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PARP inhibitors in oncology: a new synthetic lethal approach to cancer therapy

VIBEKE KRUSE UGent, Sylvie Rottey UGent, OLE DE BACKER UGent, Simon Van Belle UGent, Veronique Cocquyt UGent and Hannelore Denys UGent (2011) ACTA CLINICA BELGICA. 66(1). p.2-9
abstract
Damage to DNA has emerged as a major culprit in cancer. Mammalian cells are continuously exposed to DNA damage, caused by exogenous toxins as well as endogenous activities such as DNA replication and cellular free radical generation. It is therefore essential that cells have DNA repair mechanisms in place to preserve its genomic integrity. Interestingly, cancer cells frequently harbour defects in DNA repair pathways, leading to genomic instability. This can foster tumorigenesis, but also provides a weakness in the tumour that can be exploited therapeutically. In this context, it has been shown that homologous recombination (HR)-deficient tumour cells - including those with defects in BRCA1/2 - are highly sensitive to blockade of the base excision repair (BER) pathway via inhibition of the poly (ADPribose) polymerase (PARP) enzyme. This provides the basis for a novel 'synthetic lethal' approach to cancer therapy. Recent clinical trials have shown an enhancement of the cytotoxic effect of chemotherapy by adding a PARP inhibitor to the standard treatment. Still, clinical outcome may be even further improved if these drugs would be used as first-line therapy. In conclusion, it can be stated that an exciting new class of drugs has entered the arena of cancer therapy. However, additional clinical studies are needed before PARP inhibitors can definitely enter daily clinical practice.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
PARP inhibitors, DNA repair, POLY(ADP-RIBOSE) POLYMERASE, synthetic lethality, targeted therapy, chemopotentiation, OVARIAN-CANCER, REPAIR, BREAST, TEMOZOLOMIDE, COMBINATION, ABT-888, TUMORS
journal title
ACTA CLINICA BELGICA
Acta Clin. Belg.
volume
66
issue
1
pages
2 - 9
Web of Science type
Article
Web of Science id
000288845700002
JCR category
MEDICINE, GENERAL & INTERNAL
JCR impact factor
0.592 (2011)
JCR rank
105/153 (2011)
JCR quartile
3 (2011)
ISSN
0001-5512
DOI
10.2143/ACB.66.1.2062507
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1987400
handle
http://hdl.handle.net/1854/LU-1987400
date created
2012-01-16 15:09:42
date last changed
2015-06-17 09:54:06
@article{1987400,
  abstract     = {Damage to DNA has emerged as a major culprit in cancer. Mammalian cells are continuously exposed to DNA damage, caused by exogenous toxins as well as endogenous activities such as DNA replication and cellular free radical generation. It is therefore essential that cells have DNA repair mechanisms in place to preserve its genomic integrity. Interestingly, cancer cells frequently harbour defects in DNA repair pathways, leading to genomic instability. This can foster tumorigenesis, but also provides a weakness in the tumour that can be exploited therapeutically. In this context, it has been shown that homologous recombination (HR)-deficient tumour cells - including those with defects in BRCA1/2 - are highly sensitive to blockade of the base excision repair (BER) pathway via inhibition of the poly (ADPribose) polymerase (PARP) enzyme. This provides the basis for a novel 'synthetic lethal' approach to cancer therapy. Recent clinical trials have shown an enhancement of the cytotoxic effect of chemotherapy by adding a PARP inhibitor to the standard treatment. Still, clinical outcome may be even further improved if these drugs would be used as first-line therapy. In conclusion, it can be stated that an exciting new class of drugs has entered the arena of cancer therapy. However, additional clinical studies are needed before PARP inhibitors can definitely enter daily clinical practice.},
  author       = {KRUSE, VIBEKE and Rottey, Sylvie and DE BACKER, OLE and Van Belle, Simon and Cocquyt, Veronique and Denys, Hannelore},
  issn         = {0001-5512},
  journal      = {ACTA CLINICA BELGICA},
  keyword      = {PARP inhibitors,DNA repair,POLY(ADP-RIBOSE) POLYMERASE,synthetic lethality,targeted therapy,chemopotentiation,OVARIAN-CANCER,REPAIR,BREAST,TEMOZOLOMIDE,COMBINATION,ABT-888,TUMORS},
  language     = {eng},
  number       = {1},
  pages        = {2--9},
  title        = {PARP inhibitors in oncology: a new synthetic lethal approach to cancer therapy},
  url          = {http://dx.doi.org/10.2143/ACB.66.1.2062507},
  volume       = {66},
  year         = {2011},
}

Chicago
Kruse, Vibeke, Sylvie Rottey, OLE DE BACKER, Simon Van Belle, Veronique Cocquyt, and Hannelore Denys. 2011. “PARP Inhibitors in Oncology: a New Synthetic Lethal Approach to Cancer Therapy.” Acta Clinica Belgica 66 (1): 2–9.
APA
Kruse, V., Rottey, S., DE BACKER, O., Van Belle, S., Cocquyt, V., & Denys, H. (2011). PARP inhibitors in oncology: a new synthetic lethal approach to cancer therapy. ACTA CLINICA BELGICA, 66(1), 2–9.
Vancouver
1.
Kruse V, Rottey S, DE BACKER O, Van Belle S, Cocquyt V, Denys H. PARP inhibitors in oncology: a new synthetic lethal approach to cancer therapy. ACTA CLINICA BELGICA. 2011;66(1):2–9.
MLA
Kruse, Vibeke, Sylvie Rottey, OLE DE BACKER, et al. “PARP Inhibitors in Oncology: a New Synthetic Lethal Approach to Cancer Therapy.” ACTA CLINICA BELGICA 66.1 (2011): 2–9. Print.