Sergi Cuartero
Profile
Sergi holds a Degree in Biology (2006) from the University of Barcelona, which included one year of undergraduate training at the University of Toulouse (France), where he also did his MSc. In 2013, he completed a PhD in the Chromatin Structure and Function Lab (IBMB-CSIC and IRB Barcelona) under the supervision of Dr. M Lluisa Espinàs. His doctoral research primarily focused on investigating the proteins and genomic elements involved in transcriptional regulation through insulator elements. Following his PhD, Sergi undertook a postdoctoral position in Matthias Merkenschlager’s lab at Imperial College London/MRC London Institute of Medical Sciences (2013-2018). During this period, he identified a novel role of cohesin in controlling the activation of inflammatory gene expression. This finding shed light on the increased resistance to differentiation observed in cohesin-deficient hematopoietic progenitors and provided an explanation for the high occurrence of cohesin mutations in acute myeloid leukemia. Subsequently, Sergi was a postdoctoral researcher in Thomas Graf’s lab at the Centre for Genomic Regulation in Barcelona. Currently, he holds a junior group leader position at the Josep Carreras Leukaemia Research Institute (IJC), where he leads the Transcriptional Dynamics in Leukemia lab. The lab’s primary research interests revolve around unraveling the mechanisms that control normal and malignant hematopoiesis, with a particular focus on the roles of cohesin and CTCF.
Research
Haematopoietic differentiation is a tightly regulated process that maintains blood production throughout life. The transcriptional changes that haematopoietic cells undergo during differentiation are controlled at multiple levels and an accurate integration of all of them is essential to ensure the production of sufficient numbers of blood cells at all stages of differentiation. However, most of the acute myeloid leukaemia (AML) cases have mutations in transcriptional regulators and chromatin modifiers. These mutations alter transcriptional dynamics and can impair normal differentiation.
We study the mechanisms that regulate transcription during haematopoietic differentiation and investigate the leukaemogenic potential of mutations in transcriptional regulators and epigenetic modifiers. We are also looking into the role of mutations in proteins that drive the three-dimensional organization of the genome.
Our main goals are:
- To understand the role of mutations in hematopoietic transcription factors and chromatin regulators in acute myeloid leukaemia (AML). Using genetic models to mimic these mutations, we aim to dissect their impact on gene expression and thus understand how they promote a selective advantage.
- To characterize the impact of inflammatory signalling on normal hematopoietic differentiation and during leukemic progression. We want to understand the impact of inflammation on the progression of myeloid malignancies and how are they linked to the most common mutations.
Acute myeloid leukaemia (AML) is the one of the most aggressive forms of leukaemia, and there is an urgent need to find new treatment options. While we now know what genes are recurrently mutated in AML, we still do not understand why these mutations are malignant. Through our research, we aim to answer the following questions:
- What transcriptional mechanisms are deregulated in acute myeloid leukaemia?
- How do inflammatory signals influence leukemic progression?
- Can we use inflammatory modulation to attenuate the severity of myeloid malignancies?