How leukaemia can develop with age

How leukaemia can develop with age
Researchers from the University of Chicago Medical Center have shown that signals from bacteria that normally live in the gut can lead to a precursor situation for leukaemia. This occurs when the bacteria are allowed to wander in the body, and there are certain stem cell mutations already in place.
It is already known that approximately 15 per cent of people over 60 years of age develop a mutation (TET2) in their hematopoietic stem cells – these can lead to cancers of the blood because the TET2 mutation makes the stem cells dominant and increases the number of white cells present. This condition is called CHIP - Clonal Hematopoiesis of Indeterminate Potential.  
However, the final step to a blood cancer was not understood. In the latest study with mice it seems that wandering bacteria are the cause of the final step. If the intestinal lining becomes damaged (and in some cases, TET2 can cause this), bacteria can wander and produce localized inflammatory molecules.
The researchers hope that understanding the intestinal breakdown might lead to ways of reversing the situation.
Chris Woollams, former Oxford University Biochemist and a founder of CANCERactive said, “Yet again, it looks like cancer treatments to date have been attacking the wrong problem. Killing off the end product is looking less and less the answer in many cancers. Tackling the production line might be far more appropriate.”
1.Marlies Meisel, Reinhard Hinterleitner, Alain Pacis, Li Chen, Zachary M. Earley, Toufic Mayassi, Joseph F. Pierre, Jordan D. Ernest, Heather J. Galipeau, Nikolaus Thuille, Romain Bouziat, Manuel Buscarlet, Daina L. Ringus, Yitang Wang, Ye Li, Vu Dinh, Sangman M. Kim, Benjamin D. McDonald, Matthew A. Zurenski, Mark W. Musch, Glaucia C. Furtado, Sergio A. Lira, Gottfried Baier, Eugene B. Chang, A. Murat Eren, Christopher R. Weber, Lambert Busque, Lucy A. Godley, Elena F. Verdú, Luis B. Barreiro, Bana Jabri. Microbial signals drive pre-leukaemic myeloproliferation in a Tet2-deficient host. Nature, 2018; DOI: 10.1038/s41586-018-0125-z


2018 Research
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