Aurora kinases

Subrata Sen, Hiroshi Katayama

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Aurora kinase family of serine/threonine kinases, frequently overexpressed in human cancers and implicated in tumorigenesis, induce chromosomal instability and oncogenic transformation when expressed at elevated levels in mammalian cells in vitro and in vivo. Recent findings on the interactions of Aurora kinases with tumor suppressor gene and oncogene-regulated networks as well as involvement in other nonmitotic processes such as ciliary disassembly affecting important signaling pathways and developmental disorders termed ciliopathies, have led to a greater recognition of the functional significance of these kinases in development and disease. Among the three members of the kinase family, Aurora- A, -B, and -C identified in humans, Aurora-A and -B have been reported to express at detectable levels in most proliferating somatic cells and characterized in detail for their involvement in cellular pathways relevant to cell proliferation and development of cancer-associated phenotypes. As a result, Aurora-A and -B are being investigated as potential targets for cancer therapy and multiple agents targeting the kinases are in early phase clinical trials with some having yielded encouraging results. This chapter discusses functional involvement of Aurora kinase-A and -B in the regulation of cell proliferation and cancer-relevant cellular pathways validating their significance as cancer therapeutic targets.

Original languageEnglish
Title of host publicationTargeted Therapy of Acute Myeloid Leukemi
PublisherSpringer New York
Pages371-389
Number of pages19
ISBN (Print)9781493913930, 9781493913923
DOIs
Publication statusPublished - Jan 1 2015

Fingerprint

Aurora Kinases
Phosphotransferases
Cell proliferation
Aurora Kinase A
Neoplasms
Protein-Serine-Threonine Kinases
Aurora Kinase B
Cell Proliferation
Tumors
Genes
Chromosomal Instability
Cells
Tumor Suppressor Genes
Oncogenes
Carcinogenesis
Clinical Trials
Phenotype
Therapeutics

Keywords

  • Aurora kinases
  • Centrosomal anomalies
  • Chromosomal instability
  • Ciliopathies
  • Oncoproteins cancer cell signaling
  • Tumor suppressor proteins

ASJC Scopus subject areas

  • Medicine(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

Cite this

Sen, S., & Katayama, H. (2015). Aurora kinases. In Targeted Therapy of Acute Myeloid Leukemi (pp. 371-389). Springer New York. https://doi.org/10.1007/978-1-4939-1393-0_19

Aurora kinases. / Sen, Subrata; Katayama, Hiroshi.

Targeted Therapy of Acute Myeloid Leukemi. Springer New York, 2015. p. 371-389.

Research output: Chapter in Book/Report/Conference proceedingChapter

Sen, S & Katayama, H 2015, Aurora kinases. in Targeted Therapy of Acute Myeloid Leukemi. Springer New York, pp. 371-389. https://doi.org/10.1007/978-1-4939-1393-0_19
Sen S, Katayama H. Aurora kinases. In Targeted Therapy of Acute Myeloid Leukemi. Springer New York. 2015. p. 371-389 https://doi.org/10.1007/978-1-4939-1393-0_19
Sen, Subrata ; Katayama, Hiroshi. / Aurora kinases. Targeted Therapy of Acute Myeloid Leukemi. Springer New York, 2015. pp. 371-389
@inbook{8607a73c69de47339384f6e445938c92,
title = "Aurora kinases",
abstract = "Aurora kinase family of serine/threonine kinases, frequently overexpressed in human cancers and implicated in tumorigenesis, induce chromosomal instability and oncogenic transformation when expressed at elevated levels in mammalian cells in vitro and in vivo. Recent findings on the interactions of Aurora kinases with tumor suppressor gene and oncogene-regulated networks as well as involvement in other nonmitotic processes such as ciliary disassembly affecting important signaling pathways and developmental disorders termed ciliopathies, have led to a greater recognition of the functional significance of these kinases in development and disease. Among the three members of the kinase family, Aurora- A, -B, and -C identified in humans, Aurora-A and -B have been reported to express at detectable levels in most proliferating somatic cells and characterized in detail for their involvement in cellular pathways relevant to cell proliferation and development of cancer-associated phenotypes. As a result, Aurora-A and -B are being investigated as potential targets for cancer therapy and multiple agents targeting the kinases are in early phase clinical trials with some having yielded encouraging results. This chapter discusses functional involvement of Aurora kinase-A and -B in the regulation of cell proliferation and cancer-relevant cellular pathways validating their significance as cancer therapeutic targets.",
keywords = "Aurora kinases, Centrosomal anomalies, Chromosomal instability, Ciliopathies, Oncoproteins cancer cell signaling, Tumor suppressor proteins",
author = "Subrata Sen and Hiroshi Katayama",
year = "2015",
month = "1",
day = "1",
doi = "10.1007/978-1-4939-1393-0_19",
language = "English",
isbn = "9781493913930",
pages = "371--389",
booktitle = "Targeted Therapy of Acute Myeloid Leukemi",
publisher = "Springer New York",

}

TY - CHAP

T1 - Aurora kinases

AU - Sen, Subrata

AU - Katayama, Hiroshi

PY - 2015/1/1

Y1 - 2015/1/1

N2 - Aurora kinase family of serine/threonine kinases, frequently overexpressed in human cancers and implicated in tumorigenesis, induce chromosomal instability and oncogenic transformation when expressed at elevated levels in mammalian cells in vitro and in vivo. Recent findings on the interactions of Aurora kinases with tumor suppressor gene and oncogene-regulated networks as well as involvement in other nonmitotic processes such as ciliary disassembly affecting important signaling pathways and developmental disorders termed ciliopathies, have led to a greater recognition of the functional significance of these kinases in development and disease. Among the three members of the kinase family, Aurora- A, -B, and -C identified in humans, Aurora-A and -B have been reported to express at detectable levels in most proliferating somatic cells and characterized in detail for their involvement in cellular pathways relevant to cell proliferation and development of cancer-associated phenotypes. As a result, Aurora-A and -B are being investigated as potential targets for cancer therapy and multiple agents targeting the kinases are in early phase clinical trials with some having yielded encouraging results. This chapter discusses functional involvement of Aurora kinase-A and -B in the regulation of cell proliferation and cancer-relevant cellular pathways validating their significance as cancer therapeutic targets.

AB - Aurora kinase family of serine/threonine kinases, frequently overexpressed in human cancers and implicated in tumorigenesis, induce chromosomal instability and oncogenic transformation when expressed at elevated levels in mammalian cells in vitro and in vivo. Recent findings on the interactions of Aurora kinases with tumor suppressor gene and oncogene-regulated networks as well as involvement in other nonmitotic processes such as ciliary disassembly affecting important signaling pathways and developmental disorders termed ciliopathies, have led to a greater recognition of the functional significance of these kinases in development and disease. Among the three members of the kinase family, Aurora- A, -B, and -C identified in humans, Aurora-A and -B have been reported to express at detectable levels in most proliferating somatic cells and characterized in detail for their involvement in cellular pathways relevant to cell proliferation and development of cancer-associated phenotypes. As a result, Aurora-A and -B are being investigated as potential targets for cancer therapy and multiple agents targeting the kinases are in early phase clinical trials with some having yielded encouraging results. This chapter discusses functional involvement of Aurora kinase-A and -B in the regulation of cell proliferation and cancer-relevant cellular pathways validating their significance as cancer therapeutic targets.

KW - Aurora kinases

KW - Centrosomal anomalies

KW - Chromosomal instability

KW - Ciliopathies

KW - Oncoproteins cancer cell signaling

KW - Tumor suppressor proteins

UR - http://www.scopus.com/inward/record.url?scp=84944624388&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84944624388&partnerID=8YFLogxK

U2 - 10.1007/978-1-4939-1393-0_19

DO - 10.1007/978-1-4939-1393-0_19

M3 - Chapter

SN - 9781493913930

SN - 9781493913923

SP - 371

EP - 389

BT - Targeted Therapy of Acute Myeloid Leukemi

PB - Springer New York

ER -