Melanoma biology and new targeted therapy
By V. Gray-Schopfer, C. Wellbrock, R. Marais. Nature, 2007
1,368 citations recorded by the source corpus.
Subfields: Cell Biology, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/31254be4cf903ad28f3a4bcab93677e8c5448435
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Citations in the corpus
- Progressive Transfer Learning and Adversarial Domain Adaptation for Cross-Domain Skin Disease Classification (2020, background): “S KIN cancer is one of the most frequently diagnosed human malignancy, especially among light pigmented skin [1].”
- Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF (2013, positive): “Despite the promise and dramatic initial effects of BRAF inhibitors in the clinic, patients eventually relapse within a few months, suggesting that combination therapies may be needed to overcome intrinsic or acquired resistance (Gray-Schopfer et al., 2007; Poulikakos and Rosen, 2011).”
- Survival in BRAF V600-mutant advanced melanoma treated with vemurafenib. (2012, neutral): “Palmar–plantar erythrodysesthesia 13 (10) 2 (2) —”
- Phosphatase‐mediated crosstalk between MAPK signaling pathways in the regulation of cell survival (2008, background): “Several other studies, including work by Rosen and collaborators using chemical inhibition of the B-Raf V600E chaperone Hsp90, have further validated MEK-ERK pathway inhibition as an attractive opportunity for cancer therapy (21, 25, 26).”
- Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. (2008, positive): “The nonuniform expression of p16 INK4a in nevi has prompted speculation that senescent cells secrete a senescence-inducing agent that acts upon neighboring cells (Gray-Schopfer et al., 2007).”
- Kinase-Dead BRAF and Oncogenic RAS Cooperate to Drive Tumor Progression through CRAF (2010, background): “It has been shown that V600EBRAF is 500-fold activated, can stimulates constitutive MEK–ERK signaling in cells (Gray-Schopfer et al., 2007) and induce melanoma in mice (Dankort et al., 2009; Dhomen et al., 2009), showing that it can be a founder mutation in melanoma.”
- Broad targeting of resistance to apoptosis in cancer (2015, background): “Activated ERK in turn specifically phosphorylates a number of nuclear and cytoplasmic substrates including the ETS transcription factor, which has the net effect of providing a pro-growth and pro-survival signal [209].”