Mechanisms of tumorigenesis and novel cancer therapies have been investigated in cultured mutant cells, genetically engineered to develop tumors, but the behaviour of these cells in a normal tissue environment remains almost completely unknown. In September 1
Zhang et al. used a Nf1 mutant murine model of juvenile myelomonocytic leukaemia and performed competitive repopulation assays to quantify the proliferative advantage of hematopoietic cells that lack the NF1 tumor-suppressor gene. They found that although mutant stem cells demonstrated a growth advantage over non-mutant cells, Nf1-deficient cells did not progressively outcompete their wild-type counterparts over months of observation. The myelomonocytic leukaemia only developed in recipients ...