• sense clinically
  • think mechanistically
  • act interdisciplinarily
  • treat innovatively

Dr. Michela Serresi

Junior Group Leader
Max Delbrück Center for Molecular Medicine (Helmholtz Association)
Robert-Rössle-Straße 10
13125 Berlin

Michela.serresi@ mdc-berlin.de

Scientific Scope

Metastasis is the most common and severe complication arising in cancer patients. A question in this field that is still very much open, is how a primary cancer cell acquires metastatic traits and what are the molecular events governing this process.

Our research activity is to identify the main drivers of metastasis and clarifying their mechanisms of action. This information would enable:

  • identifying high-risk patients, and
  • design patient-tailored therapies.

We study this topic in a mouse model for lung cancer, which is the most common cancer in the western world and death by lung cancer is often caused by metastases.

We are interested in understanding the molecular mechanisms underpinning lung cancer dissemination to distal organs. While next generation sequencing technologies allowed to better understand the genetic basis of cancer, discriminating alterations that are driving the processes of tumor evolution from passenger mutations still remains a major challenge.  Moreover, extensive sequencing efforts of evolving primary and secondary tumors indicate that cancer genomes can be extremely complex and patients’ specific. Genetic screens represent powerful tools for identifying causal genes in various hallmarks of cancer progression. To address this topic, we are exploiting in vivo CRISPR-Cas9 screening strategies with dedicated and validated lung cancer animal models.

Molecular Oncology

Max-Delbrück-Center for Molecular Medicine (MDC)

Group Members

  • Sonia Kertalli, phD candidate BSIO
  • Jikke Wieriks, Erasmus student Avans University of Applied Sciences, Netherlands
  • Marialucia Massaro, Erasmus student University of Trento, Italy

Selected References

  • Ezh2 inhibition in Kras-driven lung cancer amplifies inflammation and associated vulnerability. Serresi M , Siteur B,  Hulsman D,  Company C, Schmitt MJ, Cor L , Morris B, Cesaroni M,  Proost N,   Beijersbergen R , van Lohuizen  M and Gargiulo G. J Exp Med. 2018 Dec 3;215(12):3115-3135. doi: 10.1084/jem.20180801. Epub 2018 Nov 28
  • Polycomb and lung cancer: when the dosage makes the (kind of) poison. Gargiulo G, Citterio E, Serresi M Mol Cell Oncol 2016 Feb, 2 DOI:10.1080/23723556.2016.1152345
  • Polycomb repressive complex-2 is a barrier to Kras-driven inflammation and epithelial-mesenchymal transition in non-small cell lung cancer. Serresi M, Gargiulo G, Proost N, Siteur B, Cesaroni M, Koppens M, Xie H, Sutherland KD, Hulsman D, Citterio E, Orkin S, Berns A and van Lohuizen M Cancer Cell 2016 Jan 11;29(1):17-31. doi: 10.1016/j.ccell.2015.12.006.
  • In vivo shRNA screens in solid tumors. Gargiulo G, Serresi M, Cesaroni M, Hulsman D, van Lohuizen M Nature Protocol 2014 Dec 9;(12): 2880-902
  • In vivo RNAi screen for BMI1 targets identifies TGF-B/BMP-ER stress pathway as key regulators of neural- and malignant glioma stem cell homeostasis. Gargiulo G, Cesaroni M, Serresi M, de Vries N, Hulsman D, Bruggeman SW, Lancini C, van Lohuizen M. Cancer Cell. 2013 May 13; 23(5):660-76