An Oncogene-Induced DNA Damage Model for Cancer Development

By T. Halazonetis, Vassilis G. Gorgoulis, J. Bartek. Science, 2008

1,894 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/2b6c258544618e00077a184f8fbe2b4ae6033b64

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

In Molecular Biology

In Oncology

Citations in the corpus

Dynamic EMT: a multi‐tool for tumor progression (2021, positive): “This mitigates oncogene-induced replication stress to overcome oncogene-induced senescence (OIS) in TP53 wild-type cells (Halazonetis et al , 2008) (Morel et al , 2017).”
DNA replication stress as a hallmark of cancer. (2015, background): “Subsequently, inactivation of the TP53 tumor suppressor gene and mutations in other oncogenes, notably in PIK3CA, are associated with progression from adenoma to carcinoma (43–46, 48).”
Immune parameters affecting the efficacy of chemotherapeutic regimens (2011, background): “Beyond these changes in the antigenic profile, the oncogenic stress linked to early carcinogenesis (which is shut off in later tumor progression”
Cell cycle, CDKs and cancer: a changing paradigm (2009, background): “It is therefore not surprising that human tumour cells often show constitutive activation of DNA damage signalling pathways, represented by activated ATM, CHK1 or CHK2 kinases, phosphorylated histone H2AX (γH2AX) and p53 , all of which are markers of a DNA damage respons”
Bioinspired exosome-mimetic nanovesicles for targeted delivery of chemotherapeutics to malignant tumors. (2013, background): “which is detected at the cell cycle checkpoints.(2) Therefore, for tumors to develop, tu-”
Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008, background): “In both of these cases, presence of RB seems to be beneficial to tumour progression, which is counterintuitive given the role of RB as a potent tumour suppressor; these observations might be highly relevant to cancer initiation, following the model that DNA damage signals are induced by oncogenic ac”
ATR prohibits replication catastrophe by preventing global exhaustion of RPA. (2013, positive): “Second, oncogene transformation is accompanied by elevated replication stress (Halazonetis et al., 2008), and it has been shown that expression of oncogenes is synthetically lethal with ATR deficiency (Toledo et al., 2011).”
Chromatin replication and epigenome maintenance (2012, background): “This type of replication stress can result from oncogene activation and probably contributes to carcinogenesi”
Genomic instability — an evolving hallmark of cancer (2010, background): “The first is the mutator hypothesis described above and the second is the oncogene-induced DNA replication stress model for cancer developmen”
Nucleotide Deficiency Promotes Genomic Instability in Early Stages of Cancer Development (2011, neutral): “More recently, oncogene-induced DNA replication stress was suggested as a model (Halazonetis et al., 2008).”
Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, positive): “to increase DSBs and genomic instability (Halazonetis et al., 2008), possibly through DNA hyper-replication (Bartkova et al.”
DNA damage sensing by the ATM and ATR kinases. (2013, background): “The recent discovery that ATM and ATR are activated by oncogenic stresses suggests that cancer cells may rely on the DDR pathways to survive genomic instability (Halazonetis et al. 2008).”