Too much BCR-ABL to live on, but too little BCR-ABL to die on?

摘要

The mechanistic understanding of persistence of leukemic stem cells during tyrosine kinase inhibitor therapy is an important unmet prerequisite for targeting residual CML and eradicating the disease. Unfortunately, the rarity of BCR-ABL-positive cells during major and complete molecular remission (MMR; CMR) makes it notoriously difficult to investigate genetic or biologic features of CML clones that persist in vivo under imatinib. The analysis by Chomel and colleagues on hundreds of single residual CML stem and progenitor cell clones, derived from precious marrow samples of yearlong-followed CML patients deserves respect-also for the elaborate translational approach.