| Research findings could lead to new treatments for leukaemia |
| Written by Lautaro Vargas | |
| Wednesday, 09 April 2008 | |
![]() The European Bioinformatics Institute in Cambridge Leukaemia – cancer of blood or bone marrow – is caused by mutations that allow defective blood cells to accumulate and displace healthy blood, but until now scientists have always thought that the mutation was the crucial step leading to leukaemia that should be targeted by drugs. However, the team of researchers from the European Molecular Biology Laboratory (EMBL) in Italy, the EMBL-European Bioinformatics Institute (EBI) in Cambridge UK, and the Universities of Harvard, US, and Lund, Sweden, has identified a genetic programme activated in self-renewing leukaemic cells, which is shared with similar leukaemias caused by other types of mutations. The findings, in the current issue of Cancer Cell, suggest that the cellular changes that lead to self-renewal are mutation-independent. To develop drugs with a more general efficacy it may therefore be more efficient to target the molecules and pathways shared between different cancer stem cells. Blood is generated from a small number of multipotent stem cells that divide, differentiate and give rise to the many different cell types that make up the blood. They also maintain the pool of stem cells through a process called self-renewal. While differentiating, cells acquire specific properties and functions, but lose the capacity to self-renew in the way stem cells do. Mutations interfering with this process and promoting uncontrolled proliferation of certain blood cells can lead to leukaemia. Researchers of the group of Claus Nerlov at EMBL’s Mouse Biology Unit now prove that a mutation in a protein called C/EBPa causes acute myeloid leukaemia (AML), a type of leukaemia affecting one lineage of white blood cells, in mice. “10 per cent of all patients suffering from AML have this mutation, but we could never be sure if it causes the disease,” said Peggy Kirstetter, who carried out the research in Nerlov’s lab. “By precisely reproducing the human mutation in the mouse we now proved a causative relation.” Instead of promoting uncontrolled proliferation of malignant blood stem cells, as often assumed as the cause of leukaemia, the mutation acts on already partially differentiated cells. It reprogrammes these cells to self-renew and to produce countless dysfunctional daughter cells, which displace the healthy blood cells, eventually leading to the inability to transport oxygen around in the body. “This is the first time that non-stem cell myeloid leukaemia has been generated within a healthy blood system. The findings will have profound implications for our understanding of the development and treatment of leukaemias,” added Nerlov.
Set as favorite
Bookmark
Email This
Hits: 368 Trackback(0)
Comments (0)
![]() Write comment
This content has been locked. You can no longer post any comment.
|
| < Prev | Next > |
|---|