Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis

By N. Sharpless, N. Bardeesy, Kee‐Ho Lee, D. Carrasco, D. Castrillon, A. Aguirre, Emily Wu, J. Horner, R. DePinho. Nature, 2001

859 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/a926468af5932673b122b0d7706e1d537a6beb02

How researchers see this paper

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

In Molecular Biology

1. J. Campisi
2. N. Sharpless
3. Jesús Gil
4. S. Morrison
5. R. DePinho
6. Domhnall McHugh
7. R. Weinberg
8. Shenghui He

In Oncology

1. J. Campisi
2. R. Weinberg
3. Annapoorni Rangarajan
4. Jesús Gil
5. Sue-Jean Hong
6. A. Gifford
7. R. DePinho
8. S. Morrison

In Physiology

1. J. Campisi
2. Jesús Gil
3. N. Sharpless
4. Domhnall McHugh
5. C. Sherr
6. D. Peeper
7. T. Kuilman
8. Shenghui He

Citations in the corpus

• Long non-coding RNA ANRIL is required for the PRC2 recruitment to and silencing of p15INK4B tumor suppressor gene (2010, background): “…website (http://www.nature.com/onc) N IH -PA Author M anuscript N IH -PA Author M anuscript mutations targeting each gene individually support the tumor suppression function for all three genes (Serrano et al., 1996; Kamijo et al., 1997; Krimpenfort et al., 2001, 2007; Sharpless et al., 2001).”
• Epigenetic antagonism between Polycomb and SWI/SNF complexes during oncogenic transformation (2010, positive): “However, downregulation of p16 is unlikely to be the full mechanism by which SNF5 loss drives cancer formation as tumor onset occurs much more quickly, with higher penetrance, and in a different spectrum following Snf5 inactivation than p16 inactivation (Krimpenfort et al., 2001; Sharpless et al., 2”
• The RB and p53 pathways in cancer. (2002, background): “Yet, mice lacking p16Ink4a, in particular, are tumor prone and develop a wide spectrum of cancers, particularly after exposure to chemical carcinogens or X-rays (Serrano et al., 1996; Krimpenfort et al., 2001; Sharpless et al., 2001).”
• Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “Inhibition of p38, disruption of p53 and p16, or lengthening of telomeres have all been shown to benefit aging phenotypes but carry a major caveat, as they can increase the incidence of cancer (Sharpless et al., 2001; Ito et al., 2006; Janzen et al., 2006; Shay, 2016).”
• The signals and pathways activating cellular senescence. (2005, background): “In contrast, while inactivation of p53 in the mouse germline causes widespread tumor development, p16-null mice suffer from only a narrow set of tumor types (Krimpenfort, Quon, Mooi, Loonstra, & Berns, 2001; Sharpless et al., 2001).”
• Species- and cell type-specific requirements for cellular transformation. (2004, background): “The senescence phase in primary hFS fibroblasts is seen starting at passage 53. passage hFS fibroblasts were serially infected with one of the et al., 2000; Sharpless et al., 2001).”