Expression of genes encoding centrosomal proteins and the humoral response against these proteins in chronic myeloid leukemia
Jazyk angličtina Země Řecko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
27840977
DOI
10.3892/or.2016.5226
Knihovny.cz E-zdroje
- MeSH
- centrozom imunologie metabolismus MeSH
- chronická myeloidní leukemie genetika imunologie MeSH
- dospělí MeSH
- humorální imunita * genetika MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladý dospělý MeSH
- nádorové proteiny genetika imunologie MeSH
- proteiny buněčného cyklu genetika imunologie MeSH
- regulace genové exprese u leukemie MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- studie případů a kontrol MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- nádorové proteiny MeSH
- proteiny buněčného cyklu MeSH
As the extent of centrosome abnormalities in chronic myeloid leukemia (CML) correlates with disease stage and karyotype alterations, abnormal expression of genes encoding centrosomal proteins may be an early prognostic marker of disease progression. In the present study, we showed that in comparison with healthy controls, the expression of four centrosomal genes (AURKA, HMMR, PLK1 and ESPL1) in the peripheral blood of CML patients was significantly enhanced at diagnosis and decreased to the basal level in most patients treated with imatinib mesylate for three months. In the remaining patients (17%), this decrease was delayed and was associated with worse overall survival. The detection of antibodies in sera showed that patients with higher overall antibody production had superior outcomes in terms of achieving major molecular response and failure-free survival. These data suggest that the dynamics of the response of centrosomal genes should be considered as a risk factor and immunity against centrosomal proteins may contribute to treatment response.
Citace poskytuje Crossref.org