Exome, transcriptome and miRNA analysis don’t reveal any molecular markers of TKI efficacy in primary CML patients

Table 4 Differently expressed genes involved in cancers or regulatory pathways in optimal and non-optimal responders

Gene	Localization	Gene description	Coefficient	RT-PCR, x
DAZAP2	12q12	DAZ-associated protein 2	−2.14	−1.16
UBA52	19p13.1-p12	Ubiquitin A-52 residue ribosomal protein fusion product 1	−1.86	−1.47
PRR13	12q12	Proline rich 13	−1.58	−1.52
ATG7	3p25.3	Autophagy related 7	−1.52	−2.13
LOC387820	11q24.3	DnaJ (Hsp40) homolog, subfamily B, member 7 pseudogene	1.51
PAK1	11q13-q14	p21 protein (Cdc42/Rac)-activated kinase 1	1.52
COMMD1	2p15	Copper metabolism (Murr1) domain containing 1	1.54
RAB11A	15q22.31	Member RAS oncogene family	1.55
EMP3	19q13.3	Epithelial membrane protein 3	1.76
RSAD2	2p25.2	Radical S-adenosyl methionine domain containing 2	1.83
MAP3K11	11q13.1-q13.3	Mitogen-activated protein kinase kinase kinase 11	1.83
GSTM1	1p13.3	Glutathione S-transferase mu 1	1.95
GSTM2	1p13.3	Glutathione S-transferase mu 2 (muscle)	2.01
TNFRSF1A	12p13.2	Tumor necrosis factor receptor superfamily, member 1A	2.02

Coefficients below zero correspond to elevated gene expression in optimal responders and coefficients above zero correspond to elevated gene expression in non-optimal responders

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