Selective Targeting of the G2/M Cell Cycle Checkpoint to Improve the Therapeutic Index of Radiotherapy

Abstract Despite tremendous advances in radiotherapy techniques, allowing dose escalation to tumour tissues and sparing of organs at risk, cure rates from radiotherapy or chemoradiotherapy remain suboptimal for most cancers. In tandem with our growing understanding of tumour biology, we are beginnin...

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Bibliographic Details
Published in:Clinical oncology (Royal College of Radiologists (Great Britain)) 2014-05, Vol.26 (5), p.257-265
Main Authors: Dillon, M.T, Good, J.S, Harrington, K.J
Format: Article
Language:English
Subjects:
ATR inhibition
Cell Line, Tumor
checkpoint inhibition
Checkpoint Kinase 1
Chemoradiotherapy
Chk1 inhibition
DNA - radiation effects
DNA Damage
G2 Phase Cell Cycle Checkpoints - drug effects
G2 Phase Cell Cycle Checkpoints - radiation effects
Hematology, Oncology and Palliative Medicine
Humans
M Phase Cell Cycle Checkpoints - drug effects
M Phase Cell Cycle Checkpoints - radiation effects
Neoplasms - genetics
Neoplasms - pathology
Neoplasms - therapy
Protein Kinases - drug effects
Protein Kinases - radiation effects
Radiation-Sensitizing Agents
Radiology
radiosensitisation
Receptors, Peptide - antagonists & inhibitors
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Summary:Abstract Despite tremendous advances in radiotherapy techniques, allowing dose escalation to tumour tissues and sparing of organs at risk, cure rates from radiotherapy or chemoradiotherapy remain suboptimal for most cancers. In tandem with our growing understanding of tumour biology, we are beginning to appreciate that targeting the molecular response to radiation-induced DNA damage holds great promise for selective tumour radiosensitisation. In particular, approaches that inhibit cell cycle checkpoint controls offer a means of exploiting molecular differences between tumour and normal cells, thereby inducing so-called cancer-specific synthetic lethality. In this overview, we discuss cellular responses to radiation-induced damage and discuss the potential of using G2/M cell cycle checkpoint inhibitors as a means of enhancing tumour control rates.
ISSN:0936-6555
1433-2981
DOI:10.1016/j.clon.2014.01.009