Activation of the p53 tumor suppressor can lead to cell cycle arrest. The key mechanism of
p53-mediated arrest is transcriptional downregulation of many cell cycle genes. In recent …

Oncogene activation disturbs cellular processes and accommodates a complex landscape
of changes in the genome that contribute to genomic instability, which accelerates mutation …

Upon DNA damage or other stressors, the tumor suppressor p53 is activated, leading to
transient expression of the cyclin-dependent kinase inhibitor (CKI) p21. This either triggers …

Genome instability is a hallmark of cancer, and DNA replication is the most vulnerable
cellular process that can lead to it. Any condition leading to high levels of DNA damage will …

DNA replication begins with the assembly of pre-replication complexes (pre-RCs) at
thousands of DNA replication origins during the G1 phase of the cell cycle. At the G1–S …

The clinical development of an inhibitor of cellular proteasome function suggests that
compounds targeting other components of the ubiquitin–proteasome system might prove …

The cell-cycle transition from G 1 to S phase has been difficult to visualize. We have
harnessed antiphase oscillating proteins that mark cell-cycle transitions in order to develop …

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 …

Early tumorigenesis is associated with the engagement of the DNA-damage checkpoint
response (DDR),. Cell proliferation and transformation induced by oncogene activation are …

DNA replication must be tightly regulated to ensure that the genome is accurately duplicated
during each cell cycle. When these regulatory mechanisms fail, replicative stress and DNA …