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

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

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