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Molecular Genetics: Anton Berns


Anton Berns, Ph.D ProfessorSr.Group Leader

About Anton Berns

Experimental work in the Anton Berns lab stopped.

Experimental work in my lab ended in May 2019. Some of the projects are being continued by postdocs and former colleagues. I remain active as advisor, reviewer, and as board member of supervisory committees and national and international organisations dedicated to cancer research.

Research interest:

Mouse Cancer Models
The aim was to utilize genetically engineered mouse models to define the (epi)genetic lesions involved in tumor initiation, progression, metastasis and tumor maintenance. These models were particularly suited to design and evaluate new intervention strategies.

Inducible mouse models
We have made a significant investment in developing new mouse models for a variety of tumors, using Cre/Lox mediated switching of tumor suppressor genes and oncogenes. Both transgenesis and somatic gene transfer are employed to express Cre recombinase and other genes or shRNAs in a regulatable fashion. The methodology enabled us to switch multiple oncogenes and/or tumor suppressor genes within cells in vivo at a defined time and to monitor the relevance of these genes for tumor initiation and progression. The induction of highly specific tumors within a narrow time window permited us to correlate specific genetic lesions with distinct tumor characteristics. The general picture that transpires from these studies is that the mouse cancer models show closer resemblance to the human condition when they share the same mutations. By applying sensitive in vivo imaging techniques to follow tumor growth and metastatic spread in real time in animals we not only followed tumor development longitudinally but also monitored response to genetic and pharmacological interventions.

Thoracic tumors
We focused on thoracic tumors: small cell lung cancer (SCLC), non-small cell lung cancer (NSCLC), squamous cell carcinoma (SCC) and mesothelioma. Using different sets of conditional tumor suppressor genes and oncogenes all the thoracic tumors can be induced specifically. When, for example,Rbandp53are inactivated specifically in lung, SCLC develops in nearly 100% of the mice. These tumors closely resemble human SCLC and are often heterogeneous consisting of different cell types, with either neuroendocrine or mesenchymal features. Subcutaneous grafting of each of the cell types independently gave rise to localized tumors that retained the features of the inoculated cells. However, grafting mixtures resulted in local growth as well as metastasis of the neuroendocrine cells to liver indicating that the non-neuroendocrine cells in the graft endowed the neuroendocrine cells with metastatic potential. This shows functionality of tumor cell heterogeneity. We try to uncover the underlying signaling.

An important question in our studies was the role of the cell-of-origin of these tumors. We address this by switching oncogenes and tumor suppressor genes specifically in Clara cells, Alveolar type II cells, neuroendocrine cells, basal epithelial cells of lung and in the mesothelial lining of the thoracic cavity. It appears that both the cell-of-origin and the introduced genetic lesions are critical determinants of the phenotypic characteristics of the resulting tumors. We are inquiring whether the cell of origin might also explain some of the unique features of the tumor subtypes in humans.

We were making these models more versatile by re-derivation of ES cells from them and equipping these with DNA exchange cassettes that allow us to swiftly introduced additional oncogenes, inducible shRNAs or reporters in order to test their contribution to the tumor phenotype or to the response to intervention. In this way we could also quickly evaluate the importance of putative cancer genes found by the sequencing DNA of human cancers. Furthermore, transposon-based insertional mutagenesis was conducted in these models to identify genes and pathways that strongly synergize with the driver mutations genetically inserted in these models. This will providfe us with clues what to look for in the cognate human tumors.

Parallel to these experiments we developed protocols to establish cultures from human mesothelioma and to propagate these tumors as patient derived xenografts (PDX).



Paul Krimpenfort

Academic Staff


My main scientific interest is the tumor suppressive function of the Ink4 gene family encoding the Cdk4/6 inhibitors p15Ink4b, p16Ink4a, p18Ink4c and p19Ink4d. Since Cdk4 and Cdkn6 stimulate G1 progression by phosphorylating Rb, the primary effect of Ink4 inactivation is thought to be the loss of cell cycle control. However, apart from their role in cell cycle control recent observations suggest the implication of the Ink4 proteins in tumor cell behaviour e.g. migration and invasiveness. An important issue is if and to what extent the Ink4 genes are redundant.

In addition, I am also involved in the NKI Transgenic Facility and I am a member of the Animal Experiment Committee (DEC) of the NKI.

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Key publications View All Publications

  • Mouse models for lung cancer

    Mol Oncol. 2013 Apr;7(2):165-77

    Kwon MC, Berns A.


    Link to Pubmed

Recent publications View All Publications

  • Awakening of “Schlafen11” to tackle Chemotherapy Resistance in SCLC.

    Cancer Cell. 2017;31:169-171.

    Berns, K., and Berns, A.

    Link to Pubmed
  • Comprehensive pharmacogenomic profiling of malignant pleural mesothelioma identifies a subgroup sensitive to FGFR inhibition.

    Clin Cancer Res. 2017; 23:1172.

    Quispel-Janssen JM,Badhai J, Schunselaar L, Price S, Brammeld JS, Iorio F, Kolluri, K., Garnett,M., Berns, A., Baas, P., McDermott, U., Neefjes, J., and Alifrangis, C.

    Link to Pubmed


  • Office manager

    Marij Degen

  • E-mail


  • Telephone Number

    +31 (0)20 512 9134



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