Professor Andy Hall
Director of NICR

  • Email: andy.hall@ncl.ac.uk
  • Telephone: +44 (0) 191 246 4411
  • Fax: +44 (0) 191 246 4301
  • Address: Northern Institute for Cancer Research
    Paul O'Gorman Building
    Medical School
    Framlington Place
    Newcastle upon Tyne
    NE2 4HH

Introduction

I act as Director for the Northern Institute for Cancer Research, Newcastle Cancer Centre and the Newcastle Biomedicine Biobank


Roles and Responsibilities

Director of the Northern Institute for Cancer Research

Director of the Newcastle Cancer Centre

Director of Newcastle Biomedicine Biobank

Designated Individual for the Human Tissue Authority Licence for use of human tissues for research in Newcastle University

Professor of Experimental Haematology

Honorary Consultant, Newcastle Hospitals NHS Foundation Trust

Qualifications

MBBS
MRCP
PhD
FRCPath

Memberships

American Society of Hematology
American Association for Cancer Research
British Society of Haematology
British Association of Cancer Research

 

Research Interests

Using intensive combination chemotherapy more than 80% of children with acute lymphoblastic leukaemia (ALL) achieve long-term remission. However, relapsed ALL remains the most frequent cause of death from malignancy under the age of 15. My main research focus has been the study of the biology of relapse in ALL with the aim of discovering the causes of chemoresistance and suggesting ways of improving long-term survival in relapsed disease.

Previous studies undertaken by the Molecular Pharmacology Group in Newcastle have indicated that cell line models are of limited value in predicting mechanisms of drug resistance in patients. Our research has shown this may be in part be due to the fact that the majority of lymphoid cell lines are mismatch repair defective but that this is uncommon in the clinical setting (Matheson et al, 2003 [1]). We have shown, for example, that point mutations in the glucocorticoid receptor are a common cause of steroid resistance in CCRF-CEM cells, a frequently used, mismatch repair defective, T-cell line, but do not underlie resistance in mismatch repair proficient preB697 cells (Schmidt/Irving et al, 2006 [2]) and are very uncommon in clinical samples (Irving et al 2005 [3]).

These findings have led us to alter our approach to the study of drug resistance in leukaemia to focus on the use of clinical material. We have pioneered the use of single nucleotide polymorphism microarrays to determine allelic imbalance in leukaemic cells and have demonstrated progressive loss of heterozygosity in matched samples taken at presentation and on relapse (Irving et al, 2005 [4]). Studies are underway to extend these observations in collaboration with colleagues both in the UK and abroad and to develop ways of exploiting progressive change which we have identified.

1: Matheson, E.C. and A.G. Hall, Assessment of mismatch repair function in leukaemic cell lines and blasts from children with acute lymphoblastic leukaemia. Carcinogenesis, 2003. 24(1): p. 31-8.
2. Schmidt, S., et al., Glucocorticoid resistance in two key models of acute lymphoblastic leukemia occurs at the level of the glucocorticoid receptor. Faseb J, 2006. 20(14): p. 2600-2.
3. Irving, J.A., et al., Loss of heterozygosity and somatic mutations of the glucocorticoid receptor gene are rarely found at relapse in pediatric acute lymphoblastic leukemia but may occur in a subpopulation early in the disease course. Cancer Res, 2005. 65(21): p. 9712-8.
4. Irving, J.A., et al., Loss of heterozygosity in childhood acute lymphoblastic leukemia detected by genome-wide microarray single nucleotide polymorphism analysis. Cancer Res, 2005. 65(8): p. 3053-8.