Invited speakers
(will be completed)
David Sabatini
was born in New York City to Argentine immigrant parents and obtained his bachelor’s degree at Brown University in 1990 and his MD/PhD at the Johns Hopkins School of Medicine in 1997. He completed his thesis work in the lab of Solomon H. Snyder, where he discovered mTOR. Sabatini has received a number of recognitions and has also been active in the clinical translation of his work by co-founding several biotechnology companies in the Boston area. He is currently a Senior Group Leader at IOCB Boston & Prague and was previously at MIT. He studies nutrient sensing and growth control, particularly by the mechanistic Target of Rapamycin (mTOR) pathway. This pathway is the major nutrient-sensitive growth regulator in animals and plays a central role in physiology, metabolism, aging, and cancer. Sabatini discovered the mTOR protein kinase, and most other components of the pathway, including the mTOR-containing complexes mTORC1 and mTORC2, and established them as growth regulators in cells and in vivo. He determined that nutrients signal to mTORC1 through the lysosome-associated Rag GTPases and discovered their many regulators and associated nutrient sensors. In addition to his growth-related work, Sabatini also studies small molecule metabolism and is involved in technology development, such as in generating widely used genome-scale RNAi and CRISPR/Cas9 libraries as well as organellar isolation methods. He published over 300 peer-reviewed impacted publications in the most prestigious journals like Nature, Science, Nature Medicine, Cell, Cell Metabolism, Science Advances, Cancer Discovery, etc.
Arkaitz Carracedo
Dr. Arkaitz Carracedo received his PhD in Biochemistry and Molecular Biology from the Complutense University of Madrid in 2006. After four years of postdoctoral research at Memorial Sloan-Kettering Cancer Center and Beth Israel Deaconess Medical Center, Harvard Medical School (USA), he established his independent research group at CIC bioGUNE in late 2010, focusing on the unique biological characteristics of cancer cells in vitro and in vivo, with particular emphasis on metabolic alterations. He has been an Ikerbasque Research Professor since 2011 and was appointed Distinguished Scientist at the University of the Basque Country in 2023, where he previously served as Associate Professor since 2012. Dr. Carracedo has made significant contributions to the field of cancer metabolism, with 135 scientific publications and reviews, and through the organization of internationally recognized congresses. His work has been widely recognized with numerous awards and sustained funding from major national and international agencies, including three prestigious ERC grants.
Kristýna Gloc Pimková
RNDr. Kristýna Pimková, Ph.D. (KP), is a group leader of a newly established lab. KP is focusing on the molecular underpinnings of therapeutic resistance to anti-leukemic therapy. She has a long-term interest in the role of redox signalling pathways in normal and malignant blood cell development. She gained her international postdoctoral experience at the Lund Stem Cell Center (SCC) at Lund University in Sweden, where she successfully conducted a project that identified protein redox switches in hematopoietic stem cells during ontogenesis (Redox Biology, 2022). She has also participated in the project that led to significant discoveries in splicing machinery in myelodysplastic syndrome (published in Cell, 2018). KP participates in the Biomedicine PhD program, focusing on Cell Biology and Pathology, as well as Molecular and Cellular Biology, Genetics, and Virology.
Katerina Rohlenova
Katerina Rohlenova is a junior group leader at the Institute of Biotechnology, Czech Academy of Sciences (CAS), located in the BIOCEV research center. After completing her PhD with J. Neuzil at the same institute, where she characterized a novel anti-cancer drug that later progressed to a phase I clinical trial, she joined P. Carmeliet's lab at VIB in Leuven, Belgium, to study endothelial cell metabolism. In 2020, she returned to the Czech Republic to establish the Cellular Metabolism Group. Her research focuses on metabolic communication in tumors and the vascular system, aiming to uncover how nutrient exchange drives tumor growth, therapy resistance, and endothelial inflammation, with the aim to identify selective and less toxic therapeutic strategies. Her work is supported by prestigious funding, including an ERC Starting Grant and an EMBO Installation Grant, among others. She has received several awards for her scientific achievements, such as the Werner Risau Prize and the Neuron Prize for Promising Researchers.
Petra Beran Holečková
was born in Cheb. After graduation at 1st Medical Faculty, Charles University Prague she worked at Department of Radiation Oncology, Regional Hospital Cheb. From 2002 she works in Institute of Radiation Oncology, Bulovka University Hospital and 1 st Medical Faculty of Charles University Prague. She is a deputy head of the institute. She is licenced in Clinical Oncology, Radiation Oncology and Clinical Nutrition. Nutrition in Oncology: Malnutrition occurs in 30–80% of oncology patients. Its causes are very complex: it may be due not only to the tumor itself or to oncological treatment and its complications, but also to comorbidities. Malnutrition is characterized by depletion of the body’s stores of macronutrients and micronutrients. It is caused not only by factors that reduce energy intake, but also by a primarily increased energy expenditure. In oncology patients, it leads to a deterioration in quality of life, reduced physical performance, psychological difficulties, poorer tolerance and outcomes of treatment, and a worse disease prognosis. It is an independent predictive and prognostic factor. For these reasons, nutritional care can be considered one of the most important aspects of supportive care in oncology.
Francesca Matteini
Francesca Matteini is senior postdoc researcher in the team of Dr. Maria Carolina Florian at the Bellvitge Biomedicine Research Institute (IDIBELL) in Barcelona, Spain. She started her career in Italy at university of Florence, and then for her PhD she moved to Sapienza University of Rome (Italy) joining the team of Dr. Rossella Maione. Here, she demonstrated the imprinting independent role of the long non-coding RNA Kcnq1ot1, and the catalytic independent function of the Poly(ADP-ribose)polymerase 1 (PARP1) in the transcriptional regulation of MyoD target genes during skeletal muscle differentiation. In 2019 Francesca joined the team of Dr. Florian at IDIBELL in Barcelona as postdoctoral researcher. Here she investigated the role of the Bone Marrow (BM) microenvironment in Hematopoietic Stem Cell (HSC) aging, contributed to the development of iFAST3D histology, a highly sensitive and 3D quantitative histological approach, and supported the integration of imaging data with deep learning analysis. In detail, she impacted on systemic rejuvenation strategies by showing that aged HSCs rejuvenated with CASIN are sufficient to extend health span and lifespan of the whole organism. Recently, she showed that a Notch trans-activation to cis-inhibition switch underlies HSC aging, demonstrating the crosstalk between BM niche-driven and intrinsic features of HSC aging.
Alena Pecinová
Alena Pecinová, Ph.D., is a senior researcher at the Institute of Physiology of the Czech Academy of Sciences in Prague, where she works in the Laboratory of Bioenergetics. Her research focuses on mitochondrial physiology and pathology, particularly emphasising mitochondrial metabolism and mitochondrial contributions to metabolic diseases and cancer. She has made key contributions to identifying posttranslational regulation of COX in renal carcinoma, characterising mitochondrial glycerol-3-phosphate dehydrogenase as a novel site of ROS production, and elucidating metabolic adaptations affecting insulin signalling and cancer therapy response. Alena completed her postdoctoral training at Wayne State University (Detroit, USA) and gained additional international experience during research internships in Lyon and Warsaw. She is the author of more than 50 peer-reviewed publications and corresponding or co-corresponding author of several high-impact studies, including recent findings on mitochondrial translation, metabolic syndrome predisposition, and cancer cell metabolism. Mitochondrial dysfunction is a hallmark of many rare inherited diseases, yet how cells adapt to survive under conditions of impaired energy production remains poorly understood. In this project, we uncovered a novel protective mechanism in which cells with defective oxidative phosphorylation sequester polyunsaturated fatty acids into triacylglycerols stored in lipid droplets. This adaptive response prevents lethal lipid peroxidation and ferroptosis, safeguarding membrane integrity. Our findings, confirmed in cellular models, hypoxia, and patient-derived samples, reveal a previously unrecognised lipid-based stress response with potential implications for diagnostics and therapy in mitochondrial disease.
Libor Macurek
Libor Macurek graduated in general medicine at 2nd medical faculty of Charles University in Prague. He received PhD in Cell and Developmental Biology at Faculty of Science and spent three years as postdoctoral fellow at Department of Medical Oncology at UMC Utrecht in Netherlands. Since 2013, he has been a group leader at Institute of Molecular Genetics in Prague and investigates the role of protein phosphatases in silencing the DNA damage response and in oncogenesis. Genome integrity is constantly challenged with various forms of DNA damage. Transmission of mutations to daughter cells is prevented by a temporal cell cycle arrest that allows time for DNA repair. Protein kinases ATM/ATR and tumor suppressor protein p53 are the key regulators of cellular DNA damage response. After completing DNA repair, cells recover from the checkpoint and continue proliferation. Termination of the cell cycle checkpoint is controlled by protein phosphatase PPM1D. Failure to activate the cell cycle checkpoint leads to genome instability and can promote cancer development. In the Laboratory of Cancer Cell Biology at Institute of Molecular Genetics (Czech Academy of Science) we investigate the oncogenic properties of PPM1D mutations as well as possibilities of targeting of PPM1D in human cancers.
Jaroslav Truksa
has earned his Ph.D. at the Faculty of Science, Charles University in Prague in 2005. He then moved to the Scripps Research Institute to join the lab of Ernest Beutler as a postdoctoral fellow. His work there focused mostly on hepcidin regulation, including the joint work with Bruce Beutler that identified a novel negative regulator of hepcidin, a serine protease TMPRSS6. Later, he joined the lab of Jiri Neuzil at the Institute of Biotechnology, CAS and worked on topics rfelated to mitochondrial targeting of vitamin E derivatives. Additionally, he stayed for a half-year stay at Griffith University under the supervision of prof. Jiri Neuzil, working on mitochondrial targeting of tamoxifen. In 2013 he received the „science award“from the Kellner Family Foundation and started his own lab at the Institute of Biotechnology, CAS. His research interests are iron metabolism, mitochondrial biology, molecular mechanisms of resistance and various ways how to target cancer cells. He has introduced the concept of mitochondrial iron chelation as an anti-cancer approach and is actively investigating the molecular mechanisms that confer resistance to tamoxifen and cytotoxic drugs such as taxanes and their derivatives.
Štěpána Boukalová
Štěpána Boukalová is a researcher at the Institute of Biotechnology of the Czech Academy of Sciences, focusing on cancer metabolism and mitochondria as a therapeutic target in cancer. She earned her PhD at the Institute of Physiology CAS, and later joined the Molecular Therapy Group of Prof. Jiří Neužil to develop mitochondria-targeted inhibitors of the electron transport chain (ETC) as anticancer agents and study the mechanisms of resistance to this type of therapy. Her later work has clarified the critical role of mitochondrial respiration in tumor initiation and progression, showing that de novo pyrimidine synthesis is a respiration-dependent process essential for efficient tumor formation. During a research stay with Prof. Mike Berridge at the Malaghan Institute of Medical Research in New Zealand, she contributed to discoveries on how mitochondrial gene loss shapes immune and stress-response pathways in cancer. Currently she studies the mechanism of mitochondrial complex II deficiency as a driver of paraganglioma and pheochromocytoma (PPGL). Her research demonstrates that newly identified variants in SUCLG2, a subunit of the Krebs cycle enzyme succinyl-CoA ligase (SUCL), were recently found in PPGL patients and impair the activity of mitochondrial complex II, which is a recognized tumor suppressor in PPGL. Interestingly, SUCLG2 promotes complex II assembly through a distinct splice variant, representing a moonlighting function separate from its canonical enzymatic activity. Furthermore, Štěpána is working to identify and leverage the metabolic weaknesses of complex II-deficient cancers for targeted therapy, focusing on inhibitors of ETC. Her work continues to advance the understanding of mitochondrial bioenergetics in cancer and its translational relevance in developing innovative cancer therapies.
Petr Heneberg
Metabolism Reprogramming Lab, Third Faculty of Medicine, Charles University
Petr graduated in Biology from Charles University in Prague. During his master and doctoral studies, he specialized in mast cell submembrane signaling under the supervision of Petr Dráber at the Institute of Molecular Genetics AS CR. Afterwards, in 2008-2011, Petr held a postdoc position at the Division of Stem Cell and Developmental Biology of the Ontario Cancer Institute in Toronto, Canada, where he focused on the role of protein tyrosine phosphatases in cancer onset and progression under the guidance of Benjamin G. Neel. After returning back to the Czech Republic, Petr established a laboratory affiliated with the Third Faculty of Medicine (currently called the Metabolism Reprogramming Lab). The newly formed laboratory focused on various aspects of metabolism, particularly on the effects of aberrant activity of hexokinases, first on glucokinase diabetes, later on the roles of hexokinases in cancer. The recent topics include the research on the cancer-associated reprogramming of energetic metabolism in high-grade serous ovarian carcinomas and clear cell renal carcinomas, and the analysis of the same metabolic pathways in corresponding healthy tissues. PI of several projects funded by GAČR, TAČR, AZV, IGA MZ ČR, etc.; Associated Editor of J. Environ. Manag. (since 2024), Academic Editor of PLoS ONE (since 2015), and Editorial Board member of Anti-Cancer Agents in Medicinal Chemistry (since 2011); 169 papers in peer-reviewed journals, 3648 citations (WOS).