Targeting nuclear kinases in cancer: Development of cell cycle kinase inhibitors

Todd M. Pitts, S. Lindsey Davis, S Gail Eckhardt, Erica L. Bradshaw-Pierce

Research output: Contribution to journalReview article

54 Citations (Scopus)

Abstract

Cellular proliferation is a tightly controlled set of events that is regulated by numerous nuclear protein kinases. The proteins involved include checkpoint kinases (CHK), cyclin-dependent kinases (CDK), which regulate the cell cycle and aurora kinases (AURK) and polo-like kinases (PLK), which regulate mitosis. In cancer, these nuclear kinases are often dysregulated and cause uncontrolled cell proliferation and growth. Much work has gone into developing novel therapeutics that target each of these protein kinases in cancer but none have been approved in patients. In this review we provide an overview of the current compounds being developed clinically to target these nuclear kinases involved in regulating the cell cycle and mitosis.

Original languageEnglish (US)
Pages (from-to)258-269
Number of pages12
JournalPharmacology and Therapeutics
Volume142
Issue number2
DOIs
StatePublished - Jan 1 2014

Fingerprint

Cell Cycle
Phosphotransferases
Mitosis
Protein Kinases
Neoplasms
Aurora Kinases
Cell Proliferation
Cyclin-Dependent Kinases
Nuclear Proteins
Growth
Proteins
Therapeutics

Keywords

  • Cell cycle inhibitors
  • DNA damage response
  • Mitosis inhibitors
  • Nuclear kinase inhibitor

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

Cite this

Targeting nuclear kinases in cancer : Development of cell cycle kinase inhibitors. / Pitts, Todd M.; Davis, S. Lindsey; Eckhardt, S Gail; Bradshaw-Pierce, Erica L.

In: Pharmacology and Therapeutics, Vol. 142, No. 2, 01.01.2014, p. 258-269.

Research output: Contribution to journalReview article

Pitts, Todd M. ; Davis, S. Lindsey ; Eckhardt, S Gail ; Bradshaw-Pierce, Erica L. / Targeting nuclear kinases in cancer : Development of cell cycle kinase inhibitors. In: Pharmacology and Therapeutics. 2014 ; Vol. 142, No. 2. pp. 258-269.
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