TP53 is the most commonly mutated gene in human cancer with over 100,000 literature
citations in PubMed. This is a heavily studied pathway in cancer biology and oncology with a …

MYC oncogene is a transcription factor with a wide array of functions affecting cellular
activities such as cell cycle, apoptosis, DNA damage response, and hematopoiesis. Due to …

Aims The expression of GADD153 (growth arrest and DNA damage-inducible gene 153), an
apoptosis-regulated gene, increases during endoplasmic reticulum (ER) stress. How …

In vertebrate cells, the DNA damage response is controlled by three related kinases: ATM,
ATR, and DNA-PK. It has been 20 years since the cloning of ATR, the last of the three to be …

The tumor suppressor p53 functions primarily as a transcription factor. Mutation of the TP53
gene alters its response pathway, and is central to the development of many cancers. The …

DNA damage response (DDR) pathway prevents high level endogenous and environmental
DNA damage being replicated and passed on to the next generation of cells via an …

Synthetic lethality (SL) provides a conceptual framework for tackling targets that are not
classically “druggable,” including loss-of-function mutations in tumor suppressor genes …

The multistep process of cancer progresses over many years. The prevention of mutations
by DNA repair pathways led to an early appreciation of a role for repair in cancer avoidance …

In order to maintain genomic stability, cells have developed sophisticated signalling
pathways to enable DNA damage or DNA replication stress to be resolved. Key mediators of …

Germline alterations in many genes coding for proteins regulating DNA repair and DNA
damage response (DDR) to DNA double-strand breaks (DDSB) have been recognized as …