p300/CBP and cancer
By N. Iyer, H. Özdağ, Carlos Caldas. Oncogene, 2004
652 citations recorded by the source corpus.
Subfields: Cancer Research, Developmental Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/026c45d3b40d89fc64110fda119adb1c8a9cdf09
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In Cancer Research
In Oncology
Citations in the corpus
- Tumor suppressive functions of p53. (2009, background): “For example, p53 can interact with various transcriptional activators, such as histone acetyltransferase CBP/p300 (Iyer et al. 2004), and transcriptional repressors and corepressors, such as histone deacetylases and sin3 (Zilfou et al.”
- Cancer epigenetics: from mechanism to therapy. (2012, background): “…examples of recurrent chromosomal translocations (e.g., MLL-CBP [Wang et al., 2005] and MOZ-TIF2 [Huntly et al., 2004]) or coding mutations (e.g., p300/CBP [Iyer et al., 2004; Pasqualucci et al., 2011]) involving various KATs in a broad range of solid and hematological malignancies (Figure 3).”
- Sirtuins: critical regulators at the crossroads between cancer and aging (2007, background): “The importance of HATs in cancer is highlighted by their frequent mutation, deletion and translocation in several types of cancer (Iyer et al., 2004).”
- Histone Modifications and Cancer. (2016, background): “It is increasingly evident that CBP and/or EP300 are important in cancers (e.g., transgenic mice deficient in CBP or EP300 can develop hematologic malignancies [Iyer et al. 2004]).”