Oncogene-induced senescence as an initial barrier in lymphoma development

By Melanie Braig, Soyoung Lee, C. Loddenkemper, C. Rudolph, A. Peters, B. Schlegelberger, H. Stein, B. Dörken, T. Jenuwein, C. Schmitt. Nature, 2005

1,269 citations recorded by the source corpus.

Subfields: Hematology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/efe1ae4a9d93752ce99456e5d509b7e93e72a2f9

How researchers see this paper

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

In Hematology

1. Scott W. Lowe
2. J. Campisi

In Immunology

1. J. Campisi
2. J. Kirkland
3. D. Baker
4. V. Krizhanovsky
5. Bennett G. Childs
6. F. Rodier
7. Scott W. Lowe
8. S. Friedman

In Molecular Biology

1. J. Campisi
2. J. Kirkland
3. D. Peeper
4. D. Baker
5. T. Kuilman
6. F. Rodier
7. Bennett G. Childs
8. C. Michaloglou

Citations in the corpus

• Senescence is a developmental mechanism that contributes to embryonic growth and patterning. (2013, background): “This involvement of tumorsuppressor pathways led to the identification of senescence as a potent tumor-suppressor mechanism in vivo (Braig et al., 2005; Chen et al., 2005; Collado et al., 2005; Michaloglou et al., 2005).”
• The Matricellular Protein CCN1/CYR61 Induces Fibroblast Senescence and Restricts Fibrosis in Cutaneous Wound Healing (2010, background): “Recent studies have established that cellular senescence is an important mechanism of tumour suppression, which functions by blocking the proliferation of damaged cells at risk of neoplastic transformatio”
• Senescence of activated stellate cells limits liver fibrosis (2008, background): “…a tissue culture phenomenon, recent studies demonstrate that cellular senescence imposes a potent barrier to tumorigenesis and contributes to the cytotoxicity of certain anticancer agents (Braig et al., 2005; Chen et al., 2005; Collado et al., 2005; Michaloglou et al., 2005; Schmitt et al., 2002).”
• A genetic screen implicates miRNA-372 and miRNA-373 as oncogenes in testicular germ cell tumors. (2006, background): “The senescent phenotype was recently shown to play a role in the protection from tumor development in vivo (Braig et al., 2005; Chen et al., 2005; Collado et al., 2005; Michaloglou et al., 2005).”
• DNA repair pathways as targets for cancer therapy (2008, background): “In such tumours it might be possible to use DNA repair inhibitors to make existing cancer-specific replication lesions more toxic, resulting in fatal replication lesions selectively killing oncogene-expressing cancer cell”