MembersBolis Marco, PhD, Bioinformatics
Bossi Daniela, PhD
Bressan Silvia, Visiting Research Fellow
Ceserani Valentina, MSc, Technician
Costanzo Federico, PhD, Research Scientist
Formaggio Nicolò, PhD Student
Gianfanti Federico, Visiting Research Fellow
Impellizzieri Daniela, PhD, Technician
Mosole Simone, Research Assistant (immunohistochemistry)
Theurillat Jean-Philippe, MD, Group Leader
Vallerga Arianna, PhD student
Cancer is driven by cardinal genetic alterations that activate driver genes. Driver mutations are not only essential to initiate tumorigenesis, but are also required for tumor growth and maintenance. This raises the possibility to target these mutations, opening more specific, therapeutic opportunities to treat cancer patients.
Our research group focuses on new drivers of prostate cancer with emphasis on advanced, castration-resistant disease. We aim to explore the roles of these genes in tumorigenesis with the ultimate goal to develop new therapeutic avenues for patients suffering from prostate cancer (exemplified in Fig. 1).
In addition, our group develops new strategies to empirically tailor cancer therapy in the clinic. Patient-derived tumor cells will be used to test drug responses prior treating the patient. This approach may guide decision-making in the clinic in an individualized manner (Fig. 2).
- Functional characterization of new prostate cancer drivers implicated in chromatin remodeling and protein ubiquitylation
- Engineering of small molecules against prostate cancer targets
- Generation and engineering of patient-derived cell line models
Our group is committed to train the future generation of cancer researcher. Master thesis applications are welcome at any time and we will support you with scholarships.
- 2020 Apr;16(4):e9247 PMID: 32323921
STAT3-dependent analysis reveals PDK4 as independent predictor of recurrence in prostate cancer.
- PMID: 32250342 CDCP1 overexpression drives prostate cancer progression and can be targeted in vivo. 2020 May 1;130(5):2435-2450
- PMID: 32109420 De Novo Variants in SPOP Cause Two Clinically Distinct Neurodevelopmental Disorders. 2020 Mar 5;106(3):405-411
- PMID: 32024754 TIP5 primes prostate luminal cells for the oncogenic transformation mediated by PTEN-loss. 2020 Feb 18;117(7):3637-3647
- Janouskova H, El Tekle G, Bellini E, Udeshi ND, Rinaldi A, Ulbricht A, Bernasocchi T, Civenni G, Losa M, Svinkina T, Bielski CM, Kryukov GV, Cascione L, Napoli S, Enchev RI, Mutch DG, Carney ME, Berchuck A, Winterhoff BJN, Broaddus RR, Schraml P, Moch H, Bertoni F, Catapano CV, Peter M, Carr SA, Garraway LA, Wild PJ, Theurillat JP. Opposing effects of cancer type-specific SPOP mutations on BET protein degradation and sensitivity to BET inhibitors. Accepted for publication Nat Med Jun 2017.
- PMID: 27238081 TRIM24 Is an Oncogenic Transcriptional Activator in Prostate Cancer. 2016 Jun 13;29(6):846-858
- PMID: 25278611 Prostate cancer. Ubiquitylome analysis identifies dysregulation of effector substrates in SPOP-mutant prostate cancer. 2014 Oct 3;346(6205):85-89