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Background The aim of this study is to investigate the hematological manifestations of human immunodeficiency virus (HIV) infection, the risk factors for cytopenia, and the effect of highly active anti-retroviral therapy (HAART) on cytopenia. Methods Medical records of patients treated for HIV at the Seoul National University Hospital from January 2005 to March 2010 were retrospectively reviewed. To determine the impact of HIV itself, we excluded HIV patients who had other conditions that could have resulted in hematological manifestations. Multiple logistic regression analyses were performed to identify risk factors for cytopenia. Results A total of 621 cases were investigated, and after exclusion, data of 472 patients were analyzed. The frequency of cytopenia was anemia, 3.0% (14/472); neutropenia, 10.0% (47/472); thrombocytopenia, 2.4% (12/472); lymphopenia, 25.7% (121/470); isolated cytopenia, 11.2% (53/472); and bicytopenia, 2.1% (10/472). The leading risk factor for cytopenia identified by multivariate logistic regression methods was AIDS status at initial presentation. After HAART, cytopenia was reversed in the majority of patients (thrombocytopenia, 100%; neutropenia, 91.1%; and anemia, 84.6%). Conclusion This study isolated the impact of HIV infection alone on hematologic manifestations and confirmed that these changes were reversible by HAART. Control of the HIV infection will have the main role in the management of hematological manifestations of the virus.

The blast phase in chronic myelogenous leukemia (CML) is associated with mutation of several genes. It is well known that p53 gene mutation plays a key role in the myeloid or lymphoid blast phase of CML. But for the case of the N-ras gene, the association between N-ras mutations and the blast phase of CML is not yet known. We report here on a case of detecting N-ras point mutation without p53 mutation in a 64 year-old man who suffered from the lymphoblastic blast phase of CML.

Systemic amyloidosis is a disease that displays deposition of insoluble polymeric protein fibrils in tissues and organs. We report here on a case of a 64-year-old woman who initially presented with multiple enlarged lymph nodes. Computed tomography showed multiple enlarged lymph nodes in the mediastinal, lower cervical, supraclavicular, axillary and abdominal areas. Excision biopsy of the cervical lymph nodes and the subsequent histopathology showed amorphous eosinophilic material deposits, and these revealed apple-green birefringence on a polarizing microscopic examination on the Congo-red stained slide. The patient was diagnosed with amyloidosis and she received chemotherapy consisting of melphalan and dexamethasone. During chemotherapy, she was diagnosed with breast cancer. After modified unilateral radical mastectomy, the dexamethasone was restarted and this therapy resulted in stable disease.

Background: Curcumin is a naturally occurring biologically active compound, and it has been shown to possess potent anti-inflammatory, anti-tumor and anti-oxidative properties. It is known for its anti-pro- liferative and proapoptotic effects in several cancer cells. Curcumin's effects on the mechanisms of cell survival and the expression of various cytokines were investigated in U266 cells and the in vivo effects of curcumin were examined using an animal model. Methods: Cell proliferation assay and flow cytometry were used to examine cell proliferation, along with cell cycle analysis. The protein expressions were analyzed by Western blotting and the expressed levels of cytokines were analyzed by the ELISA method. Results: Curcumin inhibited U266 cell growth in a dose-dependent and time-dependent manner. Cell cycle analysis showed an increased sub-G1 phase, a down regulated cyclinD1 expression and an induced p21 expression. Apoptosis induced a down regulated procaspase 3 expression and it induced cleaved PARP. Curcumin inhibited the IL (interleukin)-6 induced cell signal pathway via decreasing the STAT1 an 3, Erk cyclinD1 and c-myc expressions. Also, administration of 25mg/kg curcumin to a U266 animal model inhibited cancer cell engraftment in the bone marrow and it decreased the IL-6, sIL-6R and IL-8 ex- pression levels. Conclusion: Curcumin induced cell cycle arrest and apoptosis and it inhibited the IL-6 mediated signal transduction pathways in U266 cells. Similar to the in vitro results, curcumin inhibited cancer cell pro- liferation and the expression of cytokine in vivo. (Korean J Hematol 2008;43:19-27.)

Donor Lymphocyte Infusions for Patients with Relapsed Leukemia after Allogeneic Hematopoietic Stem Cell Transplantation: a 10-year Experience of Seoul National University Hospital Jin Won Kim, Byung-Su Kim, Dae-Young Kim, Ki Hwan Kim, Ji Young Rhee, Soo-Mee Bang, Inho Kim, Sung-Soo Yoon, Jong-Seok Lee, Seonyang Park and Byoung Kook Kim Department of Internal Medicine, Seoul National University Hospital, Cancer Research Institute, Seoul National University College of Medicine, Clinical Research Institute, Seoul National University Hospital, Department of Internal Medicine, Seoul Municipal Boramae Hospital, Seoul, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea

Department of Internal Medicine, Korea Cancer Center Hospital, Korea Institute of Radiological & Medical Sciences, Seoul, Department of Internal Medicine, Hallym University College of Medicine, Chuncheon, Department of Internal Medicine, Chonbuk National University Medical School, Jeonju, Department of Internal Medicine, Seoul National University Bundang Hospital, Bundang, Department of Internal Medicine, National Cancer Center, Goyang, Department of Internal Medicine, Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea 󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚󰠚

Background: Curcumin, a naturally occurring biologically active compound extracted from rhizomes of Curcuma species, has been shown to possess potent anti-inflammatory, anti-tumor and anti-oxidative properties. The effects and possible mechanism of this agent were investigated on 2 human myelogenous leukemic cell lines. Methods: K562 and KG-1 cells were the two cell lines selected. The MTT assay and flow cytometry were used to assess the cytotoxicity and for cell cycle analysis, respectively. The protein expressions were analyzed by Western blotting; the caspase activity was also checked. Results: Both cell lines showed dose-dependent susceptibility to curcumin, and the cell cycle analysis showed an increased sub-G1 phase in the KG-1 cells. In the K562 cell, curcumin down regulated the expressions of PCNA (proliferating cell nuclear antigen) and cyclins D1 and B1. The expression of Akt was also down-regulated, but caspase-3 was activated to induce cleaved PARP (polyadenosine ribose polymerase) and apoptosis. However, the expression of phospho-Erk was unaffected. Co-treatment of cyclosporin A (CsA) with curcumin resulted in an attenuation of apoptosis in the K562 cells, implying curcumin-induced apoptosis is dependent on the release of cytochrome c from the mitochondria. Conclusion: Curcumin induced cell cycle arrest and apoptosis in both human myelogenous leukemic cell lines, with the apoptosis appearing to be dependent on the release of cytochrome c from the mitochondria. (Korean J Hematol 2005;40:75-81.)

The Clinical Efficacy of Helicobacter pylori Eradication in Patients with Helicobacter pylori-positive Chronic Thrombocytopenic Purpura Bong-Seog Kim, M.D., Seung-Hyun Nam, M.D., Soo-Mee Bang, M.D., Jae Hoon Lee, M.D., Young Rok Do, M.D. , Ki Young Kwon, M.D., Hong Suk Song, M.D., Hun Mo Ryoo, M.D., Sung Hwa Bae, M.D., Min Kyoung Kim, M.D. , Kyung Hee Lee, M.D., Myung Soo Hyun, M.D., Young Jin Yuh, M.D., Eunkyung Park, M.D., Sang-Jae Lee, M.D., Sung-Soo Yoon, M.D., Seonyang Park, M.D. and Byoung Kook Kim, M.D.