Division of Molecular thoracic Oncology

Prof. Dr. Rocio Sotillo

Primary lung epithelial cells from TetO-Mad2/CCSP-rtTA/H2B-GFP mice grown in 3D culture. Overexpression of Mad2 arrests cells in mitosis and leads to chromosome missegregation.
© dkfz.de

Lung cancer is the leading cause of cancer-related deaths worldwide. During the evolution of the cancer genome, additional alterations are acquired, which often accelerate tumour growth. These alterations are translated into unique gene expression profiles that determine the malignant phenotype, including aggressiveness and therapeutic response. We employ state-of-the-art genetically engineered mouse models to understand lung cancer development considering different oncogenic drivers and genomic alterations and aim to also uncover potential markers of poor therapeutic responses.

By integrating lineage tracing mouse models, CRISPR/Cas9 technology, unbiased epigenome and single-cell transcriptome methods, we have mapped the evolutionary pathways of the cells that originate Eml4-Alk rearranged lung tumours. We focus on deciphering a comprehensive molecular characterization of Eml4-Alk driven lung adenocarcinomas and to develop new biomarkers using functional perturbations in autochthonous mouse models.

Our group has also a long-standing interest in cancer aneuploidy and chromosomal instability (CIN). Using a CIN mouse model of breast cancer, we have recently demonstrated that CIN is a mechanism to circumvent oncogene addiction. Further, we have developed and adopted innovative mouse models of human breast and lung cancer to study each step of these phenomena. These models provide a suitable setting to look at the molecular mechanisms and the influence of the immune system that orchestrates genetic instability and tumour heterogeneity as cardinal characteristics of human cancer.

Our lab has also a strong interest in the development of novel mouse models to better understand how cytosine deaminases are involved in human cancer. Our research will leverage unique systems empowering the performance of translational therapeutic studies.

To further strengthen our team we are constantly looking for talented scientists (Master students, PhD students, postdocs). In case of interest you can contact us directly (with your CV and a motivation letter).

Contact

Prof. Dr. Rocio Sotillo
Molecular thoracic Oncology (B220)
Deutsches Krebsforschungszentrum
Im Neuenheimer Feld 280
69120 Heidelberg
Tel: +49 6221 423691

Selected Publications

  • Rowald K, Mantovan M, Passos, J, Buccitelli C, Mardin BR, Korbel JO, Jechlinger M, Sotillo R.(2016) Negative selection and chromosome instability induced by Mad2 overexpression delay breast cancer but facilitate oncogene-independent outgrowth. Cell Rep.15(12): 2679-91.
  • Sotillo, R., Hernando, E., Diaz-Rodriguez, E., Teruya-Feldstein, J., Cordon-Cardo, C., Lowe, S.W., Benezra, R. (2007). Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Cancer Cell 1, 9-23.
  • Schvartzman, J.M., Duijf, P.H., Sotillo, R., Coker, C., Benezra, R. (2011). Mad2 is a critical mediator of the chromosome instability observed upon Rb and p53 pathway inhibition. Cancer Cell 19, 701-14.
  • Sotillo, R., Schvartzman, J.M., Socci, N.D., Benezra, R. (2010). Mad2-induced chromosome instability leads to lung tumor relapse after oncogene withdrawal. Nature 464, 436-440.
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