Additional file 2 of Molecular background of Philadelphia chromosome dependent enhancement of cellular growth and tyrosine kinase inhibitor sensitivity
In acute myeloid leukemia (AML), molecular heterogeneity across patients constitutes a major challenge for prognosis and therapy. AML with NPM1 mutation is a distinct genetic entity in the revised Wor
ERBB2 kinase domain mutations that were reported in solid cancers were shown along with their structural position and IC50 values against lapatinib and AEE 788. IC50 values were calculated based on Fi
Germline and somatic mutations in BRCA1predispose to breast cancer. We found that proteasome inhibitors can selectively kill BRCA1-depleted cells. The toxic response involves a deregulation of the G1/
The mutated residues in the yeast strains are presented in Table 2 for the Plasmodium-like mutants (PF) and in Table 3 for the human-like mutants (HS). Their location in the sequence and the structure