Protein expression in metastatic melanoma and the link to disease presentation in a range of tumor phenotypes

Yonghyo Kim, Jeovanis Gil, Indira Pla, Aniel Sanchez, Lazaro Hiram Betancourt, Boram Lee, Roger Appelqvist, Christian Ingvar, Lotta Lundgren, Håkan Olsson, Bo Baldetorp, Ho Jeong Kwon, Henriett Oskolás, Melinda Rezeli, Viktoria Doma, Sarolta Kárpáti, A. Marcell Szasz, István Balázs Németh, Johan Malm, György Marko-Varga

Research output: Contribution to journalArticlepeer-review


Malignant melanoma is among the most aggressive skin cancers and it has among the highest metastatic potentials. Although surgery to remove the primary tumor is the gold standard treatment, once melanoma progresses and metastasizes to the lymph nodes and distal organs, i.e., metastatic melanoma (MM), the usual outcome is decreased survival. To improve survival rates and life span, advanced treatments have focused on the success of targeted therapies in the MAPK pathway that are based on BRAF (BRAF V600E) and MEK. The majority of patients with tumors that have higher expression of BRAF V600E show poorer prognosis than patients with a lower level of the mutated protein. Based on the molecular basis of melanoma, these findings are supported by distinct tumor phenotypes determined from differences in tumor heterogeneity and protein expression profiles. With these aspects in mind, continued challenges are to: (1) deconvolute the complexity and heterogeneity of MM; (2) identify the signaling pathways involved; and (3) determine protein expression to develop targeted therapies. Here, we provide an overview of the results from protein expression in MM and the link to disease presentation in a variety of tumor phenotypes and how these will overcome the challenges of clinical problems and suggest new promising approaches in metastatic melanoma and cancer therapy.

Original languageEnglish
Article number767
Issue number3
Publication statusPublished - 2020 Mar

Bibliographical note

Funding Information:
This study was supported by the Berta Kamprad Foundation. This study was also supported by grants from the National Research Foundation of Korea, funded by the Korean government (2015K1A1A2028365 and 2016K2A9A1A03904900) and Brain Korea 21 Plus Project, and ICONS (Institute of Convergence Science), Yonsei University, Republic of Korea as well as the NIH/NCI International Cancer Proteogenome Consortium. This study was also supported by the Hungarian Scientific Research Fund (NOTKA 114460).

Publisher Copyright:
© 2020 by the authors. Licensee MDPI, Basel, Switzerland.

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research


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