prof. Olivier De Wever (PhD)
Metastasis is the main cause of death for cancer patients. To colonize distant organs, cancer cells communicate with their environment to overcome obstacles such as infiltration of foreign tissues and adaptation to supportive niches. Although metastasis is an inefficient process; we currently fail to understand it, to prevent it and to have durable responses.
In the past 16 years I and my research group dedicated its resources to improve the understanding of the communicative determinants between cancer cells and their host tissue. The results of this research can be clustered in 4 topics:
1) The creation of models to study metastasis-associated cellular activities
2) The identification of adaptive communication skills between cancer cells and host cells (cancer-associated adipose tissue and fibroblast)
3) The impact of radiotherapy on the communication skills between cancer cells and host cells
4) The exploitation of tumor-envrionment interactions as therapy or biomarker
Since I started my PhD I dedicated my scientific life to understand the involvement of the tumor environment to cancer progression. During my PhD I published seminal fundamental papers showing the importance of cancer-associated fibroblasts (CAFs) in colon cancer progression (De Wever et al., FASEBJ 2004, J Pathol 2003, J Cell Science 2004) which resulted in more than 1000 cumulative WOS citations. During my post-doc I continued to focus on the origin of CAFs (De Boeck et al., GUT 2013) and expanded my research into adipose tissue (Lapeire et al., Cancer Res 2014) and the secretory mechanisms of pro-metastatic signals (Hendrix et al., JNCI 2010, Cancer Res 2010). During my post-doc I was a regular visiting scientist at NIH (Bethesda, US) and Centre de Recherche Hôpital Saint-Antoine (Paris, France). The current lab is an ecosystem to study tumor-environment interactions including design of model systems (De Jaeghere et al., Biomaterials 2018), response to therapy of CAFs (Tommelein et al., Cancer Res 2018), and exploitation of CAFs as therapy (De Vlieghere et al., Biomaterials 2015). Several review papers are published focusing on tumor environment interactions (De Wever et al., Semin Cancer Biol 2014; De Jaeghere et al., Trends Cancer 2019). Extracellular vesicles are one communicative determinant that is under investigation in collaboration with the Hendrix lab (De Wever and Hendrix EMBOJ 2019). In my 20 years long scientific career I published more than 175 A1 papers, I have an H-index of 44 and I’m editorial board member of an important oncology journal; Cancer Research.
Laboratory of Experimental Cancer Research
- prof. Olivier De Wever - principal investigator, associate professor
- prof. An Hendrix - principal investigator, assistant professor
- dr. Elly De Vlieghere - post-doctoral fellow
- Joeri Tulkens - doctoral fellow
- Elien Alderweireldt - doctoral fellow
- dr. Emiel De Jaeghere (MD) - doctoral fellow
- dr. Arne Peirsman (MD) - doctoral fellow
- Christophe Mangodt - doctoral fellow
- Eva Blondeel - doctoral fellow
- Sam Ernst - doctoral fellow
- Robin Boiy - doctoral fellow
- Zihan Xia - doctoral fellow
- Mohammad Ghiasloo - doctoral fellow
- Stephanie Decloedt - lab technician
- Johanna Mestach - lab technician
- Sofie De Geyter - lab technician
- Sandor Dedeyne - bio informatician
- Wendy De Rycke - secretary
- Cancer-associated adipose tissue promotes breast cancer progression by paracrine Oncostatin M and Jak/STAT3 signaling. Cancer Res 2014
- The impact of disparate isolation methods for extracellular vesicles on downstream RNA profiling. J. Extracell Vesicles 2014
- Carcinoma-associated fibroblasts provide operational flexibility in metastasis. Seminars in Cancer Biology, 2014.
- Tumor-environment biomimetics delay peritoneal metastasis formation by deceiving and redirecting disseminated cancer cells. Biomaterials, 2015.
- JAK3 deregulation by activating mutations confers invasive growth advantage in extranodal nasal-type natural killer cell lymphoma. Leukemia, 2013.
- Bone marrow-derived mesenchymal stem cells promote colorectal cancer progression through paracrine neuregulin 1/HER3 signaling. Gut, 2013.
- Radiation-induced lung damage promotes breast cancer lung-metastasis through CXCR4 signaling. Oncotarget, 2015
- An ex(o)citing machinery for invasive tumor growth, Cancer Res, 2010.
- Effect of the secretory small GTPase Rab27B on breast cancer growth, invasion, and metastasis, J. Natl. Cancer Inst., 2010.
- Tenascin-C and SF/HGF produced by myofibroblasts in vitro provide convergent pro-invasive signals to human colon cancer cells through RhoA and Rac. FASEB J., 2004