SOCS-2 gene expression at diagnosis does not predict for outcome of chronic myeloid leukemia patients on imatinib treatment

Abstract

SOCS-2 gene expression at diagnosis has been suggested as a predictor of clinical outcome in chronic myeloid leukemia (CML). In this study SOCS-2 and GUS expression levels were determined by real-time PCR in pretherapeutic samples at diagnosis. First, three patient groups were compared after assessment at 48 months: optimal molecular responders (n = 35), patients with resistance to imatinib (n = 28), and blast crisis patients (n = 27). A significant difference in SOCS-2 gene expression at diagnosis was observed comparing blast crisis vs. resistant patients (p = 0.042) and optimal responders (p = 0.010). Second, a validation sample of consecutively randomized patients (n = 123) was investigated. No discriminative SOCS-2 gene expression cutoff could be derived to predict molecular or cytogenetic response, progression-free or overall survival. Although SOCS-2 gene was differentially expressed at the time of diagnosis in blast crisis patients when compared to other groups, a prognostic impact in consecutively randomized patients was not observed.

Keywords:

• SOCS-2
• chronic myeloid leukemia
• prognosis
• predictor

Acknowledgments

We would like to thank Maike Haas, Melanie Hartmann, Katrin Ackermann, Alla Elkovskaja, Melanie Müller, Cathy Huber, Julia Obländer and Ralf Bieber.

Disclosure statement

DBE and BH declare no conflicts of interest. ML and MP declare no conflicts of interest. SS declares research support from Novartis, BMS and Incyte, Honoraria from Novartis, BMS, Pfizer, Roche and Incyte. GB received educational support and honoraria from Incyte. MCM received research support and honoraria from Novartis, BMS, Incyte and Pfizer.

Additional information

Funding

This work was supported by the German Government [BMBF 01GI0270]; Deutsche Krebshilfe [Nr. 106642]; Deutsche José-Carreras Leukämiestiftung [DJCLS H09/f, H06/04v, H03/01, R05/23, AH06.01]; European Union [LSHC-CT-2004–503216]; Novartis Oncology, Nürnberg (Drs G Gerhard, S Schaffert, A Jacob and U Haus); Roche, Grenzach-Wyhlen; and Essex, Munich, Germany.