Objective To verify the clinical effect of Qinghuang powder in chronic myelogenous leukemia(CML). Methods 86 CML patients treated with Qinghuang powder, in which 28 cases also partially received herbal medicine (activating blood circulation to dissipate blood stasis). Results 62 cases had complete remission (72.1%), 14 cases partial remission (16.3 %), advance 8 cases(9.3 %), inefficiency 2 cases (2.3 %), and the total efficiency was 97.7 %. The symptom were improved after a week when patients had taken medicines. 44 cases have hepatomegalia, among them 39 cases have diminished or became normal compared to untreated. 70 cases have splenoparectasis, among them 60 cases became normal, 9 cases diminished, and 1 case had no change after treatment. It took 15.5 days in average when spleen began to diminish, and took 62.9 days to become smallest. The WBC began to decrease at 10.4 day and took 54.8 days in average became normal. The major side effect was digestive tract symptom, followed by skin pigmentation and skin excessive cornification. It could be avoided by low dosage. Conclusion Qinghuang powder could not only induce CML to CR, but also improve the clinical symptom of CML and eliminate the infiltration of leukemia cells. It has little influence to Hb and Plt.

Objective To investigate the clinical and biologic characteristics of acute myeloid leukemia (AML) with 6q deletions (6q-). Methods Two cases of with 6q deletions (6q-) were here described, and all the AML cases with 6q- found in the literature were reviewed. Results Two cases were diagnosed with AMLMt and AML-M2, respectively. Myloloid markers were positive on the leukemia cells in both cases, none of them expressing lymphocytic antigens. The karyotype of these patients were 46,XX,del(6)(q21q25),t(4; 7)(q10;q10)[3]/46,XX,del(6)(q21q25)[2]/46,XX[25], and 46,XX,del(6)(q23),t(7;11)(p15;p15)[5]/46,XX,t(7;11)' (p15;p15)[9]/46,XX [6]. Until now, 28 cases (including present 2 cases) of AML with 6q- have been documented in the world literature. Many of the AML patients with 6q -have additional chromosomal abnormalities. The breakpoints on 6q- were widely distributed from q12 to q27, mainly involved in the 6q21-23 region. Overall, the AML patients with 6q- were associated with an unfavorable clinical outcome, with a poor response to chemotherapy and a shorter duration. 6q-clone may itself confer a malignant clinical outcome. The 6q- found in some AML cases may associate with leukemogenesis via an activation of an oncogene other than myb or deletion of an antioncogene located in the long arm of chromosome 6. Conclusion Deletion of 6q is a very rare event in AML. AML with 6q- had distinct biologic features and a. poor clinical outcome.

Objective To isolate and study the phenotype and biological characteristics of chronic myelogenous leukemia-derived mesenchymal stem cells. Methods Cultivate the mesenchymal stem cells from chronic myelogenous leukemia in vitro, identify the immunophenotype by fluorescence-activated cell sorter (FACS), and detect the bcr-abl fusion gene by RT-PCR and FISH. Results The mesenchymal stem cells from chronic myelogenous leukemia can express the bcr-abl fusion gene. Conclusion These findings provide the evidence that the rearrangement of bcr-abl gene might happen at least more primitive than CD+34 CD-38 cells.