• Publications
  • Influence
DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis
During the evolution of cancer, the incipient tumour experiences ‘oncogenic stress’, which evokes a counter-response to eliminate such hazardous cells. However, the nature of this stress remainsExpand
  • 2,456
  • 108
Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints
Recent studies have indicated the existence of tumorigenesis barriers that slow or inhibit the progression of preneoplastic lesions to neoplasia. One such barrier involves DNA replication stress,Expand
  • 1,677
  • 66
53BP1 loss rescues BRCA1 deficiency and is associated with triple-negative and BRCA-mutated breast cancers
Germ-line mutations in breast cancer 1, early onset (BRCA1) result in predisposition to breast and ovarian cancer. BRCA1-mutated tumors show genomic instability, mainly as a consequence of impairedExpand
  • 753
  • 52
  • PDF
A CHEK2 genetic variant contributing to a substantial fraction of familial breast cancer.
CHEK2 (previously known as "CHK2") is a cell-cycle-checkpoint kinase that phosphorylates p53 and BRCA1 in response to DNA damage. A protein-truncating mutation, 1100delC in exon 10, which abolishesExpand
  • 446
  • 33
Distinct spatiotemporal dynamics of mammalian checkpoint regulators induced by DNA damage
Cell cycle checkpoints are signal transduction pathways activated after DNA damage to protect genomic integrity. Dynamic spatiotemporal coordination is a vital, but poorly understood aspect, of theseExpand
  • 482
  • 23
REV7 counteracts DNA double-strand break resection and affects PARP inhibition
Error-free repair of DNA double-strand breaks (DSBs) is achieved by homologous recombination (HR), and BRCA1 is an important factor for this repair pathway. In the absence of BRCA1-mediated HR, theExpand
  • 316
  • 20
53BP1 functions in an ATM-dependent checkpoint pathway that is constitutively activated in human cancer
53BP1 is a conserved nuclear protein that is implicated in the DNA damage response. After irradiation, 53BP1 localizes rapidly to nuclear foci, which represent sites of DNA double strand breaks, butExpand
  • 438
  • 17
Retinoblastoma-protein-dependent cell-cycle inhibition by the tumour suppressor p16
D-TYPE cyclins, in association with the cyclin-dependent kinases Cdk4 or Cdk6, promote progression through the Gl phase of the cell cycle1–6 by phosphorylating the retinoblastoma protein (RB)7,8. TheExpand
  • 922
  • 16
The combined status of ATM and p53 link tumor development with therapeutic response.
While the contribution of specific tumor suppressor networks to cancer development has been the subject of considerable recent study, it remains unclear how alterations in these networks areExpand
  • 264
  • 13
Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type- and insult-dependent manner and follow expression of p16ink4a
Cellular senescence, an irreversible proliferation arrest evoked by stresses such as oncogene activation, telomere dysfunction, or diverse genotoxic insults, has been implicated in tumor suppressionExpand
  • 231
  • 13
  • PDF