• Publications
  • Influence
Final version of 2009 AJCC melanoma staging and classification.
Revised melanoma staging system has been made that reflect the improved understanding of this disease and will be formally incorporated into the seventh edition of the AJCC Cancer Staging Manual and implemented by early 2010. Expand
Inhibition of mutated, activated BRAF in metastatic melanoma.
Treatment of metastatic melanoma with PLX4032 in patients with tumors that carry the V600E BRAF mutation resulted in complete or partial tumor regression in the majority of patients. Expand
Improved survival with vemurafenib in melanoma with BRAF V600E mutation.
Vemurafenib produced improved rates of overall and progression-free survival in patients with previously untreated melanoma with the BRAF V600E mutation in a phase 3 randomized clinical trial. Expand
Dissecting the multicellular ecosystem of metastatic melanoma by single-cell RNA-seq
The cellular ecosystem of tumors is begin to unravel and how single-cell genomics offers insights with implications for both targeted and immune therapies is unraveled. Expand
Combined BRAF and MEK inhibition in melanoma with BRAF V600 mutations.
Dabrafenib and trametinib were safely combined at full monotherapy doses, and the rate of pyrexia was increased with combination therapy, whereas the rates of proliferative skin lesions was nonsignificantly reduced. Expand
Survival in BRAF V600-mutant advanced melanoma treated with vemurafenib.
  • J. Sosman, Kevin B Kim, +22 authors A. Ribas
  • Medicine
  • The New England journal of medicine
  • 23 February 2012
Vemurafenib induces clinical responses in more than half of patients with previously treated BRAF V600-mutant metastatic melanoma, and the median overall survival in this study with a long follow-up was approximately 16 months. Expand
Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma
The structure-guided discovery of PLX4032 (RG7204), a potent inhibitor of oncogenic B-RAF kinase activity, and a remarkably high 81% response rate in metastatic melanoma patients treated at an oral dose of 960 mg twice daily are described, demonstrating that BRAF-mutant melanomas are highly dependent on B- RAF kinases activity. Expand
Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion.
It is found that stroma-mediated resistance is common, particularly to targeted agents, and the systematic dissection of interactions between tumours and their micro-environment can uncover important mechanisms underlying drug resistance. Expand
Improved overall survival in melanoma with combined dabrafenib and trametinib.
Dabrafenib plus trametinib, as compared with vemurafenib monotherapy, significantly improved overall survival in previously untreated patients with metastatic melanoma with BRAF V600E or V600K mutations, without increased overall toxicity. Expand
RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)
The model that inhibition of ERK signalling by RAF inhibitors is dependent on levels of RAS–GTP too low to support RAF dimerization is supported and a novel mechanism of acquired resistance in patients is identified: expression of splicing isoforms of BRAF(V600E) that dimerize in a RAS-independent manner. Expand