Background. A human PIM-2 is proto-oncogene that encodes serine/threonine kinase which interacts with various signalling molecules. hPIM-2 is highly expressed in haematopoietic tissues and in leukaemic and lymphoma cell lines which is consistent with a role during haematopoiesis and during oncogenic transformation. The aim. The aim of the study was to investigate whether the human PIM-2 is altered in acute myeloblastic leukaemia (AML) and acute lymphoblastic leukaemia (ALL). Patients. Thirty-seven patients were included: 22 with AML and 15 with ALL (10 with T and 5 with B subtype), aged 21–70 (x=41). Twenty-two patients reached complete remission (CR). Bone marrow samples were collected at the time of diagnosis. Control samples were obtained from 8 healthy donors.

Methods. We analyzed hPIM-2 expression by quantitative RT-PCR analysis. RNA was isolated from 3mlns mononuclear cells by using standard methods (TriPure Reagent, Roche Diagnostics). cDNA was synthesized by AMV reverse transcriptase (Finnzyme). Sequence for primers was forward, 5′-CTTTCCTTCCAATACCCCA-3′ and reverse, 5′-CCATCTTCCATTCCTTCCC-3′. As a n internal control c-ABL was used with primers c-ABL: 5′-CCCAACCTTTTCGTTGCACTGT-3′ and 5′-TGA CTGGCGTGATGTAGTTGCTT-3′. The intensity of each band was compared densitometrically.

Results. Expression of the hPIM-2 in all leukemic patients (n=37) and both subgroups: AML (n=22) and ALL (n=15) was significantly higher than in normals (p=0,0001; p=0,0009; p=0.0002, respectively). Patients who reached CR expressed hPIM-2 significantly lower than patients with primary resistance to chemotherapy (with no CR) (p= 0,01). Moreover we have found the correlation between hPIM-2 expression and patients age (r=0,45, p=0,005) and WBC in peripheral blood (r=0,34, p=0,04). Summary. PIM-2 expression is increased in patients with AML and ALL Our data indicate that expression of hPIM-2 could be considered as an additional prognostic marker in patients with AML and ALL.

Author notes

Disclosure: No relevant conflicts of interest to declare.