49
Views
5
CrossRef citations to date
0
Altmetric
Article

INCREASED EXPRESSION OF MULTIDRUG RESISTANCE GENE (MDR1) AT RELAPSE IN A CHILD WITH ACUTE LYMPHOBLASTIC LEUKEMIA

, MD, MSc, , MD, PhD, , MD, PhD, , PhD, , MD, PhD, , MD, PhD & , MD, PhD show all
Pages 489-494 | Received 11 Jan 2006, Accepted 27 Mar 2006, Published online: 09 Jul 2009
 

Abstract

Modern treatment protocols lead to complete remission in a high proportion of patients with childhood acute lymphoblastic leukemia (ALL). However, a large number of them show a relapse of the disease. Treatment failure in these patients is mainly attributable to de novo or acquired resistance to a wide variety of cytotoxic drugs, which is called multi drug resistance (MDR). Expression of multi drug resistance 1 gene (MDR1) is implicated in the drug-resistance mechanism. In order to contribute further information we present a rare case of a 15-month old girl with newly diagnosed CALLA positive pre-B acute lymphoblastic leukemia with favourable prognostic factors at diagnosis who experienced a relapse of the disease. Using reverse transcriptase polymerase chain reaction method, m-RNA expression of the MDR1 gene upon relapse, was five-fold compared with that at diagnosis. This is the first report on increased mRNA expression at relapse in a paired sample of a child with ALL in our region.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.