Objective To investigate the bone marrow supernatant expression of sclerostin in the patients with multiple myeloma (MM) and to clarify its clinical signification .Methods The sclerostin level was quantified by using ELISA ,and the gene expression of sclerostin was determined by RT-PCR .Results The sclerostin level was (0 .54 ± 0 .21)pg/mL in the MM group ,which was sig-nificantly higher than (0 .31 ± 0 .06)pg/mL in the control group (t=5 .67 ,P<0 .01) .The sclerostin level was (0 .65 ± 0 .17) pg/mL in the recurrent and refractory MM group ,which was significantly higher than (0 .47 ± 0 .21) pg/mL in the control group and the newly diagnosed group (t=8 .44 ,3 .27 ,P<0 .01) ,RT-PCR verified that the BMMNC of most patients expressed sclerostin gene .The expression of sclerostin in the MM group was negatively correlated with alkaline phosphatase (ALP)(r= -0 .379 ,P=0 .005) ,and positively related with the correction blood calcium ,bone loss points ,serum β2-micro globulin(β2-GM ) ,proportion of serum M protein and clinical International Staging System (ISS) stages .The median follow-up periods were 29(6-65) months ,the low sclerostin group had the median survival period of 48(6-65) months and the high sclerostin group had the median survival pe-riod of 24(6-52) months ,the difference between them had statistical significance (χ2 = 12 .74 ,P< 0 .01) .Conclusion Its level may reflect the bone destruction ,osteogenesis inhibition degree and myeloma burden ,and reflect the median survival period of MM patients to some extent .

ObjectiveTo investigate the expression of CCL2 and its effects on the proliferation and adhesiveness on leukemia cells in patients with acute lymphoblastic leukemia(ALL). MethodsThe bone marrow mesenchymal cells (BMMSC) and bone marrow mononuclear cells (BMMNC) of 30 ALL patients and 30 healthy controls were studied, and CCL2 level was evaluated by ELISA. CCL2 gene mRNA level in ALL was determined by RT-PCR. The cell proliferation and adhesiveness were detected by MTT assays. The cell counts were measured by flow cytometry. ResultsThe BM plasma levels of CCL2 in patients at diagnosis were significantly higher than that in healthy controls [(780.12±129.61) pg/ml vs (120.49±25.21) pg/ml,t =4.96, P =0.00]. Supernatant levels of CCL2 in BMMSC were significantly higher than that of BMMNC [(572.38±35.39) pg/ml vs (193.85±15.45) pg/ml,t =5.37,P =0.00]in vitro.CCL2 cannot induce leukemia proliferation alone,but could induce leukemia proliferation in BMMNC and BMMSC co-culture in a dose- and time-dependent manner.CCL2 could increase the leukemia adhesive to the BMMSC compared with control (r =0.824,P =0.02).ConclusionPatients with B type ALL had higher levels of CCL2 which was secreted by BMMSC. The leukemia could induce the BMMSC to secrete CCL2. CCL2 could promote the survival and proliferation of leukemia in the presence of BMMSC and BMMNC, and enhance ALL cells adhesion toBMMSC in a dose-dependent manner.