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Oncogenomics: William Faller

William Faller

William Faller, Ph.DJr. Group Leader

About William Faller

Research interest

The Faller lab is studying the role that RNA translation plays in models of cancer. In recent years it has become clear that cancer cells use multiple mechanisms to up-regulate oncogenes and down-regulate tumour suppressor genes. Much of the focus of this research has been on modulators of transcription; however we now estimate that transcriptional control only explains 30% to 40% of protein level variation. One of the major reasons for this discrepancy is thought to be differences in RNA translation.

Colorectal cancer (CRC) is the second most common cause of cancer mortality, with around 700,000 deaths annually. While this number has been steadily decreasing over the last 4 decades, this has largely been as a result of screening programs, and our treatment options have lagged behind.

Our lab uses mouse models of CRC to study the effect that changes in RNA translation have on this disease. We have previously shown that CRC cells require increased RNA translation in order to proliferate. We also showed that by blocking this RNA translation we could protect mice from the disease. Our aim is now to fully understand the role that RNA translation plays, in order to identify therapeutic targets and potentially develop drugs that can target this process.

We have also pinpointed the elongation phase of RNA translation as being a crucial level of regulation in CRC. Interestingly, this regulation via elongation is specific for a subset of pro-proliferative RNAs. We want to understand why certain genes are regulated in this manner and others not. If we can understand this mechanism it may provide us with a rationale for targeting abnormal elongation in cancer with chemotherapy. Alternatively, by understanding which particular genes are regulated like this, it may be possible to target them instead. For example, we have shown that Cyclin D3 is controlled by elongation, while other highly homologous family members (Cyclin D1 and Cyclin D2) are not. Given its role as a regulator of the cell cycle, we are now trying to elucidate the importance of Cyclin D3 in the context of cancer.

Our lab aims to combine the use of innovative technologies with state-of-the-art mouse models, in order to give us a much more thorough understanding of the role that RNA translation plays in cancer, while at the same time identifying many new, exciting therapeutic targets for the disease.



Rob van der Kammen

Technical Staff


I am an experienced technician (>25 years) in cell biology, molecular biology and mouse models (In possession of art.12).   Started my career in Utrecht under supervision of Dr. Jansen and Dr de Pagter-Holthuizen where I worked on IGF1 and IGF-2.

In 1988 I joined the group of Dr. J Collard at the NKI , where I worked quite succesfully on Tiam1(mousemodels, skincancer). In 2009  I shifted gear and moved to the group of Metello Innocenti and worked on the formin Diaph3 and on  conditional mouse models regarding ARPC4 deletionto study the role of the Arp2/3 complex  in the skin. At present I relocated to the group of William Faller,  a new appointed groupleader at the NKI where I will work on intestinal cancer models (in vivo as well as in vitro).



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Eric Pintó Barbera

PhD Student


I studied Biomedical Science at the University of Lleida (Spain) in which I carried out a project working on the role of VEGFR2/3 in the p110a-dependent sprouting angiogenesis using mouse models.

I obtained my Master's degree in Cancer Research (University of Barcelona, Spain) and performed an internship at the NKI. I worked on a CRIPSR-Cas9-based screen to identify AR-associated enhancers that are important for proliferation of prostatic cancer cells.

My PhD project aims to study the role of RNA translation in the oncogenic process in APC-driven models of colorectal cancer with the ultimate goal of identifying novel targets for therapy.

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Joana Silva



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Key publications View All Publications

  • mTORC1-mediated translational elongation limits intestinal tumour initiation and growth.

    Nature. 2015;22:517:497-500

    Faller WJ, Jackson TJ, Knight JR, Ridgway RA, Jamieson T, Karim SA, Jones C, Radulescu S, Huels DJ, Myant KB, Dudek KM, Casey HA, Scopelliti et al.

    Link to Pubmed

Recent publications View All Publications

  • A YY1-dependent increase in aerobic metabolism is indispensable for intestinal organogenesis.

    Development. 2016;143:3711-3722

    Kumar N, Srivillibhuthur M, Joshi S, Walton KD, Zhou A, Faller WJ, Perekatt AO, Sansom OJ, Gumucio DL, Xing J, Bonder EM, Gao N, White...

    Link to Biologist
  • Fascin expression is increased in metastatic lesions but does not correlate with progression nor outcome in melanoma

    Melanoma Res. 2015;25:169-72

    Ma Y, Faller WJ, Sansom OJ, Brown ER, Doig TN, Melton DW, Machesky LM.

    Link to Pubmed


  • Office manager

    Marij Degen

  • E-mail

  • Telephone Number

    +31 (0)20 512 9134



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