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Proffered Paper Session 1

207 - Downregulation of USP28 confers poorer overall survival to melanoma patients and causes resistance to RAF inhibitors

Date

05 Mar 2018

Session

Proffered Paper Session 1

Presenters

Azad Saei

Citation

Annals of Oncology (2018) 29 (suppl_3): iii7-iii9. 10.1093/annonc/mdy048

Authors

A. Saei1, M. Palafox2, T. Benoukraf3, N. Kumari4, P. Iyengar3, Z.F. Bin Adam Isa3, H. Yang3, W.L. Tam1, V. Serra2, P. Eichhorn3

Author affiliations

  • 1 Genome Institute of Singapore, A*STAR, 138672 - Singapore/SG
  • 2 Vall d’Hebron Institute of Oncology (VHIO), Vall d’Hebron University Hospital, 08035 - Barcelona/ES
  • 3 Cancer Science Institute of Singapore, 117599 - Singapore/SG
  • 4 Biochemistry, National University of Singapore, 119228 - Singapore/SG
More

Resources

Abstract 207

The mutation in BRAF kinase at V600 has been frequently reported in nearly 50% of melanoma patients resulting in the hyper-activation of MAPK pathway. As such, various inhibitors which target mutant BRAF have been developed including vemurafenib and dabrafenib both of which have demonstrated significant clinical outcomes. Nevertheless, both primary and acquired resistance reduce the overall response of patients to the therapy. So, the search of efficient biomarkers to stratify melanoma patients has become an imperative subject of research to enhance the efficacy of RAF inhibitor treatments and to decrease the rate of side effects due to the therapy. The mechanism of ubiquitination in controlling various functions such as stabilization of a protein cannot be neglected. A number of ubiquitin regulatory enzymes have been already shown to act on and regulate various component of MAPK pathway.

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