Oral examination in a patient with a history of acute lymphoblastic leukemia (ALL) and allogeneic hematopoietic cell transplantation (HCT) needs considerations of leukemia relapse and graft-versus-host disease (GVHD). Oral manifestations may contribute to early detection of relapse or systemic complications making accurate oral examination and diagnosis significant. We report a case of a large tumor like mass arising in a patient with a history of ALL and HCT. The patient had been diagnosed with ALL relapse and was being treated with chemotherapy, and furthermore was suspected of GVHD development.

Bovine leukemia virus (BLV) is the causative agent of enzootic bovine leukosis. This study was conducted to clarify the seroprevalence of BLV in the Republic of Korea. Blood samples were obtained from Korean native cattle farms in all provinces of South Korea except Jeju. A commercial indirect enzyme-linked immunosorbent assay with 4,498 samples to detect antibodies against BLV was conducted. The results revealed that the prevalence of BLV was dependent upon age, with increasing prevalence among cattle occurring until they were 5 years old. The highest seroprevalence in cattle was observed in Chungnam (29.6%) and the lowest was observed in Jeonnam (2.6%). The mean overall prevalence for BLV antibodies in the survey was 10.2%, indicating that BLV is widespread nationwide.

L-아스파라기나제는 급성 림프모구백혈병 환자에서 사 용이 증가하는 약물로, 췌장염은 이 약제의 중요한 합병증 중 하나이며, 항암화학치료 중 이에 대한 주의가 필요하다. 급성 췌장염은 드물지만 치명적 합병증인 괴사성 췌장염 으로 진행할 수 있으며 빠른 진단과 적절한 처치가 중요하다. 본 증례는 괴사성 췌장염에 동반된 췌관 누출 그리고 췌장가성낭이 경유듀적 췌관 스텐트 삽입으로 호전되었던 증례이다. 향후 이러한 L-아스파라기나제 유발 췌장염 및 췌관 누출의 치료를 위한 다양한 접근 및 안전성에 대해 추가적인 연구가 요구된다.

An Australian cattle dog (case 1: 6-year-old castrated male) and a Shih-Tzu dog (case 2: 8-year-old castrated male) were referred to the Gyeongsang Animal Medical Center due to anorexia and depression. Physical examinations, complete blood counts, serum chemical analysis, radiography, ultrasonography, and bone marrow biopsy were performed. Upon physical examinations of cases 1 and 2, enlargement of superficial lymph nodes was not identified. Hematologic findings in these dogs included leukocytosis with severe lymphocytosis, anemia, and thrombocytopenia. Upon radiography, both dogs showed splenomegaly. Upon examination of a peripheral blood smear in case 1, immature lymphoid cells, featuring decreased nuclear chromatin condensation and nuclear pleomorphism, were present. Biopsy samples of the bone marrow in case 1 revealed hypercellularity as well as a large number of immature lymphoblastic cells similar in shape to cells in the peripheral blood. The characteristic morphological features of peripheral blood and bone marrow samples in case 2 were small lymphocytes. Thus, the dogs were tentatively diagnosed with acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL), respectively. After diagnosis, the CLL patient was administered chlorambucil and prednisolone therapy. Due to its similarity to human leukemia, the canine leukemia model provides a valuable model for research into human leukemia.

Skin-derived precursor cells (SKPs) are multipotent, sphere-forming and embryonic neural crest‐related precu- rsor cells that can be isolated from dermis. It is known that the properties of porcine SKPs can be enhanced by leuke- mia inhibitory factor (LIF) which is an essential factor for the generation of embryonic stem cells in mice. In our pre- sent study, to enhance or maintain the properties of murine SKPs, LIF was added to the culture medium. SKPs were treated with 1,000 IU LIF for 72 hours after passage 3. Quantitative real time RT‐PCR was then performed to quantify the expression of the pluripotent stem cell specific genes Oct4, Nanog, Klf4 and c‐Myc, and the neural crest specific genes Snai2 and Ngfr. The results show that the expression of Oct4 is increased in murine SKPs by LIF treatment whereas the level of Ngfr is decreased under these conditions. Interestingly, LIF treatment reduced Nanog exp- ression which is also important for cell proliferation in adult stem cells and for osteogenic induction in mesenchymal stem cells. These findings implicate LIF in the maintenance of stem- ness in SKPs through the suppression of lineage differen- tiation and in part through the control of cell proliferation.

The experimental manipulation of protooncogenes and their gene products is a valuable research tool for the study of human neoplasia. In this study, the recently identified human cervical cancer protooncogene (HccR-2) was expressed in transgenic mice under the control of the tetracycline regulatory system. The phenotype observed was similar in many respects to human chronic neutrophilic leukemia (CNL). Thus, the HccR-2 transgenic mouse model is important not only for investigating the biological properties of the HccR-2 protooncogene in vivo, but also for analyzing the mechanisms involved in the progression of CNL.

The experimental manipulation of protooncogenes and their gene products is a valuable research tool for the study of human neoplasia. In this study, the recently identified human cervical cancer protooncogene (HccR-2) was expressed in transgenic mice under the control of the tetracycline regulatory system. Mice expressing the HccR-2 transgene showed an altered myeloid development characterized by an increased percentage of mature and band-form neutrophils in the peripheral blood, liver and spleen. This phenotype is similar to human chronic neutrophilic leukemia (CNL) in many ways, which is a rare chronic myeloproliferative disorder (CMD) that presents as a sustained leukocytosis of mature neutrophils with a few or no circulating immature granulocytes, an absence of peripheral blood monocytosis, basophilia, or eosinophilia, and an infiltration of neutrophils into the liver, spleen and kidney. Thus, the HccR-2 transgenic mouse model is imperative not only for investigating the biological properties of the HccR-2 protooncogene in vivo, but also for analyzing the mechanisms involved in the progression of CNL.

Covalent modifications of histone tails have fundamental roles in chromatin structure and transcriptional activity of a target locus. One of such modifications, Methylation at Lysine 9 of histone H3 (H3-K9) causes several epigenetic phenomena including heterochromatin formation, transcriptional regulation and DNA methylation. Setdb1, H3-K9 specific histone methyltransferase, functions in gene silencing, heterochromatin formation and essential role for early development. Here, we demonstrate that Setdb1 associates with promyelocytic leukemia (Pml) protein from the early stage of mouse development and is a constitutive member of PML nuclear bodies (PML-NBs) that have been linked to many cellular processes such as apoptosis, DNA damage responses, and transcriptional regulation. Immunostaining of mouse blastocyst showed that Setdb1 and Pml signals were scattered in nucleus as a few speckles and microinjected Pmlmyc signals colocalize with Setdb1 signals. This colocalization was observed in mEF and the punctate signals of Setdb1 were observed to be present in every nucleus of mEFs and dividing cells with condensed chromosomes. Arsenic treatment, which induces Pml degradation, also caused Setdb1 signals to disappear. Setdb1 knockdown resulted in disassembly of PML-NBs and immunoprecipitation results demonstrated physical interactions between Setdb1 and Pml. These data suggest that Setdb1 was associated in PML-NB and Setdb1 has important function in maintenance of PML-NB structure.

Emodin is a bioactive compound isolated from the root and rhizomes of Rheum plamatum L. (polygenaceae), which is known as a traditional Chinese and Japanese medicine. In the present study, the effect of emodin on YD-15 mucoepidermoid carcinoma cells and its molecular mechanism were investigated. This study shows that emodin significantly inhibits the growth of YD-15 cells. Activation of caspase-3 and PARP is triggered by emodin and it increases sub-G1 population and the number of YD-15 cells with nuclear condensation and fragmentation. In addition, we found that emodin significantly decreases myeloid cell leukemia 1(MCL-1). These results suggest that MCl-1 is an important molecule for emodin-induced apoptosis. Taken together, emodin inhibits cell viability and induces apoptosis via down-regulation of MCL-1 and it can be a new potent anticancer drug candidate for the treatment of mucoepidermoid carcinoma

[Background] Cordyceps militaris is a traditional popular mushroom, produces an important bioactive compound Cordycepin (3’-deoxyadenosine) used for the tonic and medicinal purpose in eastern Asia. Cordycepin is reported to possess many pharmacological activities including immunologically stimulating, anti-tumor, anti-virus, and anti-infection effects. [Methods] Growth inhibition of human leukemia cells was assessed by MTT assays. The determination of apoptotic cell death was performed by flow cytometry analysis, agarose gel electrophoresis and DAPI fluorescent staining methods. The apoptotic-regulated gene markers in both death receptor- and mitochondria-mediated apoptotic pathways were detected by RT-PCR and Western blot analysis etc. [Results] It was found that inhibition of cell proliferation was observed for human leukemia U937 and THP-1 cells treated with cordycepin in a dose-dependent manner. Cordycepin induced morphological change and apoptotic cell death such as formation of apoptotic bodies, DNA fragmentation and increased populations of apoptotic-sub G1 phase. Apoptosis of U937 and THP-1 cells by cordycepin was associated with a down-regulation of anti-apoptotic Bcl-2 and inhibitor of apoptosis proteins (IAPs) expression. Cordycepin treatment induced the proteolytic activation of caspase-3, caspase-8 and caspase-9, and a concomitant inhibition of poly(ADP-ribose) polymerase (PARP), β-catenin and phospholipase (PLC)-γ1 protein. Conclusions: Our results indicated that the apoptotic processes caused by cordycepin are mediated by the regulation of the Bcl-2 and caspase family in human leukemia U937 and THP-1 cells. Our data also suggested that cordycepin may be a potential chemotherapeutic agent for the treatment of leukemia cancer patients.

Facial numbness restricted to the distribution of the mental nerve(mental neuropathy) is called "numb chin syndrome". The clinical importance of this syndrome is associated with first recognition of involvement of malignant diseases. The malignant neoplasm with numb chin syndrome show rapid progression and high mortality. We present a 43-year-old female who had been treated by radiotherapy for precursor T-cell leukemia/lymphoma involving the central nervous system( CNS) previously and later developed mental nerve invasion without central nervous system recurrence. MRI images revealed the CNS tumor mass remitted, and there was no identified peripheral nervous system(PNS) involvement including the mental nerve invasion, nevertheless the patient complained of consistent numbness and pain on right mandibular area. This is the first case of precursor T-cell leukemia/lymphoma accompanying mental nerve invasion without recurrence for central nervous system. Proper interpretation for mental neuropathy may lead to the prompt diagnosis and therapeutic intervention.

Cordycepin (3’-deoxyadenosin), a polyadenylation specific inhibitor, is the main functional component in Cordyceps militaris which is one of the top three famous traditional Chinese medicine. It has been shown to possess many pharmacological activities including immunologically stimulating, anti-cancer, anti-bacterial, and anti-virus, anti-infection effects. However, its anti-cancer molecular mechanisms are poorly understood. In this study, the apoptotic effects by cordycepin were investigates in human leukemia cells. Treatment of cordycepin significantly inhibited cells growth in a concentrationdependent manner by inducing apoptosis, as evidenced by morphological change and apoptotic cell death such as formation of apoptotic bodies, DNA fragmentation and increased populations of sub-G1. Induction of apoptosis by cordycepin was associated with modulation of Bcl-2 and inhibitor of apoptosis proteins (IAP) family expression. Cordycepin also increased reactive oxygen species (ROS) generation, activation of casepase-3, caspase-8, caspase-9, cleavage of poly(ADP-ribose) polymerase (PARP), β-catenin and phospholipase C (PLC)-γ1 protein. The quenching of ROS generation by N-acetyl-L-cysteine administration, a scavenger of ROS, reversed the cordycepin-induced apoptosis effects. Theresults suggested that cordycepin may be a potential chemotherapeutic agent for the treatment of leukemia patients [This work was supported by Blue-Bio Industry RIC at Dong-Eui University as a RIC (08-06-07) program of ITEP under Ministry of Knowledge Economy].

Cordycepin (3’-deoxyadenosine) is a polyadenylation specific inhibitor, one of the components of Cordyceps militaris. It has been shown to possess many pharmacological activities including immunologically stimulating, anti-tumor, anti-virus, and anti-infection effects. However, its molecular mechanisms are poorly understood. In this study, the apoptotic effects by cordycepin were investigated in human leukemia cells. Cordycepin treatment inhibited leukemia cells growth a concentration-dependent manner by inducing apoptosis,as evidenced by morphological change and apoptotic cell death such as formation of apoptotic bodies, DNA fragmentation and increased populations of apoptoticsub G1 phase. Induction of apoptosis by cordycepin in leukemia cells were associated with modulation of Bcl-2 member and inhibitor of apoptosis (IAP) proteins expression. Cordycepin also increased ROS generation, activation of caspase-3, caspase-8, caspase-9, cleavage of poly(ADP-ribose) polymerase (PARP), -catenin and phospholipase (PLC)-1 protein. Both the this effect by cordycepin treatment were significantly inhibited by NAC, a ROS scavenger, demonstrating the important role of ROS in the observed cytotoxic effect. This results suggested that cordycepin may be a potential chemotherapeutic agent for the treatment of leukemia patients.

The differentiation of leukemia cells into mature cells is a major target of the human leukemia therapy. As differentiated leukemia cells lose their proliferative and tumor-forming abilities, differentiation inducers may be useful for the treatment of leukemia. In this study, the experiments were designed to determine whether diallyl disulfide (DADS) regulates expressions of tumor suppressor protein PTEN (phosphatase and tension homologue) in HL- 60 cells. DADS causes upregulation of PTEN in a time- and dose-dependent manner, which was correlated with decrease of phospho-Akt level. These results suggest that DADS induces upregulation of PTEN in human leukemia cells. These results suggest that DADS may be a useful anticancer agent for management of human leukemia.

In this study, the apoptotic effects of the actin disruption agent, latrunculin B(LB) have been investigated on p53 deficient chronic myeloid leukemia cell line K562. A dose-dependent decrease in K562 cell proliferation was observed after LB treatment with maximum decrease in cell proliferation being at 1.5μM where the percent inhibition was 66.53%. F-actin stained with TRITC-phalloidin was shown as a peripheral ring or appeared diffusely distributed throughout the cytoplasm in untreated cells, this actin ring was decreased following LB treatment, and even large focal actin aggregates were formed. Treatment of K562 with LB(1.5μM) generated ROS substantially. LB activated expression in a dose-dependent manner. Therefore it can be concluded that LB, depolymerising agent of actin, induces apoptosis by producing ROS and up-regulating NF-kB and COX-2 activation.

In order to study the antitumoral effect of Selaginella tamariscina extracts, the cytotoxicities to human histiocytic leukemia cells (U937) and lymphocyte were measured by MTT method. The water extract of Selaginella tamariscina was partitioned into chloroform (CHCl₃), ethylacetate (EtAc), n-butanol (BuOH) and water (H₂O), successively. CHCl₃, EtAc and BuOH fractions of Selaginella tamariscina showed the cytotoxicity to the U937 cells but they had no effect on the cytotoxicity of lymphocyte under the same conditions. The tumor-specific cytotoxicity of Selaginella tamariscina fractions might have been attributed to their genotoxic effect on actively proliferating cells. The expression of p53 tumor suppressor gene was then evaluated by northern blotting. The increased expression of p53 was induced by Selaginella ramariscina fraction V but no expression of p53 was induced by CHCl₃, EtAc, and BuOH fractions of Selaginella tamariscina. These results suggested that the increased expression of p53 induced by Selaginella tamariscina water extract (fraction V) should be required for the cytotoxicity on U937 and the other fractions of Selaginella tamariscina mediated the U937 disruption.