As a haematologist, I am interested in how blood cells are produced from stem cells, and how this process is corrupted in blood diseases. Blood cells are critical for health and wellbeing. They carry oxygen throughout the body, fight infection and control bleeding. Throughout our lifetime, blood cells need to be replaced in a constant, tightly controlled manner.

Our division has revealed many of the genes that are critical for blood cell development. Many of these genes are also involved in the development of blood diseases, such as leukaemia and lymphoma in children, adolescents and adults. By understanding the processes that control blood cell development, I aim to advance the treatment of blood diseases for both children and adults.

Research interest

Our laboratory focuses on the use of genetic approaches to decipher mechanisms which regulate blood cells in normal development and disease. This involves in vitro and in vivo model systems which can be manipulated to understand how genes such as transcription factors, signaling molecules and cell receptors control these processes.

By integrating fundamental biology with translational approaches using genomics and chemical biology, we aim to develop a strong basis for the understanding of blood development and disease, to allow precision medicine approaches for rational drug design.

My research interests are:

  • the control of haemopoietic stem cells and blood cell development.
  • the role of genes in blood cell development and function in health and disease. This includes investigating the causes of childhood blood cancer such as Down syndrome-associated leukaemia, as well as acute leukaemias with poor prognosis.
  • the role of signaling molecules and receptors in control of blood cell production and development of myeloproliferative disorders.
  • the mechanisms that underly blood cancer development, in particular how changes in gene expression can promote the development of blood cancers from pre-cancerous stages in children and adults. We are particularly focussed on investigating acute lymphoblastic leukaemia (the most common paediatric cancer) and how to develop new therapies against aggressive subtypes of this disease.
  • the mechanisms which determine how blood cancers respond to treatment.


Selected publications from Dr Ashley Ng

Ng AP, Kauppi M, Metcalf D, Hyland CD, Josefsson EC, Lebois M, Zhang JG, Baldwin TM, Di Rago L, Hilton DJ, Alexander WS. Mpl expression on megakaryocytes and platelets is dispensable for thrombopoiesis but essential to prevent myeloproliferation. Proc Natl Acad Sci U S A. 2014 Apr 7;111(16):5884-9. PMID: 24711413.

Stevenson WS, Morel-Kopp MC, Chen Q, Liang HP, Bromhead CJ, Wright S, Turakulov R, Ng AP, Roberts AW, Bahlo M, Ward CM. GFI1B mutation causes a bleeding disorder with abnormal platelet function. J Thromb Haemost. 2013 Nov;11(11):2039-47. PMID: 23927492.

Tang JZ, Carmichael CL, Shi W, Metcalf D, Ng AP, Hyland CD, Jenkins NA, Copeland NG, Howell VM, Zhao ZJ, Smyth GK, Kile BT, Alexander WS. Transposon mutagenesis reveals cooperation of ETS family transcription factors with signaling pathways in erythro-megakaryocytic leukemia. Proc Natl Acad Sci U S A. 2013 Apr 9;110(15):6091-6. PMID: 23533276.

Ng AP, Kauppi M, Metcalf D, Di Rago L, Hyland CD, Alexander WS. Characterization of thrombopoietin (TPO)-responsive progenitor cells in adult mouse bone marrow with in vivo megakaryocyte and erythroid potential. Proc Natl Acad Sci U S A. 2012 Feb 14;109(7):2364-9. PMID: 22308484.

Ng AP, Hyland CD, Metcalf D, Carmichael CL, Loughran SJ, Di Rago L, Kile BT, Alexander WS. Trisomy of Erg is required for myeloproliferation in a mouse model of Down syndrome. Blood. 2010 May 13;115(19):3966-9. PMID: 20007548.

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