Junior Postdoctoral Researcher

The Josep Carreras Leukaemia Research Institute (IJC) is a comprehensive cancer research center dedicated to conduct research and drive innovation in the epidemiological, preventive, clinical, translational, and basic aspects of leukaemia and other hematologic malignancies, with the final aim of finding a cure for these diseases. It was created in 2010, and since then has experienced an exponential growth.

The IJC is also part of the network of Excellence Research Centers of Catalonia (CERCA) and was accredited as a Severo Ochoa Center of Excellence by the Ministry of Science, Innovation, and Universities in 2024. Since 2018, the Institute has also been accredited by the Scientific Foundation of the Spanish Association Against Cancer (FCAECC) Additionally, IJC is one of the centers integrated into the Institut de Recerca Germans Trias i Pujol (IGTP) accreditation as Accredited Health Research Institute (IIS) by the Carlos III Health Institute (ISCIII) .

The IJC's main headquarters is located within the Can Ruti Biomedical Campus, alongside other leading biomedical institutions, providing direct access to cutting‑edge scientific and technological facilities, as well as complementary community services. The IJC has six locations integrated into reference hospitals : Hospital Germans Trias i Pujol, Hospital Clínic, Hospital Sant Pau, Hospital Josep Trueta, Hospital del Mar and Hospital San Joan de Déu. This facilitates close collaboration between basic and clinical researchers, fostering translational research that integrates basic science with clinical practice in clinical settings.

We are looking for a Postdoctoral Researcher to join the Epigenetic Control of Haematopoiesis Group, led by Dr. José Luis Sardina.

Our research aims to understand the molecular mechanisms that regulate cell identity and fate during human haematopoiesis and how their dysregulation contributes to immune dysfunction and haematological malignancies. We combine functional genomics, epigenomic and single‑cell approaches with experimental models of human haematopoiesis to define how regulatory mechanisms shape normal and malignant cell states. Recent work from the group has identified vulnerabilities regulating haematopoietic progenitor and leukaemic cell states through genome‑wide CRISPR screening (Kodali et al., Nature Cell Biology, 2024), established a causal role for DNA methylation in regulating human immune cell fate using CRISPR‑based epigenome editing (Valcárcel et al., Science Advances, 2025), and identified and functionally validated TET2‑dependent regulatory targets in human myeloid commitment, including an AGO2 regulatory axis linking TET2‑dependent epigenetic regulation to RNA biology and leukemic fitness (Lazarenkov et al., bioRxiv, 2026).

Within this broader research programme, the present project focuses on the largely unexplored role of TET2‑dependent epigenetic regulation during human lymphoid development. We combine cutting‑edge epigenomic and single‑cell approaches applied to primary human lymphoid cells, together with hiPSC‑based differentiation, CRISPR‑mediated genetic and epigenetic editing, and patient‑derived samples, to define how TET2 regulates early lymphoid commitment and competence. The project integrates computational analysis of newly generated DNA methylation and single‑cell multi‑omics data, CRISPR epigenome‑editing approaches, and complementary public datasets. Our preliminary findings identify TET2 as a major TET dioxygenase during early human lymphoid commitment and reveal extensive epigenetic remodelling at key stages of lymphoid development. We will investigate how TET2‑dependent epigenetic programmes regulate lymphoid competence and how their progressive disruption, including in ageing, clonal haematopoiesis, and primary immunodeficiencies, may contribute to immune dysfunction and lymphoid malignancy. By defining how TET2‑dependent epigenetic programmes are established during normal lymphoid development and how they become disrupted in disease, the project will provide a mechanistic framework linking epigenetic regulation to immune dysfunction, ageing, and lymphoid malignancy.

• Contribute to the design, execution, and interpretation of experimental studies addressing the role of TET2 in human lymphoid development, using primary human cells, hiPSC‑based differentiation, and CRISPR‑mediated genetic and epigenetic approaches.

• Perform and further develop computational analyses and integration of epigenomic and single‑cell datasets generated within the project, including DNA methylation, transcriptomic, and other relevant multi‑omics datasets.

• Develop and implement experimental and computational approaches within the overall research framework of the project , with scope for inde