Please use this identifier to cite or link to this item:
Scopus Web of Science® Altmetric
Type: Journal article
Title: The development of cytokine receptor antagonists as potential therapeutic agents for the myeloproliferative disorders
Author: Ramshaw, H.
Lopez, A.
Bardy, P.
Citation: Current Pharmaceutical Design, 2002; 8(5):357-368
Publisher: Bentham Science Publ Ltd
Issue Date: 2002
ISSN: 1381-6128
Statement of
Hayley Ramshaw, Angel Lopez and Peter Bardy
Abstract: The aetiology of the myeloproliferative disorders and, in particular, of the myeloid leukaemias is unknown. The transformation of cells is primarily due to molecular aberrations leading to excessive cellular signalling and proliferation. In addition cytokines and their receptors may play a role in leukaemogenesis by increasing the proliferative capacity of leukaemic cells and extending their life span. Chemotherapeutic agents are regularly used to treat patients with leukaemia but they are non-discriminatory treatments that kill both healthy and cancer cells. Consequently patients receiving chemotherapy suffer unwanted toxicities in both the haematological and other systems. Therapies that specifically target malignant cells sparing normal cells are being investigated in a number of contexts. Cytokine antagonists can target growth factor-dependent cells by obstructing the interaction between cytokine and receptor. In this review we will discuss the myeloproliferative disorders in particular the leukaemias, the cytokines involved in leukaemogenesis, and the therapeutic potential of new agents that block specific cytokines.
Keywords: Animals
Myeloproliferative Disorders
Granulocyte-Macrophage Colony-Stimulating Factor
Receptors, Cytokine
Recombinant Proteins
Description: Copyright © 2002 Bentham Science Publishers Ltd.
DOI: 10.2174/1381612023396005
Description (link):
Appears in Collections:Aurora harvest 4
Medicine publications

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.