Inflammation Pharmacology and Cell Death
Kaufmann Group

Our lab studies how cells decide to live or die, and why this matters for health and disease. We focus on a group of proteins called the BCL-2 family, which act as key “switches” controlling a major form of programmed cell death (PCD), known as apoptosis. When apoptosis is disturbed, it can contribute to diseases such as cancer or chronic inflammation. We are also interested in BH3 mimetics, a new class of targeted anti-cancer drugs that directly target the apoptotic machinery by inhibiting pro-survival BCL-2 family proteins. Our research investigates how these compounds kill cancer cells, how resistance arises, and how their therapeutic efficacy can be improved. Another longstanding major focus is the pro-apoptotic BCL-2 family member BOK, which is often reduced in cancer. We have shown that BOK not only influences cell death but also affects how cells grow, respond to stress, and regulate the metabolism of nucleotides.

We also investigate how immune cells, especially neutrophils, die during inflammation. These cells are essential for fighting infections but can cause damage to surrounding healthy tissue if they persist too long. We study how signals from the environment control their lifespan and how different types of cell death interact. This includes understanding how cells switch between apoptosis (a non-inflammatory form of PCD) and necroptosis (a more inflammatory form of PCD), which could help develop new treatments for chronic inflammatory diseases.
Another focus is on allergic effector cells, such as mast cells and basophils. We study how these cells respond to stress and how their survival is regulated. Building on this, we have developed cell model systems that allow precise and standardized testing of allergic reactions in vitro. These platforms can improve diagnosis of allergies, including many food allergies, and help us better understand both classical (IgE-driven) and non-classical (“pseudoallergic”) responses.

         

Project leader: Prof. Thomas Kaufmann

Image: Philippe JeanRichard

Connecting BOK to DNA damage in lung cancer

BOK is a member of the cell death-regulating BCL-2 family and is frequently repressed in cancer. Recent work identified an unexpected role of BOK in nucleotide metabolism (PMID: 31311867). In this project, we found that loss of BOK makes p53-deficient lung cancer cells more vulnerable to DNA damage and highly dependent on ATR-mediated DNA repair pathways for survival. By inhibiting ATR with the clinically relevant inhibitor ceralasertib, we induced pronounced DNA damage and cell death specifically in BOK/p53-deficient tumour cells. Our findings uncover a new connection between BOK, nucleotide metabolism, and genome stability, and suggest that reduced BOK levels may represent a therapeutically exploitable vulnerability in lung cancer (JeanRichard et al 2026; and highlighted in editorial).

Project leader: Prof. Thomas Kaufmann

Image: Thomas Kaufmann

Targeting lung cancer cells with BH3 mimetics

Non-small cell lung cancer (NSCLC) is often resistant to conventional therapies that rely on DNA damage to trigger apoptosis. In this project, we investigate whether directly targeting the apoptotic machinery could overcome this resistance. We found that simultaneous inhibition of the pro-survival proteins BCL-XL and MCL-1 using BH3 mimetics induced extremely rapid and potent apoptosis in the majority of NSCLC cell lines tested — often within less than one hour and independent of p53 status. Importantly, newer BCL-XL inhibitors and PROTAC-based approaches retained strong efficacy while potentially reducing side effects. Our findings identify a major apoptotic vulnerability in NSCLC with promising therapeutic potential. Besides therapeutic efficacy we are also interested in understanding resistance mechanisms that may develop upon BH3 mimetics treatment.

Project leader: Prof. Thomas Kaufmann

Image: Gergely Gyimesi

Regulation of BOK mRNA stability by TRIM28

TRIM28 is best known as a transcriptional regulator involved in chromatin organisation, gene silencing, DNA damage responses, and cancer progression. Building on our previous discovery that TRIM28 negatively regulates the pro-apoptotic protein BOK through elements in the BOK mRNA 3′UTR (PMID: 30471638), this project uncovered an unexpected new role for TRIM28 as an RNA-binding protein. We identified a domain in TRIM28 as a novel RNA-binding domain that directly binds BOK mRNA and promotes its degradation. Importantly, this process also depends on the RING domain of TRIM28, which confers E3 ubiquitin ligase activity, indicating that ubiquitination is a critical part of this newly identified RNA decay pathway. We are currently investigating which proteins are modified by TRIM28-dependent ubiquitination and how this regulates mRNA stability. Since related TIF1 family members (TRIM24, TRIM33, and TRIM66) also contain the RNA-binding domain, we are further exploring whether RNA binding represents a broader function of the TIF1 family, which additional mRNAs are targeted, and in which cancer types these mechanisms are relevant. Notably, we observed an inverse correlation between TRIM28 and BOK expression in lung cancer and other carcinomas, suggesting that this pathway may contribute to tumour progression.

Project leader: Prof. Thomas Kaufmann

New In Vitro Approaches to Study Allergy

Our lab has co-developed an advanced in vitro mast cell activation platform that enables sensitive and standardized functional testing of allergic reactions using human IgE (PMID: 34418424). This mast cell activation test (MAT)-based technology allows us to investigate how food allergens trigger immune responses and how processes such as gastrointestinal digestion or food processing influence allergenicity. Current projects focus on cow milk allergy and αGal syndrome (red meat allergy). We also study pseudoallergic reactions, which mimic classical allergies but occur independently of IgE. Our goal is to improve the mechanistic understanding, diagnosis, and future treatment of allergic diseases.

Prof. Dr. Thomas Kaufmann, PhD

Group members

former Group members

Ali Jazaeri, PhD (2021-2026)

Oihane Ofogo, internship student (2025)

Baris Budak, master student (2024-2025)

Fredrik Holm, master student (-2025)

Jana Lea Roth (2023)

Lea Wilhelm, MSc Pharm. (2022)

Dr. Samara Naim, PhD (2021); postdoc (2021)

Livia Pulfer, MSc. Pharm. (2020-2021)

Fabrizo Motta, MSc (2020-2021)

Peymaneh Zahiroddini MSc (2019 - 2020)

Dr. Yuniel Fernandez Marrero, PhD (2017); postdoc (2017-19)

Noah Schnüriger, MSc (2019)

Estefanía Lucendo Gutiérrez, visiting PhD student Valencia (2019)

Anthony Marchand, visiting student EPFL (2018)

Ramona Reinhart, PhD (2017)

Angela Fallegger, BMSc (2017)

Dr. Tatiana Rabachini de Almeida, postdoc (2011- 2016)

Simone Wicki, PhD (2016)

Nicole Tochtermann, MMed (2016)

Dr. Erika Moravcikova, postdoc (SciEx fellow, 2014-15)

Emanuel Lauber, BMSc (2015)

Ursina Gurzeler, PhD (2013)

Nohemy Echeverry, PhD (2012)

Laetitia Roh, Diploma/BSc (2011)

Short Curriculum Vitae

Prof. Dr. THOMAS KAUFMANN, PhD

Date of Birth:  May 16, 1976

Nationality:  Swiss

Office Address:  Institute of Pharmacology
  Medical Faculty
  University of Bern
  Inselspital, INO-F
  3010 Bern, CH-Switzerland
  Email: thomas.kaufmann@pki.unibe.ch
  Tel: +41 (0)31 684 09 06

ACADEMIC DEGREES
2014 Associate Professor, Medical Faculty, University of Bern (CH)
2011 'Venia Docendi' (Habilitation) in Experimental Pharmacology, University of Bern (CH)
2003  PhD in Biochemistry, Institute of Biochemistry, University of Fribourg (CH)
2000  Diploma in Biochemistry, Institute of Biochemistry, University of Fribourg (CH)

CAREER HISTORY AND POSITIONS HELD
2013-  Principal Investigator (Dozent I), Institute of Pharmacology, University of Bern, Switzerland
2008-2013 SNSF Assistant Professor, Institute of Pharmacology, University of Bern, Switzerland
2004-2007 Postdoctoral research fellow with Prof Andreas Strasser, Molecular Genetics of Cancer Division, The Walter and Eliza Hall Institute of Medical Research (WEHI), Melbourne, Australia
2003-2004 Postdoctoral research fellow Institute of Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, Germany
2000 - 2003 PhD-student with Prof Christoph Borner, Institute of Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, Germany
1995-2000 Studies in Biochemistry, University of Fribourg, Switzerland

GRANTS, FELLOWSHIPS AND AWARDS
2014 - 2017 SNSF Project Grant (D-A-CH) 310030E-150805
2014 - 2017 SNSF Project Grant 31003A_149387
2013 - 2015 Swiss Cancer League Research Grant; KFS-3014-08-2012
2012 - 2014 3R Foundation Research Grant; 127-11
2012 – 2013 Prolongation SNSF Professorship, Swiss National Science Foundation; PP00P3_139190/1
2008 – 2012 SNSF Professorship, Swiss National Science Foundation; PP00A-119203
2011 Best Poster Award, 19th ECDO meeting, Sep 14-17 2011, Stockholm (SWE)
2009 Research grant from the ‘Novartis Foundation for Biological-Medical Research’, Novartis, Basel (CH)
2006 – 2007 Postdoctoral fellowship for advanced researchers, Swiss National Science Foundation; PA00A-111430
2006 Postdoctoral fellowship ‘Novartis Foundation, formerly Ciba-Geigy-Jubiläumsstiftung’ (Novartis, Switzerland)
2005/2006 Postdoctoral fellowship ‘Roche Research Foundation’ (Roche, Switzerland)
2004 – 2005 Postdoctoral fellowship for prospective researchers, Swiss National Science Foundation; PBFRA-104383
2004 ’Faculty Prize’, Faculty of Science, University of Fribourg (CH)
2000 ’Syngenta Crop Protection Monthey SA 2000’ prize

MEMBERSHIPS AND HONORARY POSTS
- Member of the World Allergy Organization (WAO) Special Committee on Eosinophils, Mast Cells & Basophils (since 2013)
- Editorial Board Member of peer-reviewed journals: Allergy, Cell Death and Disease, Frontiers in Molecular and Cellular Oncology
- Member of the expert committee 'Cell Biology' within the Graduate School for Cellular and Biomedical Sciences, University of Bern; since 2009
- Member of the following associations: Swiss Society for Allergology and Immunology (SAAI), since 2013; European Cell Death Organization (ECDO), since 2008; Swiss Society of Experimental Pharmacology (SSEP), since 2008; Swiss Society for Biochemistry (BIO), since 2000; Swiss Society for Cell Biology, Molecular Biology and Genetics (ZMG), since 2000

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