Expression and function of CXCR2, CXCR7 of acute leukemic cells in rat.

OBJECTIVE: To investigate the expression and function of chemokine receptor CXCR2 and CXCR7 in the rat with acute leukemia. METHODS: Flow cytometry and RT-PCR were used to detect the CXCR2, CXCR7 expression on the bone marrow cell surface of the acute leukemia group and the control group. RESULTS: The bone marrow cell surface CXCR2, CXCR7 relative fluorescence intensity of the observation group was significantly higher than the control group (P<0.05). The CXCR7 expression of the extramedullary infiltration group was significantly higher than non-extramedullary infiltration group (P<0.05). The CXCR2, CXCR7mRNA median expression level of the observation group was higher than the control group. The CXCR2 expression and CXCR7 expression of the observation group was positively correlated, and the correlation coefficient was 0.782 (P<0.01). CONCLUSIONS: The chemokine receptor CXCR2 and CXCR7 are highly expressed in acute leukemia, which may be associated with the occurrence of leukemia.

[Comparison of clinical implications of p16 deletion in childhood and adult B-lineage acute lymphoblastic leukemia].

OBJECTIVE: To investigate and compare the clinical implications of p16 deletion in childhood and adult B-lineage acute lymphoblastic leukemia (B-ALL). METHODS: A total of 129 cases of de novo childhood (73 cases) and adult (56 cases) B-ALL were examined genetically and immunologically using G-banding techniqhe, interphase fluorescence in situ hybridization (I-FISH) and immunophenotyping by flow cytometry, and their clinical data were retrospectively analyzed. RESULTS: Of 73 childhood cases, the prevalences of homozygous deletion, hemizygous deletion and no deletion of p16 were 24.7% (18 cases), 6.8% (5 cases) and 68.5% (50 cases) respectively, and of 56 adult cases, the incidences as of 14.3% (8 cases), 8.9% (5 cases) and 76.8% (43 cases) respectively. The incidence of p16 deletion between the two groups had no significant difference (P = 0.338). In both groups, patients with or without p16 deletion had no significant difference in terms of white blood cells (WBC) count at diagnosis, BM blast percentage, chromosome karyotype, extra-infiltration and CR1 rate. Of note, there were 2 cases, each in childhood and adult, showed no deletion at the time of diagnosis, their p16 deletions occurred at relapse. The deletion of p16 was associated with poor overall survival and event-free survival (EFS) in both childhood and adults. According to the standard of NCI risk stratification, we divided patients of two groups into standard and high risk category respectively, and performed further analysis. The significance of different risk category in children and adults was disparity. The overall survival (OS) rates of deletion and no deletion of p16 were 45.3% and 79.8% (P = 0.006) in children, and 7.7% and 22.6% (P = 0.002) in adults, respectively. EFS rates of deletion and no deletion of p16 were 33.5% and 58.1% (P = 0.008) in children, and 0 and 10.9% (P < 0.01) in adults, respectively. Of the standard risk category in children, OS rates of deletion and no deletion of p16 were 46.8% and 89.3% (P = 0.015) respectively, and EFS rates of deletion and no deletion of p16 as of 40.9% and 82.1% (P = 0.007) respectively. Of the high risk category in children, OS rates of deletion and no deletion of p16 were 41.7% and 67.4% (P = 0.193) respectively, and EFS rates of deletion and no deletion of p16 were 25.0% and 25.6% (P = 0.305) respectively. Of the standard risk category in adults, OS rates of deletion and no deletion of p16 were 20.0% and 46.9% (P = 0.092) respectively, and EFS rates of deletion and no deletion of p16 were 0 and 25.0% (P = 0.062) respectively. Of the high risk category in adults, OS rates of deletion and no deletion of p16 were 0 and 12.4% (P < 0.001) respectively, and EFS rate of deletion and no deletion of p16 was 0 and 4.8%(P < 0.001), respectively. CONCLUSION: This study indicated that deletion of p16 was associated with poor prognosis in both childhood and adult B-ALL, which highlighted an important significance to define the status of p16 in both childhood and adult B-ALL for predicting prognosis and guiding clinical intervention.

[Treatment efficacy of imatinib mesylate versus allogeneic hematopoietic stem cell transplantation for patients with chronic myeloid leukemia in chronic phase].

OBJECTIVE: To compare the treatment efficacy of imatinib mesylate versus allogeneic hematopoietic stem cell transplantation (allo-HSCT) for patients with chronic myeloid leukemia in chronic phase. METHODS: The efficacy, overall survival, progression-free survival and adverse events were evaluated in 198 patients on these two therapies from February 2002 to December 2012 at our hospital. One hundred and fifteen cases in imatinib group (n = 115) received imatinib at an initial daily dose of 400 mg and then dose was adjusted according to blood routine test and therapy response. All patients were evaluated for hematologic, cytogenetic and molecular responses every 1-3 months. The allo-HSCT group (n = 83) received myeloablative preconditioning regimen and methotrexate (MTX) and cyclosporine A (CsA) were used for graft-versus-host disease (GVHD) partially plus mycophenolate mofetil (MMF) and antihuman thymocyte globulin (ATG). The engraftment evidence and evolution of cytogenetic and molecular response was conventionally detected after allo-HSCT. RESULTS: In imatinib group, 59 of 86 (68.6%) cases achieved complete cytogenetic response (CCyR) in the 12 months after therapy, while 67 of 70 (95.7%) cases achieved CCyR in allo-HSCT group. The relapse rates of two groups were 14.8% (17/115) , 12.3% (10/81) respectively. The adverse reaction of imatinib in imatinib group was obviously much more tolerable for patients compared with frequently occurred GVHD and infection in allo-HSCT group. The 10-year cumulative overall survival (OS) rate was 93.9% in imatinib group and 77.1% in allo-HSCT group (P = 0.015). And the 10-year cumulative progression-free survival (PFS) rate was 86.1% in imatinib group versus 88.0% in allo-HSCT group (P = 0.508) . For Sokal rating stratified analysis, the cumulative OS rates of two groups were 96.4% and 68.0% (P = 0.049) for intermediate-risk patients, 92.6% and 57.1% (P = 0.017) for high-risk patients while the cumulative PFS rates of two groups were 89.3% and 88.0% for intermediate-risk patients (P = 0.942), 70.4% and 85.7% for high-risk patients (P = 0.405). The rates of OS and PFS were not significantly different for low-risk patients. The cumulative OS rates of two groups were 94.7% and 73.5% (P = 0.009) for those ≥ 30 years old and the cumulative PFS rates of two groups 84.2% and 94.1% respectively (P = 0.147). CONCLUSION: Imatinib mesylate is superior to allo-HSCT for patients with chronic myeloid leukemia in chronic phase.

[N'-(3-Meth-oxy-2-oxidobenzyl-idene-κO)benzohydrazidato-κN',O]tris-(pyridine-κN)cobalt(III) perchlorate.

In the mononuclear title compound, [Co(III)(C(15)H(12)N(2)O(3))(C(5)H(5)N)(3)]ClO(4), the Co(III) ion is coordinated by three pyridine mol-ecules and one N'-(3-meth-oxy-2-oxidobenzyl-idene)benzohydrazidate Schiff base ligand in an O,N,O'-tridentate manner. The Co(III) ion adopts a distorted CoN(4)O(2) octa-hedral coordination environment.