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Dr Ingo Ringshausen

107-Ringshausen-2017Dr Ingo Ringshausen

Haematopoietic stem cells and malignancies


Laboratory: Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre 

Departmental Affiliation: Haematology


Ingo Ringshausen studied medicine at the Johannes Gutenberg University in Mainz/ Germany and London/ Canada. After his graduation in 1999 he started his medical training in Internal Medicine and Haematology/ Oncology at the Technical University in Munich. Between 2003 and 2006 he joined the group of Gerard Evan at UCSF on a postdoctoral fellowship. After his board certification in 2010 he became a Consultant in the Department of Haematology/ Oncology in Munich and subsequently an independent group leader. 

In 2014 he joined the Department of Haematology in Cambridge and is now appointed as Consultant Haematologist at Addenbrooke’s hospital and a Principal Investigator at the CSCI.



Cancer Research UK, Kay Kendall Leukaemia Fund


 Ringshausen research 2018

Malignant B cells (yellow) actively remodel Bone marrow mesenchymal stromal cells (Nestin+ cells are GFP positive, endothelial cells are in red).



Chronic lymphocytic leukaemia (CLL) is the most common leukaemia in western countries. Although CLL is a putative mature B cell malignancy, it has very recently been shown that the maturation of CD34+CD38- HSPC from CLL patients is skewed towards the lymphoid linage. Importantly, the majority of stem and progenitor cells from CLL patients carry disease specific mutations in NOTCH1, SF3B1, TP53 and XPO. These recent reports suggest that the initial oncogenic events can occur at the earliest stages of B cell specification in the stem cell compartment. 

Our group previously demonstrated that malignant cells actively re-program mesenchymal stromal cells, a process that is dependent on the activation of NF-κB and essential for disease propagation. We are now interested in understanding how clonal evolution from a pre-malignant progenitor to a treatment-resistant B cell malignancy affects the activation and reprogramming of niche cells in the bone marrow microenvironment and how this contributes to microenvironment-mediated drug resistance. Related to this, we are investigating how the lymphoma-remodelled microenvironment impairs normal HSC biology, leading to bone marrow failure.


Ringshausen Group 2017

Group Members

Jingyu Chen, Maurizio Mangolini, Andrew Moore, Eugene Park, Antonella Santoro, Vijitha Sathiaseelan


Plain English

Similar to normal blood stem cells, malignant cells from patients with B cell lymphomas require signals from their surrounding environment for cell survival and proliferation. Thus, benign bystander cells provide crucial support for malignant cells, mediated by direct cell-cell contact and soluble factors. Understanding these cell-cell communications from a molecular viewpoint opens new directions to treat blood-born malignancies. Specifically, we want to understand: 1. How this cell-cell communication changes over time? Are malignant cells from patients with relapsed disease equally dependent on these signals? 2. How does this communication between malignant cells and their micro-environment affects the function of normal haematopoietic stem cells and the production of normal blood cells? 

Key Publications


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