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Publications (3)0 Total impact

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    ABSTRACT: The study was aimed to explore the possible roles of survivin and P63 protein in the development and progression of B cell non-Hodgkin's lymphoma (B-NHL) and their relation with cell apoptosis and proliferation. TdT-mediated dUTP nick end labeling (TUNEL) and immunohistochemistry were used to detect the survivin and P63 protein expression, cell apoptosis and proliferating cell nuclear antigen (PCNA) level in 43 cases of B-NHL and 10 cases of reactive hyperplasia lymphoid (RHL) tissues. The results indicated that the positive rates of survivin and P63 protein expression were 69.8% (30/43) and 82.7% (30/43) respectively. The expression of survivin and P63 protein was 10% (1/10) and 40% (4/10) in RHL tissues of 10 cases. The expression of survivin in aggression B-NHL was higher than that in indolent B-NHL (83.3% vs 46.2%, P < 0.01). The expression of P63 proteins in aggressive B-NHL was higher than that in indolent B-NHL (86.7% vs 76.9%, P > 0.05). Apoptotic index (AI) and proliferation index (PI) correlated positively with expression of survivin (r = 0.429, P < 0.01; r = 0.348, P < 0.01), and so do with expression of P63 proteins (r = 0.451, P < 0.01; r = 0.369, P < 0.05). In addition, AI and PI were positively related (r = 0.598, P < 0.001). It is concluded that survivin may participate in the regulation mechanism of B-NHL cell apoptosis and proliferation, P63 as an oncogene enhances proliferation and takes part in the development of B-NHL. There may be a close relationship between survivin and P63 protein in the regulation of lymphocyte proliferative kinetics.
    Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 02/2007; 15(1):99-102.
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    ABSTRACT: To investigate the anti-chronic myeloid leukemia (CML) effect of cytotoxicity T lymphocytes (CTL) activated by dendritic cells (DC) pulsed with freeze thaw K562 lysates antigen. DC were achieved by healthy donors peripheral blood monocytes which were induced by granulocyte-macrophage colony stimulating factor (GM-CSF) and IL-4. On the sixth day, these cells were collected. One part of them was used to prove that they were DC from morphology and phenotypes. The other part was pulsed with K562 lysates and the lysate-loaded DC were compared with immature DC from phenotypes. The expression of IL-12 and IFNgamma in supernatant, the mixed lymphocytes reaction and the specific cytotoxicity against leukemia cells were tested. Freeze thaw K562 lysate up-regulated the expression of various differentiation antigens of DC, such as CD(1a) (27.40 +/- 5.00)% vs (15.40 +/- 2.34)%, CD(80) (61.35 +/- 5.35)% vs (42.00 +/- 2.77)%, CD(83) (93.30 +/- 3.48)% vs (25.15 +/- 4.02)%, CD(86) (85.25 +/- 4.39)% vs (37.25 +/- 3.20)%, CD(40) (89.80 +/- 7.18)% vs (35.95 +/- 4.06)% and HLA-DR (49.50 +/- 5.45)% vs (17.15 +/- 3.61)%. Simultaneously, the expression of IL-12 rose after DC were loaded with tumor lysates after 24 hours (P < 0.05). The T cells from healthy donors and CML patients, proliferated by antigen loaded DC, could induce IFNgamma increase (P < 0.01). The proliferation of T cells had distinct relation with the time of antigen loaded with DC. These T cells had specific cytotoxicity against K562 and HLA partial matching CML cells. DC pulsed with K562 lysates can stimulate T cells, and can keep high immunocompetence with specific cytotoxicity against K562.
    Zhonghua nei ke za zhi [Chinese journal of internal medicine] 12/2006; 45(12):1013-6.
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    ABSTRACT: To explore the expression of myeloid cell leukemia 1 (MCL-1) proteins and survivin and its correlation with cell apoptosis as well as with the development and progression of B cell non-Hodgkin's lymphoma (B-NHL). TdT-mediated dUTP nick end labeling and immunohistochemistry were used to study cell apoptosis and expression of MCL-1 proteins and survivin proteins in 43 patients with B-NHL and 10 with reactive hyperplasia (RH) lymphoid tissue. The positive rate of MCL-1 proteins and survivin proteins was 58.1% (25/43) and 69.8% (30/43) respectively. The expression of MCL-1 proteins was not detected in RH lymphoid tissue, but that of survivin was detected in 10.0% (1/10). The expression of MCL-1 proteins in aggressive B-NHL was higher than that in indolent B-NHL (70.0 % vs 30.8 %, P < 0.05). The expression of survivin in aggressive B-NHL was also higher than that in indolent B-NHL (80.0% vs 46.2%, P < 0.05). Apoptotic index (AI) was not correlated positively with the expression of MCL-1, but correlated positively with the expression of survivin (r = 0.429, P < 0.01). MCL-1 and survivin were correlated positively in B-NHL (r = 0.598, P < 0.001). MCL-1 proteins as family member of BCL-2 have no influence on apoptosis but survivin may participate in the regulation mechanism of B-NHL apoptosis. It is indicated that the two proteins with a close relationship may take part in the development and progression of B-NHL.
    Zhonghua nei ke za zhi [Chinese journal of internal medicine] 03/2006; 45(2):133-5.