p53 in survival, death and metabolic health: a lifeguard with a licence to kill

By F. Kruiswijk, Christiaan F. Labuschagne, Karen H. Vousden. Nature reviews. Molecular cell biology, 2015

1,009 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology

View Paper: https://www.semanticscholar.org/paper/199df5a69ddcf23969267473cda46bc30ae0d0d0

How researchers see this paper

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

In Cancer Research

1. Navdeep S. Chandel
2. Ralph J. Deberardinis
3. Jesús Gil
4. W. Zou
5. Arul M. Chinnaiyan
6. P. Jat
7. E. Lengyel
8. J. Campisi

In Oncology

1. Jesús Gil
2. W. Zou
3. M. Guo
4. Haolan Wang
5. Yongheng Chen
6. P. Jat
7. E. Lengyel
8. John Calvin Reed

Citations in the corpus

• Mutant p53 as a guardian of the cancer cell (2018, neutral): “help the cell adapt to and survive mild stress conditions, including oxidative and metabolic stress [7].”
• Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “107 Ammonia is a prevalent product of cellular metabolism.”
• Loss of BRCA1 in the cells of origin of ovarian cancer induces glycolysis: A window of opportunity for ovarian cancer chemoprevention (2017, background): “The p53 mutation in the immortalized IOSE and fallopian tube cells could alter metabolism (25); therefore, nonimmortalized primary human FTECs and FTSCs were also tested.”
• Autophagy-Independent Functions of the Autophagy Machinery (2019, background): “The ultimate metabolic catastrophe promoted by the absence of ATG7 irrespective of bona fide autophagic responses may reflect the ability of p53 to support the maintenance of metabolic homeostasis at baseline (Kruiswijk et al., 2015).”
• Radiotherapy and immunotherapy promote tumoral lipid oxidation and ferroptosis via synergistic repression of SLC7A11 (2019, background): “Along this line, p53 contributes to tumor-cell survival but also promotes tumor-cell death (35).”
• Revisiting the hallmarks of cancer. (2017, neutral): “[35] Kruiswijk F, Labuschagne CF and Vousden KH.”
• Fundamentals of cancer metabolism (2016, background): “Loss of p53 increases glycolytic flux to promote anabolism and redox balance, two key processes that promote tumorigenesis (19).”
• Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021, background): “Additional signals and persistent stress can lead to sustained expression of p53 and activation of p16INK4A contributing to a long lasting cell cycle arrest (Sharpless and DePinho, 2006; Salama et al., 2014; Kruiswijk et al., 2015).”
• Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “Although transient increases in p53 levels can enact a quiescent state and activate DNA repair processes, during senescence, there is a sustained induction of p53 (Salama et al., 2014; Kruiswijk et al., 2015).”
• Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging (2017, background): “…of nuclei of senescent cells showed FOXO4 to reside within these PML bodies, adjacent to 53BP1-containing DNA-SCARS (Figure 2D; Movies S1 andS2; Figures S2E–S2I). p53 controls both apoptosis and senescence (Kruiswijk et al., 2015) and localizes to DNA-SCARS in senescent cells (Rodier et al., 2011).”