Senescence in tumours: evidence from mice and humans

By M. Collado, Manuel Serrano. Nature Reviews. Cancer, 2010

1,152 citations recorded by the source corpus.

The importance of cellular senescence, which is a stress response that stably blocks proliferation, is increasingly being recognized. Senescence is prevalent in pre-malignant tumours, and progression to malignancy requires evading senescence. Malignant tumours, however, may still undergo senescence owing to interventions that restore tumour suppressor function or inactivate oncogenes. Senescent tumour cells can be cleared by immune cells, which may result in efficient tumour regression. Standard chemotherapy also has the potential to induce senescence, which may partly underlie its therapeutic activity. Although these concepts are well supported in mouse models, translating them to clinical oncology remains a challenge.

Subfields: Biotechnology, Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/1c93d2135e14ecff48dff94701976488d6d6a1ff

How researchers see this paper

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

In Biotechnology

In Immunology

In Physiology

Citations in the corpus

Aging, Cellular Senescence, and Cancer (2012, background): “There is little doubt that the senescence growth arrest suppresses the development of cancer (8, 48, 136).”
Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “Senescent cells are detected in culture and in vivo by a variety of markers, including the senescence-associated β-galactosidase (SAβgal) [28], p16 [39], telomere-associated DNA damage foci [40], senescence-associated heterochromatin foci [41], and several other molecules; all of these markers have ”
Exosomes maintain cellular homeostasis by excreting harmful DNA from cells (2017, neutral): “1 2 3 4 5 6 siRNA(2): siRNA(1): Alix Rab27a Control”
Mechanisms and functions of cellular senescence. (2018, neutral): “In fact, senescence is best known as a potent anticancer mechanism that prevents malignancies by limiting the replication of preneoplastic cells (10).”
The essence of senescence. (2010, neutral): “DEC1, DCR2 (Collado et al. 2005), and PAI1 (Goldstein et al. 1994) have also been used as senescence biomarkers (Collado and Serrano 2010).”
The dynamic nature of autophagy in cancer. (2011, background): “There is a wealth of literature demonstrating the anti-proliferative effects of high levels of oncogenic Ras expression in primary cells as a barrier to transformation (Collado and Serrano 2010; Kuilman et al. 2010), and, perhaps in the initial stages of transformation, autophagy provides a barrier.”
Programmed cell senescence during mammalian embryonic development. (2013, positive): “For instance, cyclin-dependent kinase inhibitors p21 and p27 also contribute to senescent phenotypes (Collado and Serrano, 2010).”
Lamin B1 loss is a senescence-associated biomarker (2012, background): “They have also been shown to accumulate at sites of age-related pathology, both degenerative and preneoplastic (Parrinello et al., 2005; Campisi and d’Adda di Fagagna, 2007; Jeyapalan and Sedivy, 2008; Collado and Serrano, 2010).”
Radiation-induced cell death mechanisms (2010, methodology): “However, also molecules involved in the DNA damage response (DDR) as well as novel markers obtained from microarray studies have been used as surrogate markers of this process [ 121 ].”
Hallmarks of cancer: the next generation. (2011, neutral): “…has undermined this notion, in that excessively elevated signaling by oncoproteins such as RAS, MYC, and RAF can provoke counteracting responses from cells, speciﬁ-cally induction of cell senescence and/or apoptosis (Collado and Serrano, 2010; Evan and d’Adda di Fagagna, 2009; Lowe et al., 2004).”