BRAFE600-associated senescence-like cell cycle arrest of human naevi

By C. Michaloglou, Liesbeth C. W. Vredeveld, M. Soengas, C. Denoyelle, T. Kuilman, C. C. A. M. Horst, D. Majoor, J. Shay, W. Mooi, D. Peeper. Nature, 2005

2,216 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/bfbf433cb25b4a5e054e35a6850376801a03b87d

How researchers see this paper

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

In Cell Biology

1. Walter Kolch
2. J. Campisi
3. L. Larue
4. J. Pouysségur
5. Joseph Schlessinger
6. Meenhard Herlyn
7. S. Meloche

In Molecular Biology

1. J. Campisi
2. Jesús Gil
3. Manuel Serrano
4. D. Peeper
5. T. Kuilman
6. F. d’Adda di Fagagna
7. Masashi Narita
8. Zhijian J. Chen

In Physiology

1. J. Campisi
2. Jesús Gil
3. Manuel Serrano
4. F. d’Adda di Fagagna
5. D. Peeper
6. T. Kuilman
7. Zhijian J. Chen
8. M. Collado

Citations in the corpus

• Cellular senescence and its effector programs (2014, background): “2010) in several murine and human premalignant lesions (Braig et al. 2005; Chen et al. 2005; Collado et al. 2005; Lazzerini Denchi et al. 2005; Michaloglou et al. 2005), reinforcing the tumor-suppressive role of senescence (Narita and Lowe 2005).”
• Senescence is a developmental mechanism that contributes to embryonic growth and patterning. (2013, methodology): “…it is a proven and reliable marker of senescence in vivo in many settings, including premalignant lesions (Chen et al., 2005; Collado et al., 2005; Michaloglou et al., 2005), chemotherapy and tumor regression (Schmitt et al., 2002; Xue et al., 2007), premature aging (Baker et al., 2011; Keyes et…”
• Analysis of BRAF V600E mutation in 1,320 nervous system tumors reveals high mutation frequencies in pleomorphic xanthoastrocytoma, ganglioglioma and extra-cerebellar pilocytic astrocytoma (2011, background): “It has previously been demonstrated that BRAF mutation results in an induction of p16 and that this leads to senescence in human melanocytic nevi [28].”
• The regulation of INK4/ARF in cancer and aging. (2006, neutral): “For example, in cultured human cells, senescence generally occurs in the setting of increased expression of p16 INK4a , but not ARF, and enforced RAS-RAF activation also appears to induce only p16 INK4a in human cells (Huot et al., 2002; Michaloglou et al., 2005; Munro et al., 1999).”
• Discovery of a selective inhibitor of oncogenic B-Raf kinase with potent antimelanoma activity (2008, background): “Note that certain premalignant cells such as those found in benign nevi also demonstrate frequent expression of B-RafV600E (20, 21), and it remains unclear how these cells avoid transformation to a malignant state.”
• Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. (2008, positive): “Significantly, p16 INK4a expression was not induced by BRAFV600E in 16 of the 17 melanocyte KD cell lines.”
• Targeting the Mitogen-Activated Protein Kinase RAS-RAF Signaling Pathway in Cancer Therapy (2012, background): “Marked activation of theMAPKpathway can also suppress cellular growth in normal and cancer cells by inducing cellular senescence [39,40].”