@article{3087212,
    title = "Expression, prognostic significance and mutational analysis of protein tyrosine phosphatase SHP-1 in chronic myeloid leukemia",
    author = "Papadopoulou, V. and Kontandreopoulou, E. and Panayiotidis, P. and Roumelioti, M. and Angelopoulou, M. and Kyriazopoulou, L. and Diamantopoulos, P.T. and Vaiopoulos, G. and Variami, E. and Kotsianidis, I. and Athina Viniou, N.",
    journal = "Clinical Lymphoma Myeloma and Leukemia",
    year = "2016",
    volume = "57",
    number = "5",
    pages = "1182-1188",
    publisher = "Taylor and Francis Ltd.",
    doi = "10.3109/10428194.2015.1090573",
    keywords = "BCR ABL protein;  protein tyrosine phosphatase SHP 1;  BCR ABL protein;  protein kinase inhibitor;  protein tyrosine phosphatase SHP 1, adult;  aged;  amino acid sequence;  Article;  autoregulation;  cancer prognosis;  chronic myeloid leukemia;  clinical article;  comparative study;  controlled study;  exon;  female;  gene expression;  gene frequency;  human;  male;  mutational analysis;  pathogenesis;  priority journal;  protein binding;  protein expression;  real time polymerase chain reaction;  reverse transcription;  case control study;  dna mutational analysis;  gene expression regulation;  genetics;  Leukemia, Myelogenous, Chronic, BCR-ABL Positive;  middle aged;  mortality;  mutation;  myeloid leukemia;  prognosis;  single nucleotide polymorphism;  treatment outcome;  very elderly;  young adult, Adult;  Aged;  Aged, 80 and over;  Case-Control Studies;  DNA Mutational Analysis;  Female;  Fusion Proteins, bcr-abl;  Gene Expression Regulation, Leukemic;  Humans;  Leukemia, Myelogenous, Chronic, BCR-ABL Positive;  Leukemia, Myeloid, Chronic-Phase;  Male;  Middle Aged;  Mutation;  Polymorphism, Single Nucleotide;  Prognosis;  Protein Kinase Inhibitors;  Protein Tyrosine Phosphatase, Non-Receptor Type 6;  Treatment Outcome;  Young Adult",
    abstract = "The protein tyrosine phosphatase SHP-1 dephosphorylates BCR-ABL1, thereby serving as a potential control mechanism of BCR-ABL1 kinase activity. Pathways regulating SHP-1 expression, which could be exploited in the therapeutics of TKI-resistant chronic myeloid leukemia (CML), remain unknown. Moreover, the questions of whether there is any kind of SHP-1 deregulation in CML, contributing to disease initiation or evolution, as well as the question of prognostic significance of SHP-1, have not been definitively answered. This study shows moderately lower SHP-1 mRNA expression in chronic phase CML patients in comparison to healthy individuals and no change in SHP-1 mRNA levels after successful TKI treatment. Mutational analysis of the aminoterminal and phosphatase domains of SHP-1 in patients did not reveal genetic lesions. This study also found no correlation of SHP-1 expression at diagnosis with response to treatment, although a trend for lower SHP-1 expression was noted in the very small non-responders group of the 3-month therapeutic milestone. © 2015 Taylor and Francis."
}