ena-STUDY-Children's Medical Research Institute-16-12-2014-02:55:54:141-466
NGS whole genome sequencing from five murine lymphoid tumours (m137, m189, m191, m209, m313 and m97) and one control sample C57B1/6 Sca1+ progenitor cells.
Our study demonstrates that by increasing the number of “young” wild-type bone marrow progenitors the development of malignancy can be prevented. Importantly, in all cases the malignant clones arose from the wild-type donor cell population, and not in the immunodeficient host cells. We conclude that self-renewal in the thymus can result from limiting, not just eliminating, progenitor cells that contribute to lymphopoiesis and that these early thymocytes are a substrate for oncogenesis via the acquisition of additional genetic legions due to off-target recombination events.
Our study demonstrates that by increasing the number of “young” wild-type bone marrow progenitors the development of malignancy can be prevented. Importantly, in all cases the malignant clones arose from the wild-type donor cell population, and not in the immunodeficient host cells. We conclude that self-renewal in the thymus can result from limiting, not just eliminating, progenitor cells that contribute to lymphopoiesis and that these early thymocytes are a substrate for oncogenesis via the acquisition of additional genetic legions due to off-target recombination events.