Cellular senescence as a tumor-suppressor mechanism.

By J. Campisi. Trends in Cell Biology, 2001

938 citations recorded by the source corpus.

Subfields: Biotechnology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/c3a1ebe5e9b50a9a33a6e469d56bac202f5a7a77

How researchers see this paper

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

In Biotechnology

1. J. Campisi
2. F. d’Adda di Fagagna
3. H. Okada
4. T. Mak
5. Jesús Gil
6. Scott W. Lowe
7. R. Hoffman
8. Erik Sahai

In Molecular Biology

1. J. Campisi
2. Jesús Gil
3. F. d’Adda di Fagagna
4. A. Krtolica
5. Scott W. Lowe
6. J. Fridman
7. T. Mak
8. H. Okada

In Physiology

1. J. Campisi
2. Jesús Gil
3. Scott W. Lowe
4. F. d’Adda di Fagagna
5. A. Krtolica
6. C. Schmitt
7. T. Mak
8. H. Okada

Citations in the corpus

• Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence. (2003, neutral): “In fact, human fibroblasts almost never spontaneously es-between 3 and 5 days postselection (Figure 1C), a time when these cells stopped incorporating BrdU and be-cape replicativesenescence and cannotbe transformed unless the process is disabled (Campisi, 2001).”
• Nuclear structure in cancer cells (2004, background): “Cellular senescence is a permanent form of cell-cycle arrest that also limits the proliferation of damaged cells, and therefore seems to be an important antitumour mechanis”
• Oxygen sensitivity severely limits the replicative lifespan of murine fibroblasts (2003, background): “Replicative senescence limits the proliferation of many cell types in culture and in vivo”
• A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy. (2002, background): “Tumors lacking both programs rapidlyis controlled by the p53 and p16/Rb tumor suppressor pathways (Campisi, 2001). progress to a lethal stage, suggesting that post-damage responses are almost completely responsible for CTXTo determine whether CTX-induced cytostasis has features of cellular…”
• Pathways of apoptotic and non-apoptotic death in tumour cells (2004, background): “Senescence can also be induced by various cellular stresse”
• A DNA damage checkpoint response in telomere-initiated senescence (2003, background): “This model may therefore be of relevance in terms of the proposed role of senescence as a tumour-suppressor mechanis”
• Glycolytic enzymes can modulate cellular life span. (2005, background): “cells achieve a limited number of population doublings before entering a growth-arrested state known as replicative senescence (6, 7).”
• Cellular senescence: when bad things happen to good cells (2007, background): “One such mechanism was cellular senescence, which stops incipient cancer cells from proliferatin”
• Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. (2005, background): “These pathways are governed by a the gatekeeper tumor suppressor proteins p53 and r pRB (Bringold and Serrano, 2000; Lundberg et al., c 2000; Campisi, 2001).”