as a target in human acute myeloid leukemia

Banerji¹,

Frumm²,

Ross³

et al. 2012

J. Clin. Invest.

102

112

View full text Add to dashboard Cite

show abstract

“…to protect leukaemia cells from apoptosis mediated by chemotherapeutic drugs [25,26]. Here we explored whether BM stroma may provide the protection from CART-cell-mediated cytolysis.…”

Section: Bone Marrow Stroma Protects Leukaemia Cells From Cart-cell Cmentioning

confidence: 99%

Antileukemic potency of CD19-specific T cells against chemoresistant pediatric acute lymphoblastic leukemia

Dolnikov

Shen

Klamer

et al. 2015

Experimental Hematology

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“…3). This study also provided the first validation that BIO could be an effective anti-cancer agent in vivo and was confirmed in a mouse model of acute myeloid leukemia (AML), in which BIO treatment induced AML cell apoptosis and prevented host engraftment (Song et al 2010).…”

Section: Bio Reversinementioning

confidence: 81%

Some leopards can change their spots: potential repositioning of stem cell reprogramming compounds as anti-cancer agents

et al. 2016

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Glycogen synthase kinase−3β inhibitors suppress leukemia cell growth

Cited by 38 publications

References 36 publications

The intersection of genetic and chemical genomic screens identifies GSK-3α as a target in human acute myeloid leukemia

The intersection of genetic and chemical genomic screens identifies GSK-3α as a target in human acute myeloid leukemia

Antileukemic potency of CD19-specific T cells against chemoresistant pediatric acute lymphoblastic leukemia

Some leopards can change their spots: potential repositioning of stem cell reprogramming compounds as anti-cancer agents

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