Daniel Peeper is the Head of the Department of Molecular Oncology & Immunology and chairs both the Scientific Faculty Council and the Translational Research Board at the Netherlands Cancer Institute (NKI). He holds a professorship in Functional Oncogenomics at the VU University Medical Center (VUmc) and was elected as member of Oncode (a funded network of elected scientists in fundamental oncology from across the Netherlands).

Peeper studied Medical Biology at the VU University and received his PhD in the laboratory of Alex van der Eb at the University of Leiden (1994), for his work on adenoviral oncoproteins and cell cycle proteins. He received his postdoctoral training in the laboratories of Mark Ewen (Dana-Farber Cancer Institute, Harvard Medical School, Boston) and René Bernards (NKI). In 2002, Peeper became Assistant Professor and three years later Associate Professor at NKI. Also in that year, he was elected as an EMBO Young Investigator.

In 2002 and 2006, he received NWO VIDI and VICI awards, respectively for his functional oncogenomic studies. In 2007, he received the first KWF Queen Wilhelmina Award, by her Majesty the Queen Beatrix and the minister of Education, for his work on melanoma in collaboration with W. Mooi. In the same year, he received the Society for Melanoma Research Jr. Researcher Award. In 2008, Peeper was appointed affiliate Professor at the VUmc and was elected as EMBO member. In 2013, he received, together with colleagues including A Berns and M Stratton (Sanger Inst.), an ERC Synergy grant (€15 million) for the development of combinatorial cancer therapy. In 2015, he received the Outstanding research award by the Society for Melanoma Research and in 2016 he was elected to become a member of Academia Europaea. In 2017, he was invited to join Oncode.

Peeper has been a member of the European Association for Cancer Research (EACR) Board since 2013, and he also serves on the EACR Conference committee.

Highlights of the Peeper lab include their discoveries that a genomic screen for anoikis resistance can be used to identify metastasis genes (Nature 2004); that Oncogene-Induced cellular Senescence (OIS) serves as a potent in vivo tumor suppressor mechanism limiting cancer progression (Nature 2005; New Engl J Med 2006); the identification of several OIS-associated oncogenes (Nat Cell Biol 2005; Nat Rev Cancer 2006); that OIS is associated with the activation of an inflammatory transcriptome (Cell 2008; Nat Rev Cancer 2009; Genes Dev 2010); the identification of a novel candidate melanoma suppressor gene (EMBO J, 2011) and of a key mechanism of human melanomagenesis involving abrogation of OIS by reduction of PTEN expression (Genes Dev 2012). His laboratory also identified a prognostic breast cancer genetic signature and a factor essential to drive metastasis (PNAS 2013) and discovered that pyruvate dehydrogenase kinase (PDK1) acts as a critical switch for the execution of OIS and serves as an attractive drug target in melanoma (Nature 2013). Peeper and his team demonstrated the power of in vivo shRNA dropout screens for drug target identification (Cell Rep. 2014, Oncotarget 2016) and discovered a new mechanism mediating broad resistance to targeted therapy in melanoma (Nature Commun 2014). They also identified multiple resistance mechanisms to BRAF targeted therapy in a melanoma patient (EMBO Mol Med 2015) and developed a new bioinformatic tool to determine copy number alterations in cancer (Genome Biol 2015).

In addition, they established a large melanoma PDX platform that they used to identify a novel resistance mechanism of melanoma to BRAF inhibition (Cell Rep. 2016), and identified a prognostic genetic network driving human breast cancer (Oncotarget, 2017). Recently, they dissected the mechanism of cancer drug addiction and provided PoC of how this vulnerability may be used clinically (Nature 2017). Most recently, his lab developed a new concept for rational treatment combination: in collaboration with the biotech company Genmab it was demonstrated that melanoma intratumor heterogeneity is effectively targeted by a combination of an AXL-ADC (antibody-drug conjugate) and BRAF pathway inhibitors. By attacking distinct tumor subpopulations, these treatments act in a cooperative fashion, ensuring more durable responses (Nature Medicine 2018).

• 2016: Elected Member of Academia Europaea

• 2015: Society for Melanoma Research (SMR) Outstanding Researcher Award

• 2009: Queen Wilhelmina Award by the Netherlands Cancer Society

• 2008: Elected EMBO Member

• 2007: Society for Melanoma Research (SMR) Jr. Researcher Award

• 2006: VICI Award by the Netherlands Organisation for Scientific Research (NWO)

• 2005: Elected EMBO Young Investigator (YIP)

1. Boshuizen, J., Koopman, L. A., Krijgsman, O., Shahrabi, A., Gresnigt–van den Heuvel, E., Ligtenberg, M. A., ... & Pencheva, N. (2018). Cooperative targeting of melanoma heterogeneity with an AXL antibody-drug conjugate and BRAF/MEK inhibitors. Nature medicine.

2. Kong, X., Kuilman, T., Shahrabi, A., Boshuizen, J., Kemper, K., Song, J. Y., ... & Peeper, D. S. (2017). Cancer drug addiction is relayed by an ERK2-dependent phenotype switch. Nature, 550(7675), 270.

3. Kaplon, J., Zheng, L., Meissl, K., Chaneton, B., Selivanov, V. A., Mackay, G., ... & Gottlieb, E. (2013). A key role for mitochondrial gatekeeper pyruvate dehydrogenase in oncogene-induced senescence. Nature, 498(7452), 109.

4. Kuilman, T., Michaloglou, C., Vredeveld, L. C., Douma, S., van Doorn, R., Desmet, C. J., ... & Peeper, D. S. (2008). Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. Cell, 133(6), 1019-1031.

5. Michaloglou, C., Vredeveld, L. C., Soengas, M. S., Denoyelle, C., Kuilman, T., Van Der Horst, C. M., ... & Peeper, D. S. (2005). BRAF E600-associated senescence-like cell cycle arrest of human naevi. Nature, 436(7051), 720.