Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints
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Summary
It is shown that oncogene-induced senescence is associated with signs of DNA replication stress, including prematurely terminated DNA replication forks and DNA double-strand breaks, and, together with apoptosis, provides a barrier to malignant progression.
- Type
- article
- Published
- 2006-11-01
- Cited by
- 2,050
- References
- 30
- OpenAlex
- https://openalex.org/W2041156660
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:4406956
Keywords
DNA damage, Senescence, Carcinogenesis, Oncogene, Biology
References
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Cited by
- Development of an shRNA screen to identify mediators of cellular senescence in human breast epithelial cells
- Developing a systems-based understanding of hematopoietic stem cell cycle control.
- Ionizing radiation and aging: rejuvenating an old idea
- The Vitamin D Receptor as Tumor Suppressor in Skin.
- The genome and epigenome of malignant melanoma
- Stemming out of a new PML era?
- The many facets of the Tim-Tipin protein families’ roles in chromosome biology
- Transcriptional regulation of cellular senescence
- Senescence and pre-malignancy: how do tumors progress?
- CLCA2 as a p53-inducible senescence mediator.
- Polyploid cells rewire DNA damage response networks to overcome replication stress-induced barriers for tumour progression
- Wnt Antagonist SFRP1 Functions as a Secreted Mediator of Senescence
- Bexarotene Induces Cellular Senescence in MMTV-Neu Mouse Model of Mammary Carcinogenesis
- Oncogenes induce genotoxic stress by mitotic processing of unusual replication intermediates
- The DNA damage checkpoint response to replication stress: A Game of Forks
- Working hard for recovery: mitotic kinases in the DNA damage checkpoint
- Dissecting the telomere-independent pathways underlying human cellular senescence
- Cdc6 cooperates with c-Myc to promote genome instability and epithelial to mesenchymal transition (EMT) in zebrafish
- Role of sirtuins in chronic obstructive pulmonary disease
- Trial Watch: Targeting ATM–CHK2 and ATR–CHK1 pathways for anticancer therapy
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