UCL  IRIS
Institutional Research Information Service
UCL Logo
Please report any queries concerning the funding data grouped in the sections named "Externally Awarded" or "Internally Disbursed" (shown on the profile page) to your Research Finance Administrator. Your can find your Research Finance Administrator at http://www.ucl.ac.uk/finance/research/post_award/post_award_contacts.php by entering your department
Please report any queries concerning the student data shown on the profile page to:

Email: portico-services@ucl.ac.uk

Help Desk: http://www.ucl.ac.uk/ras/portico/helpdesk
Publication Detail
NF-κB activation mediates resistance to IFNΒ in MLL-rearranged acute lymphoblastic leukemia
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Tracey L, Streck CJ, Du Z, Williams RF, Pfeffer LM, Nathwani AC, Davidoff AM
  • Publication date:
    01/01/2010
  • Pagination:
    806, 812
  • Journal:
    Leukemia
  • Volume:
    24
  • Issue:
    4
  • Status:
    Published
  • Print ISSN:
    0887-6924
Abstract
Acute lymphoblastic leukemia (ALL) harboring the t(4;11) translocation is associated with a very poor prognosis; innovative treatment strategies are required to improve the current 5-year survival rate of 30-40%. Interferon Β (IFNΒ) has shown promise in the treatment of both solid and hematologic malignancies, although the short half-life and toxicity associated with high doses have limited its clinical utility. To overcome these limitations, we investigated the effect of continuous, gene transfer-mediated delivery of IFNΒ using adeno-associated virus (AAV)-mediated expression, on ALL cells with the t(4;11) translocation. We found that this method of IFNΒ delivery resulted in complete remission of leukemia in a murine model. However, leukemic cells eventually became resistant to IFNΒ and relapse was observed. Activation of NF-B was identified as a mechanism for IFNΒ resistance, and inhibition of NF-B activity in resistant cells sensitized cells to IFNΒ. IFNΒ combined with agents that inhibit NF-B could have therapeutic potential in the treatment of children with mixed lineage leukemia subtype ALL. © 2010 Macmillan Publishers Limited All rights reserved.
Publication data is maintained in RPS. Visit https://rps.ucl.ac.uk
 More search options
UCL Researchers
Author
Research Department of Haematology
University College London - Gower Street - London - WC1E 6BT Tel:+44 (0)20 7679 2000

© UCL 1999–2011

Search by