Apoptosis in cancer.
By Scott W. Lowe, Athena W. Lin. Carcinogenesis, 2000
1,191 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/a801859934f9f0e8be0c226d0c8bbb3f8e29e1e3
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In Molecular Biology
In Oncology
Citations in the corpus
- Apoptosis A Link between Cancer Genetics and Chemotherapy (2002, background): “…the alternative reading frame product of the INK4a/ARF tumor suppressor locus. p19ARF, in turn, can both disable apoptosis and accelerate tumor development in transgenic mice (Attardi and Jacks, 1999;binds and inactivates Mdm2, leading to p53 activation (Lowe and Lin, 2000; Sherr and Weber, 2000).”
- Control of apoptosis by p53 (2003, background): “Conversely, the ability of oncogenes such as Myc to sensitize cells to chemotherapy may explain, in part, the therapeutic index of certain chemotherapeutic agents to begin with (Lowe and Lin, 2000; Pelengaris et al., 2002).”
- Autophagy as a cell death and tumor suppressor mechanism (2004, background): “The contribution of loss of type I apoptotic responses to cancer formation is now well established and has been extensively analysed at the molecular level over recent years (Hanahan and Weinberg, 2000; Lowe and Lin, 2000; Green and Evan, 2002).”
- Apoptosis and melanoma chemoresistance (2003, background): “The identification of Bcl-2 as an oncogene that prevented apoptosis served as a catalyst for one of the most prolific areas of research in molecular oncology that revealed apoptosis as a critical tumor control mechanism (Lowe and Lin, 2000; Igney and Krammer, 2002; Johnstone et al., 2002).”