Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC.

Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC. Research Abstract Details 

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Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC. Abstract Text:

Andrei Goga,Dun Yang,Aaron D Tward,David O Morgan,J Michael Bishop,

Tumor cells have a dysregulated cell cycle that may render their proliferation especially sensitive to the inhibition of cyclin-dependent kinases (CDKs), important regulators of cell cycle progression. We examined the effects of CDK1 inhibition in the context of different oncogenic signals. Cells transformed with MYC, but not cells transformed by a panel of other activated oncogenes, rapidly underwent apoptosis when treated with small-molecule CDK1 inhibitors. The inhibitor of apoptosis protein BIRC5 (survivin), a known CDK1 target, is required for the survival of cells overexpressing MYC. Inhibition of CDK1 rapidly downregulates survivin expression and induces MYC-dependent apoptosis. CDK1 inhibitor treatment of MYC-dependent mouse lymphoma and hepatoblastoma tumors decreased tumor growth and prolonged their survival. As there are no effective small-molecule inhibitors that selectively target the MYC pathway, we propose that CDK1 inhibition might therefore be useful in the treatment of human malignancies that overexpress MYC.

Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC. Publishing Authors By Initials

A Goga,D Yang,AD Tward,DO Morgan,JM Bishop,

For similar proteins: dna-binding proteins: tumor suppressor protein p53 research abstracts see: proteins: dna-binding proteins: tumor suppressor protein p53 research

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Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Nature medicine

VOLUME: 13

Page Numbers: 820-7

Journal Abbreviation: Nat. Med.

ISSN: 1078-8956

DAY: 24

MONTH: 06

YEAR: 2007

Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 9502015

Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC. Keywords Mesh Terms:

KEYWORDS: Tumor Suppressor Protein p53

MESH TERMS: metabolism

Chemical & Substance for Abstract: Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC. Information

Substance Name: CDC2 Protein Kinase

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC.

AFFILIATION: Department of Medicine, Division of Hematology/Oncology, University of California, San Francisco, San Francisco, California 94143-0552, USA. andrei.goga@ucsf.edu

Country: United States

AGENCY: United States NIGMS

GRANT: R01 GM69901

ACRONYM: GM

MEDLINETA: Nat Med

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