Book contents
- Frontmatter
- Dedication
- Contents
- List of Contributors
- Preface
- Part 1.1 Analytical techniques: analysis of DNA
- Part 1.2 Analytical techniques: analysis of RNA
- Part 2.1 Molecular pathways underlying carcinogenesis: signal transduction
- 10 HER
- 11 The insulin–insulin-like growth-factor receptor family as a therapeutic target in oncology
- 12 TGF-β signaling in stem cells and tumorigenesis
- 13 Platelet-derived growth factor
- 14 FMS-related tyrosine kinase 3
- 15 ALK: Anaplastic lymphoma kinase
- 16 The FGF signaling axis in prostate tumorigenesis
- 17 Hepatocyte growth factor/Met signaling in cancer
- 18 PI3K
- 19 Intra-cellular tyrosine kinase
- 20 WNT signaling in neoplasia
- 21 Ras
- 22 BRAF mutations in human cancer: biologic and therapeutic implications
- 23 Aurora kinases in cancer: an opportunity for targeted therapy
- 24 14-3-3 proteins in cancer
- 25 STAT signaling as a molecular target for cancer therapy
- 26 The MYC oncogene family in human cancer
- 27 Jun proteins and AP-1 in tumorigenesis
- 28 Forkhead box proteins: the tuning forks in cancer development and treatment
- 29 NF-κB and cancer
- Part 2.2 Molecular pathways underlying carcinogenesis: apoptosis
- Part 2.3 Molecular pathways underlying carcinogenesis: nuclear receptors
- Part 2.4 Molecular pathways underlying carcinogenesis: DNA repair
- Part 2.5 Molecular pathways underlying carcinogenesis: cell cycle
- Part 2.6 Molecular pathways underlying carcinogenesis: other pathways
- Part 3.1 Molecular pathology: carcinomas
- Part 3.2 Molecular pathology: cancers of the nervous system
- Part 3.3 Molecular pathology: cancers of the skin
- Part 3.4 Molecular pathology: endocrine cancers
- Part 3.5 Molecular pathology: adult sarcomas
- Part 3.6 Molecular pathology: lymphoma and leukemia
- Part 3.7 Molecular pathology: pediatric solid tumors
- Part 4 Pharmacologic targeting of oncogenic pathways
- Index
- References
23 - Aurora kinases in cancer: an opportunity for targeted therapy
from Part 2.1 - Molecular pathways underlying carcinogenesis: signal transduction
Published online by Cambridge University Press: 05 February 2015
- Frontmatter
- Dedication
- Contents
- List of Contributors
- Preface
- Part 1.1 Analytical techniques: analysis of DNA
- Part 1.2 Analytical techniques: analysis of RNA
- Part 2.1 Molecular pathways underlying carcinogenesis: signal transduction
- 10 HER
- 11 The insulin–insulin-like growth-factor receptor family as a therapeutic target in oncology
- 12 TGF-β signaling in stem cells and tumorigenesis
- 13 Platelet-derived growth factor
- 14 FMS-related tyrosine kinase 3
- 15 ALK: Anaplastic lymphoma kinase
- 16 The FGF signaling axis in prostate tumorigenesis
- 17 Hepatocyte growth factor/Met signaling in cancer
- 18 PI3K
- 19 Intra-cellular tyrosine kinase
- 20 WNT signaling in neoplasia
- 21 Ras
- 22 BRAF mutations in human cancer: biologic and therapeutic implications
- 23 Aurora kinases in cancer: an opportunity for targeted therapy
- 24 14-3-3 proteins in cancer
- 25 STAT signaling as a molecular target for cancer therapy
- 26 The MYC oncogene family in human cancer
- 27 Jun proteins and AP-1 in tumorigenesis
- 28 Forkhead box proteins: the tuning forks in cancer development and treatment
- 29 NF-κB and cancer
- Part 2.2 Molecular pathways underlying carcinogenesis: apoptosis
- Part 2.3 Molecular pathways underlying carcinogenesis: nuclear receptors
- Part 2.4 Molecular pathways underlying carcinogenesis: DNA repair
- Part 2.5 Molecular pathways underlying carcinogenesis: cell cycle
- Part 2.6 Molecular pathways underlying carcinogenesis: other pathways
- Part 3.1 Molecular pathology: carcinomas
- Part 3.2 Molecular pathology: cancers of the nervous system
- Part 3.3 Molecular pathology: cancers of the skin
- Part 3.4 Molecular pathology: endocrine cancers
- Part 3.5 Molecular pathology: adult sarcomas
- Part 3.6 Molecular pathology: lymphoma and leukemia
- Part 3.7 Molecular pathology: pediatric solid tumors
- Part 4 Pharmacologic targeting of oncogenic pathways
- Index
- References
Summary
The Aurora kinase (AK) family members, Aurora kinase A (AURKA), Aurora kinase B (AURKB), and Aurora kinase C (AURKC) are a collection of highly related and conserved serine/threonine kinases that regulate key cellular functions, mitosis, and multiple signaling pathways. AK dysfunction can cause aneuploidy, mitotic arrest, and cell death. Several studies have reported amplification and/or over-expression of AURKA and AURKB in various human cancers. Additionally, transgenic mouse model studies have established AURKA as a bona fide oncogene. AURKA over-expression in tumors is often associated with gene amplification, genetic instability, dedifferentiated morphology, and poor prognosis. AURKB over-expression is frequently observed in a variety of tumors along with AURKA. AURKB over-expression has also been correlated with increased genetic instability and poor clinical outcome. The function of AURKC in cancer biology is relatively less studied. Given their association with tumorigenesis, both AURKA and AURKB have been targeted for cancer therapy. Currently, a number of selective and non-selective AK inhibitors are being tested in pre-clinical and clinical settings as anti-tumor agents. This chapter reviews the structure, biology and physiological functions of AKs and is an overview of small-molecule modulators of AKs for targeted cancer therapy.
- Type
- Chapter
- Information
- Molecular OncologyCauses of Cancer and Targets for Treatment, pp. 278 - 292Publisher: Cambridge University PressPrint publication year: 2013