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Profile

Biography

Ian Hitchcock is a Professor of Experimental Haematology based in the Centre for Immunology and Infection. He was awarded his BSc and PhD in Biology from the Department of Biology at the University of York, before becoming a postdoctoral fellow in the laboratory of Professor Kenneth Kaushansky in the Department of Medicine at the University of California San Diego. In 2007 he was made an Assistant Professor at the University of California San Diego and moved to the Department of Medicine at Stony Brook University, New York in 2010. He has been at the University of York since July 2014.    

Career

University of York

BSC in Biology (1999)

University of York

PhD in Biology (2003)

University of California San Diego

Postdoctoral Fellow (2003-2007)

Assistant Professor (2007-2010)

Stony Brook University School of Medicine

Assistant Professor (2010-2014)

University of York

Lecturer in Biomedical Sciences (2014-2017)

Professor of Experimental Haematology (2017 - )

Research

Overview

• Myeloproliferative neoplasms
• Regulation of haematopoietic cytokine signalling
• Platelet signalling and function
• Thrombosis and haemostasis

Blood cell production (haematopoiesis) is tightly regulated by a number of different factors to ensure that the numbers of circulating blood cells are maintained within a physiological range. Haematopoietic cytokines and their receptors are essential in regulating blood cell production, and consequently, aberrant haematopoietic cytokine singling can often lead to haematological malignancies or myelodysplatic syndromes. Our lab is interested in the molecular mechanisms of haematopoietic cytokine signalling and how mutations in cytokine receptors and their associated proteins cause haematological disorders and vascular complications in humans.

Projects

Thrombopoietin signalling and myeloproliferative neoplasms

The Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) are a group of haematological malignancies characterised by hyperproliferation of myeloid cells, often leading to over production of red blood cells, platelets and neutrophils. The most common mutation in patients with MPNs is JAK2V617F, an activating mutation in a kinase essential for initiation of haematopoietic cytokine signalling. This project is investigating the roles of the cytokine thrombopoietin and its receptor c-MPL in regulating JAK2V617F-positive MPNs and to target this signalling axis as a new way to treat haematological malignancies.

Dysfunctional haemostasis and thrombosis in myeloproliferative neoplasms  

The most common cause of morbidity and mortality in patients with JAK2V617F-positive MPNs is thrombosis and, conversely, bleeding disorders. We are investigating why this mutation leads to dysfunctional haemostasis and thrombosis in these patients and what cell types are responsible for causing these defects with particular focus on the roles of endothelial cells and megakaryocytes.

The roles of gender in haematological malignancies

In many cancers, including the haematological malignancies, gender plays a critical role in disease development, progression and outcome. We are looking at the cellular and molecular mechanisms that regulate the development of three JAK2V617F-positive MPNs; essential thrombocythaemia, polycythaemia vera and primary myelofibrosis, and how these differ between males and females.

Identifying and characterising rare MPL and JAK2 mutations

Although the most common mutations of MPL and JAK2 have already been identified, rare acquired and congenital mutations to these genes are frequently identified. Our lab is working with clinical partners to identify these rare mutations and characterise how they affect cell signalling and function both in vitro and in vivo, especially in comparison with the more common mutations. We hope that this work will provide insight into disease mechanisms and potentially identify whether current therapies will apply to these rare cases. 

Research group(s)

Publications

Selected publications

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