Identification_of_collaborating_mutations_in_CBP_null_leukaemias__Huntley_Uni__of_Cambridge. Identification_of_collaborating_mutations_in_CBP_null_leukaemias__Huntley_Uni__of_Cambridge

Cbp null mice develop lymphoid leukaemias and lymphomas with long latency and incomplete penetrance suggesting that other mutations are required for disease progression. They also demonstrate a defined, preleukaemic phase with the presence of aberrant cells in the blood, marrow and spleen but no frank disease characteristics. We hypothesise that loss of Cbp facilitates the development of leukemia and we also want to identify mutations that collaborate with Cbp loss by performing exome sequencing on bulk tumour DNA. DNA from matched normal tissue is available in roughly 50% of cases. In addition we would like to perform exome sequencing on haematopoietic stem cells, pre-leukaemic stem cells and bulk leukaemic tissue from some mice to identify at which stage during disease progression these collaborating mutations are acquired.