Biomedical subjects

Ming Yu

Publications and source records attributed to Ming Yu.

At least 19 recordsLinked to original sources

PubMed2026

Identification of a novel human gut microbes and microbial metabolites related genes signature for prognostic implication in head and neck squamous carcinomas.

BACKGROUND: The gut microbiota acts as a critical driver influencing the pathogenesis, therapeutic response, and clinical outcomes across various cancer types. This study aimed to investigate the prognostic value of human gut microbes and microbial metabolites related genes (HGMMMRGs) in head and neck squamous cell carcinoma (HNSCC). METHODS: We constructed a prognostic risk model comprising 19 core HGMMMRGs using LASSO penalized regression and a multivariate Cox proportional hazards model. The predictive performance of the model was evaluated through Kaplan-Meier analysis, receiver operating characteristic (ROC) curves, nomograms, and concordance index. In addition, functional enrichment analysis was performed on the differentially expressed risk genes. Furthermore, the relationship between the immune microenvironment of HNSCC and the risk diagnostic model was examined. Western blot analysis was used to assess the expression levels of IL10 in both HNSCC tissues and adjacent normal tissues. Finally, the correlation between IL10 and the gut microbiota was explored. RESULTS: This study developed a risk score model integrating 19 HGMMMRG genes, which can serve as a tool to guide prognosis and immune microenvironment assessment in HNSCC patients. Survival analysis showed that patients in the high-risk group had significantly worse outcomes (P < 0.05). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed significant enrichment of differentially expressed genes (DRLs) and immune-related pathways. Western blot analysis further confirmed that IL10 was highly expressed in HNSCC, and the abundance of Faecalibacterium prausnitzii and Enterococcus durans colonies was correlated with IL10 expression. CONCLUSION: We developed a prognostic model for HGMMMRGs that can be effectively used to predict OS in patients with HNSCC. Second, Faecalibacterium prausnitzii and Enterococcus durans can influence the prognosis of patients with HNSCC by mediating the expression IL10 and thereby affecting the prognosis of HNSCC patients. Thus, human gut microbes and microbial metabolite-related genes may be another promising strategy for the treatment of patients with HNSCC.

HNSCC↗

PubMed2024

Molecular Analysis of Persistent and Recurrent Barrett's Esophagus in the Setting of Endoscopic Therapy.

INTRODUCTION: Early neoplastic progression of Barrett's esophagus (BE) is often treated with endoscopic therapy. Although effective, some patients are refractory to therapy or recur after apparent eradication of the BE. The goal of this study was to determine whether genomic alterations within the treated BE may be associated with persistent or recurrent disease. METHODS: We performed DNA sequencing on pre-treatment esophageal samples from 45 patients who were successfully treated by endoscopic therapy and did not recur as well as pre-treatment and post-treatment samples from 40 patients who had persistent neoplasia and 21 patients who had recurrent neoplasia. The genomic alterations were compared between groups. RESULTS: The genomic landscape was similar between all groups. Patients with persistent disease were more likely to have pre-treatment alterations involving the receptor tyrosine kinase pathway ( P = 0.01), amplifications of oncogenes ( P = 0.01), and deletions of tumor suppressor genes ( P = 0.02). These associations were no longer significant after adjusting for patient age and BE length. More than half of patients with persistent (52.5%) or recurrent (57.2%) disease showed pre-treatment and post-treatment samples that shared at least 50% of their driver mutations. DISCUSSION: Pre-treatment samples were genomically similar between those who responded to endoscopic therapy and those who had persistent or recurrent disease, suggesting there is not a strong genomic component to treatment response. Although it was expected to find shared driver mutations in pre-treatment and post-treatment samples in patients with persistent disease, the finding that an equal number of patients with recurrent disease also showed this relation suggests that many recurrences represent undetected minimal residual disease.

Humans↗

PubMed2006

PIAS3 induction of PRB sumoylation represses PRB transactivation by destabilizing its retention in the nucleus.

Progesterone receptor (PR) plays a critical role in cell proliferation and differentiation, and its transcriptional activity is known to be modulated by cofactor proteins. In the present study, we demonstrated that in the presence of progesterone, protein inhibitor of activated STAT-3 (PIAS3) significantly inhibited the PR transcriptional activity and the expression of progesterone-responsive genes. Reduction of endogenous PIAS3 by PIAS3 small-interfering RNA enhanced PR transactivation in a ligand-dependent manner. PIAS3 interacted with PR both in vitro and in vivo and the interaction was enhanced by progesterone. Furthermore, our findings suggested that PIAS3 strongly induced PRB sumoylation at three sites, Lys-7, Lys-388 and Lys-531. In addition, novel roles in PRB nuclear retention and transactivation were identified for these sites. Our data also suggested that PIAS3 was recruited in a largely hormone-dependent manner in response to a progesterone-responsive promoter. Finally, we demonstrated that PIAS3 inhibited the DNA-binding activity of PR and influenced its nuclear export as well as PR transactivation. Taken together, these data strongly suggested that PIAS3 played an important physiological role in PR function.

Animals↗

PubMed2006

Protein kinase casein kinase 2 mediates inhibitor-kappaB kinase and aberrant nuclear factor-kappaB activation by serum factor(s) in head and neck squamous carcinoma cells.

We showed previously that the signal transcription factor nuclear factor-kappaB (NF-kappaB) is aberrantly activated and that inhibition of NF-kappaB induces cell death and inhibits tumorigenesis in head and neck squamous cell carcinomas (HNSCC). Thus, identification of specific kinases underlying the activation of NF-kappaB could provide targets for selective therapy. Inhibitor-kappaB (IkappaB) kinase (IKK) is known to activate NF-kappaB by inducing NH(2)-terminal phosphorylation and degradation of its endogenous inhibitor, IkappaB. Casein kinase 2 (CK2) was previously reported to be overexpressed in HNSCC cells and to be a COOH-terminal IKK, but its relationship to NF-kappaB activation in HNSCC cells is unknown. In this study, we examined the contribution of IKK and CK2 in the regulation of NF-kappaB in HNSCC in vitro. NF-kappaB activation was specifically inhibited by kinase-dead mutants of the IKK1 and IKK2 subunits or small interfering RNA targeting the beta subunit of CK2. CK2 and IKK kinase activity, as well as NF-kappaB transcriptional activity, was shown to be serum responsive, indicating that these kinases mediate aberrant activation of NF-kappaB in response to serum factor(s) in vitro. Recombinant CK2alpha was shown to phosphorylate recombinant IKK2 as well as to promote immunoprecipitated IKK complex from HNSCC to phosphorylate the NH(2)-terminal S32/S36 of IkappaBalpha. We conclude that the aberrant NF-kappaB activity in HNSCC cells in response to serum is partially through a novel mechanism involving CK2-mediated activation of IKK2, making these kinases candidates for selective therapy to target the NF-kappaB pathway in HNSCC.

Carcinoma, Squamous Cell↗

PubMed2006

Potent inhibition of the CD4-dependent T cell response by J2, a novel nonpeptide organic ligand of CD4 D1.

The interaction between CD4 and major histocompatibility complex (MHC) class II proteins is critical for the activation of CD4+ T cells, which are involved in transplantation reactions and a number of autoimmune diseases. It is known that the CD4 N-terminal immunoglobulin variable region-like domain (D1) is directed toward and reaching into the two membrane-proximal domains of the MHC class II molecule. Thus, compounds targeted to D1 would be expected to function as the inhibitors of the interaction of CD4 and class II MHC molecules. In this study, we used a computer-based design method to screen thousands of non-peptidic compounds in a molecular database and identified a group of compounds as potential ligands of CD4 D1. These small organic compounds were then synthesized and tested by actual biological assays. One of them, named J2, which possessed favorable activity, was obtained. Experimental data showed that J2 could specifically block stable CD4-MHC class II binding and elicit significant inhibition of immune responses in vitro and in vivo. All the results demonstrated the therapeutic potential of this compound as a novel immunosuppressive agent.

Acrylamides↗

PubMed2006

Expression and distribution of HSP27 in response to G418 in different human breast cancer cell lines.

Heat shock proteins (HSPs) play an important role in folding, intracellular localization and degradation of cellular proteins. However, the cellular role of HSP27 is not completely understood. The conflicting results have been reported regarding stress-induced nuclear translocation of HSP27. In this study, human breast cancer cells transiently and stably expressing HSP27-EGFP chimera were utilized to observe the intracellular localization of HSP27. The data show that the transient and stable expression of HSP27-EGFP displayed distinguishingly cellular localization. The nuclear translocalization of HSP27-EGFP was correlated with the presence of G418. Experiments carried out with different human breast cancer cell lines revealed clearly different distribution patterns of endogenous HSP27. The subcellular distribution of endogenous HSP27 appeared diffuse throughout the cytoplasm in MDA435 cells. In MCF-7 and SKBR3 cells, the accumulation of the protein was distinctly seen along the cell membrane and around nucleus. Moreover, the nuclear translocation of endogenous HSP27 was stimulated by G418 only in MDA435 cells, but not in MCF-7 and SKBR3 cells. Overexpression of HSP27 has been associated with resistance to cisplatin and doxorubicin. The correlation of the expression pattern of HSP27 with the drug resistance may need to be investigated. Further studies on the intracellular function of HSP27 may take into account its interaction proteins in the cells. It may provide useful information for the identification of sensitivity of carcinoma cells to the chemotherapeutic drugs and development of more specific agents to circumvent HSP27.

Blotting, Western↗

PubMed2006

A novel cis-acting element in Her2 promoter regulated by Stat3 in mammary cancer cells.

Stat3 plays important roles in the development of breast malignancies and oncogenesis. In the present study, a palindromic cis-acting element displaying repression activity in breast cancer cells expressing low level of Her2 was found in Her2 promoter. Deletion analysis showed that the novel element was located within Pal2 region spanning nucleotides -529 to -505. The sequence analysis of Pal2 region revealed a DNA sequence (TTAAGATAA) homologous to the binding site of Stat3, starting from position -529 to -521bp. By reporter assay, Pal2 was found to be regulated by constitutive activated Stat3C. A stimulatory effect both on Her2 mRNA and protein expressions was observed in MCF-7 cells stably expressing Stat3C, suggesting that Stat3 regulated Her2 expression. Using ChIP assays the binding of Stat3 to Her2 promoter was confirmed. The data obtained in this study indicate constitutive activated Stat3 regulates Her2 expression. Further investigation of differential effects of Stat3 exerting on breast cancer cells expressing Her2 at different levels will provide more insights into the roles of Stat3 in Her2 expression as well as the regulation of diverse biological activities.

Base Sequence↗

PubMed2006

[The features of postprandial glucose state in type 2 diabetes mellitus].

OBJECTIVE: To study the features of postprandial glucose state in individuals with normal glucose regulation (NGR) and type 2 diabetes (T2DM) and the relations between hemoglobin A1c (HbA1c) and postprandial glucose in T2DM. METHODS: 41 NGR individuals and 60 newly diagnosed T2DM patients without previous management in Shanghai were measured by continuous glucose monitoring system for 3 days. The postprandial glucose spike (PGS), time to PGS (Deltat), postprandial glucose excursion (PPGE), duration of postprandial glucose (DUR) and incremental area under the curve of postprandial glucose (IAUC) were calculated in each individual. RESULTS: (1) The levels of PGS and Deltat in the T2DM group were significantly higher than those of the NGR group (all P < 0.01). The levels of PPGE, DUR and IAUC of the T2DM group were 5.87 mmol/L +/- 0.19 mmol/L, 14.1 h +/- 0.3 h and 2.04 mmol.L(-1).d +/- 0.09 mmol.L(-1).d respectively, all significantly higher than those of the NGR group (2.10 mmol/L +/- 0.12 mmol/L, 8.3 h +/- 0.4 h and 0.43 mmol.L(-1).d +/- 0.03 mmol.L(-1).d respectively, all P < 0.01). The breakfast had higher PGS and lower Deltat than those of lunch and dinner in the T2DM group (both P < 0.01). The PPGE was arranged from high to low in the order of breakfast, dinner and lunch. The highest IAUC appeared during dinner. (2) There was a significantly correlation between PPGE and IAUC (r = 0.93, P < 0.01) in the T2DM group. After being adjusted by preprandial glucose, the partial correlation of HbA1c and IAUC disappeared (before r = 0.29, P = 0.03, after P = 0.05). (3) The relative contribution of postprandial glucose to overall glucose levels in the T2DM group was significantly higher than that of the NGR group (18.1% +/- 0.8% vs 8.0% +/- 0.7%, P < 0.01), but both were significantly lower than those of preprandial glucose. (4) Relative contribution of postprandial hyperglycemia to overall diurnal hyperglycemia decreased progressively from the lowest to the highest quarter of HbA1c. By contrast, the relative contribution of preprandial hyperglycemia showed a significant increase with increasing levels of HbA1c. Postprandial hyperglycemia played a major role when the HbA1c level below 7.5% (P < 0.05). CONCLUSION: (1) The features of postprandial glucose state in T2DM is representative in the delay of PGS and excessive glucose excursion for a long time after the ingestion of a meal. (2) HbA1c can't reflect postprandial glucose excursions. PPGE can be used as a simple clinic index to evaluate the amplitude of postprandial glucose excursions. (3) Postprandial glucose excursions play a major role in T2DM suffering from mild or moderate hyperglycemia. The present results suggest that postprandial hyperglycemia is an important target for intervention when T2DM patients are approaching the ideal glycemic control.

Adult↗

PubMed2006

Role of superoxide and angiotensin II suppression in salt-induced changes in endothelial Ca2+ signaling and NO production in rat aorta.

Male Sprague-Dawley rats were maintained on a low-salt (LS) diet (0.4% NaCl) or changed to a high-salt (HS) diet (4% NaCl) for 3 days. Increases in intracellular Ca2+ ([Ca2+]i) in response to methacholine (10 microM) and histamine (10 microM) were significantly attenuated in aortic endothelial cells from rats fed a HS diet, whereas thapsigargin (10 microM)-induced increases in [Ca2+]i were unaffected. Methacholine-induced nitric oxide (NO) production was eliminated in endothelial cells of aortas from rats fed a HS diet. Low-dose ANG II infusion (5 ng x kg(-1) x min(-1) iv) for 3 days prevented impaired [Ca2+]i signaling response to methacholine and histamine and restored methacholine-induced NO production in aortas from rats on a HS diet. Adding Tempol (500 microM) to the tissue bath to scavenge superoxide anions increased NO release and caused N(omega)-nitro-L-arginine methyl ester-sensitive vascular relaxation in aortas from rats fed a HS diet but had no effect on methacholine-induced Ca2+ responses. Chronic treatment with Tempol (1 mM) in the drinking water restored NO release, augmented vessel relaxation, and increased methacholine-induced Ca2+ responses significantly in aortas from rats on a HS diet but not in aortas from rats on a LS diet. These findings suggest that 1) agonist-induced Ca2+ responses and NO levels are reduced in aortas of rats on a HS diet; 2) increased vascular superoxide levels contribute to NO destruction, and, eventually, to impaired Ca2+ signaling in the vascular endothelial cells; and 3) reduced circulating ANG II levels during elevated dietary salt lead to elevated superoxide levels, impaired endothelial Ca2+ signaling, and reduced NO production in the endothelium.

Angiotensin II↗

PubMed2006

The rational designed antagonist derived from the complex structure of interleukin-6 and its receptor affectively blocking interleukin-6 might be a promising treatment in multiple myeloma.

Human interleukin-6 is involved in the maintenance and progression of several diseases such as multiple myeloma (MM), rheumatoid arthritis, or osteoporosis. Our previous work demonstrated that an interleukin-6 antagonist peptide (named PT) possessed potential bioactivity to antagonize the function of hIL-6 and could efficiently induce the growth arrest and apoptosis of XG-7 and M1 cells in a dose-dependent manner. In this study, the theoretical interaction of the peptide PT with its receptor was analyzed further more with molecular docking and molecular dynamics methods. The theoretical studies showed that PT possessed very high affinity to interleukin-6R and offered a practical means of imposing long-term blockade of interleukin-6 activity in vivo. According to the theoretical results, the biological evaluation of PT was researched on two different cells models with more sensitive approaches: (1) The antagonist activity of PT was studied on the interleukin-6 dependent MM cells (XG-7) cultured with interleukin-6. In the other interleukin-6 dependent MM cells (SKO-007), they survived themselves by auto/paracrine without the exogenous interleukin-6, and also could be antagonized by PT. The therapeutic value of PT only limited on the interleukin-6 dependent category in MM. (2) Myeloid leukemia M1 cells were induced for growth arrest and apoptosis in response to interleukin-6. The results supported our previous findings and showed that PT could be evaluated by protecting the cells from interleukin-6 induced apoptosis. In conclusion, PT could induce interleukin-6-dependent XG-7 and SKO-007 cells to apoptosis while inhibit interleukin-6-stimulated apoptosis in M1 cells.

Antineoplastic Agents↗

PubMed2006

Inhibitory effect of antisense vascular endothelial growth factor RNA on the profile of hepatocellular carcinoma cell line in vitro and in vivo.

AIM: To evaluate the effect of antisense vascular endothelial growth factor (VEGF) RNA (PCMV-FGEV) transfection on the profile of hepatocellular carcinoma (HCC) SMMC-7721 cells in vitro and in vivo. METHODS: SMMC-7721 cells were transfected with PCMV-FGEV antisense, PCMV-VEGF sense and empty vector plasmid encapsulated by lipofectamine as antisense group, sense group and control group respectively. The positive cell clones were selected with G418. The stable transfection and expression of VEGF in the cells were determined by RT-PCR and immunohistochemistry. Cell proliferation was observed by MTT assay. FACS analysis was used to determine the effect of PCMV-FGEV transfection on cell apoptosis. The growth of transfected cells in vivo was also observed in nude mice. RESULTS: VEGF expression was reduced in SMMC-7721 transfected with PCMV-FGEV, which was confirmed by RT-PCR and immunohistochemistry. No effect of PCMV-FGEV transfection was found on cell proliferation and cell apoptosis of SMMC-7721 in vitro. The growth of cells transfected with PCMV-FGEV was slow in nude mice and accompanied with obvious apoptosis. The latent time of tumors in the antisense group was 25.0 +/- 1.8 d, which was longer than that in sense and control groups (F = 19.455, P < 0.01). The average tumor weight in antisense group (0.96 g +/- 0.28 g) was the smallest among the three groups (F = 21.501, P < 0.01). CONCLUSION: The expression of VEGF can be inhibited by antisense PCMV-FGEV. Antisense PCMV-FGEV has no effect on cell proliferation and apoptosis of SMMC-7721 in vitro but can inhibit tumor growth and induce cell apoptosis in vivo.

Animals↗

PubMed2006

Establishment of a cell model based on FKBP12 dimerization for screening of FK506-like neurotrophic small molecular compounds.

FK506 is an efficient immunosuppressive agent with an increasing number of clinical applications. It has been approved to prevent rejection in transplant patients and be efficacious in several autoimmune diseases. Its immunosuppressive activity results from binding to receptor proteins designated as immunophilins (i.e., FKBP12, FK506 binding protein). Recent studies have suggested that FK506 can promote neurite outgrowth as a 2nd activity. Furthermore, it has been shown that the neurotrophic property of FK506 is independent of its immunosuppressive action. Although the mechanism of its neurotrophic activity has not yet been well elucidated, FKBP12 is identified as a drug target, and much effort has been directed toward the design of FKBP12-binding molecules, which are neurotrophic but non-immunosuppressive, for clinical use. In this present study, the authors constructed a stable cell line, which underwent apoptosis upon treatment by AP20187, a wholly synthesized, cell-permeable dimeric FK506 derivative, based on FKBP12-mBax dimerization. This AP20187-mediated apoptosis was rapidly reversed by the addition of an FKBP12-binding competitor molecule (FK506 or rapamycin), indicating that this cell line might be used to screen FK506 derivatives. Using the screening model, hundreds of synthetic FK506 analogs were analyzed. A promising compound, named N308, was obtained. The results showed that N308 could inhibit AP20187-induced gene-modified target cell apoptosis and elicit augmentation of neurite extension from both cultured PC-12 cells and chicken dorsal root ganglia cultures.

Animals↗

PubMed2006

Encapsulation of quinine by beta-cyclodextrin: excellent model for mimicking enzyme-substrate interactions.

An inclusion complex formed by beta-cyclodextrin and quinine has been investigated in solution and in the solid state, in which the quinoline ring and the aliphatic ring locate in different hydrophobic cavities, respectively. The study on the inclusion geometry and weak interactions shows that the difference in conformation for this complex is a result of three main packing arrangement considerations, which can provide an ideal model mimicking enzyme-substrate interactions.

Biomimetic Materials↗

PubMed2006

Sequestering ErbB2 in endoplasmic reticulum by its autoinhibitor from translocation to cell surface: an autoinhibition mechanism of ErbB2 expression.

ErbB2 is differentially overexpressed in tumor versus host tissues, suggesting that an autoregulation mechanism may modulate the expression of ErbB2 and control cell growth. A truncated ErbB2 extracellular domain, herstatin has been shown to bind to ErbB2 and inhibit the growth of tumor cells expressing ErbB2. In the present study, the interaction of herstatin and ErbB2 in vivo was observed by confocal microscopy. The aggregation of ErbB2 and herstatin was found in endoplasmic reticulum (ER). The decrease of ErbB2 on the cell surface was accompanied with the increased colocalization of ErbB2 and herstatin in the cytoplasm, suggesting that the formation of ErbB2/herstatin complex may prevent transit from ER to cell surface of ErbB2. The formation of ErbB2 and herstatin complex was further confirmed by immunoprecipitation. The results demonstrate that sequestering ErbB2 molecules intracellularly by herstatin may be a possible mechanism of the cell growth inhibition.

Animals↗

PubMed2006

Directing energy flow through quantum dots: towards nanoscale sensing.

Nanoscale sensors can be created when an expected energetic pathway is created and then that pathway is either initiated or disrupted by a specific binding event. Constructing the sensor on the nanoscale could lead to greater sensitivity and lower limits of detection. To this end, quantum dots (QDs) can be considered prime candidates for the active components. Relative to organic chromophores, QDs have tunable spectral properties, show less susceptibility to photobleaching, have similar brightness, and have been shown to display electro-optical properties. In this review, we discuss recent articles that incorporate QDs into directed energy flow systems, some with the goal of building new and more powerful sensors and others that could lead to more powerful sensors.

Journal Article↗

PubMed2006

Proteomics-based identification of autoantibodies in the sera of healthy Chinese individuals from Beijing.

The identification of panels of tumor antigens that elicit an antibody response may have utility in cancer screening, diagnosis and in establishing prognosis. However, autoantibodies normally exist in sera of healthy individuals and are enormously diversified. To explore the reservoir of autoantibody in healthy population, we performed a proteomics investigation of autoantibody profiles in the sera of 36 healthy Chinese individuals from Beijing, which may provide valuable reference information to the identification of disease-specific autoantibodies. The results showed that autoantibody profiles varied individually, but some autoantibodies were identified at a high frequency in the healthy population. The autoantibodies against alpha-enolase and those against heterogeneous nuclear ribonucleoprotein L were positive in more than 50% of the sera samples. The autoantibodies identified in more than 20% of samples included those against annexin II, F-actin capping protein beta subunit and calreticulin. Some of these autoantibodies have been previously reported to be involved in autoimmune conditions and cancers. Autoantibodies in the healthy population are important as a foundation from which disease-specific autoantibodies can be defined. Thus our report on autoantibodies in healthy individuals may be useful as a reference for defining new autoantibody biomarkers.

Adult↗

PubMed2006

A novel neutralizing monoclonal antibody against both ricin toxin A and ricin toxin B, and application of a rapid sandwich enzyme-linked immunosorbent assay.

Two strains of neutralizing monoclonal antibodies (MAbs) anti-ricin, both B chain and A chain, named 3D74 and 4C13, were generated efficiently. The two antibodies recognized different epitopes located in a separated toxin structure domain characterized by enzyme-linked immunosorbent assay (ELISA) and Western blotting. 3D74 recognized space conformation epitope, whereas 4C13 recognized linearity epitope of ricin. 4C13 possessed a novel neutralizing ability; the safe period for intraperitoneal injection of 100 microg of antibody was 30 min after intraperitoneal injection of 2 microg of ricin (10 times LD50). Using 3D74 and 4C13 as pair-matching antibodies, we established sandwich ELISA and rapid ELISA for detection of ricin. The detection sensitivities were 31.3 and 156 pg/ml, respectively. Rapid sandwich ELISA was sufficiently sensitive and was performed easily for ricin detection without any special instruments.

Animals↗

PubMed2006

Analysis of an anti-B lymphocyte stimulator monoclonal antibody B7 and its binding activity to myeloma and lymphoma cell lines.

Although there is convincing evidence of a link between B lymphocyte stimulator (BLyS) and the proliferation and survival of malignant B cells, previous observations about BLyS expression on B lymphoma cells were contradictory. In this study, BLyS expression on human lymphoma and myeloma cell lines was evaluated by Fluorescence-Activated Cell Sorter (FACS). First, specificity of a monoclonal antibody (MAb) against BLyS, was analyzed. The results showed that MAb B7 was immunoglobulin G(3) (IgG(3)) and recognized recombinant human BLyS specifically. In addition, MAb B7 bound to the histiocyte lymphoma cell line U937 in dosage-dependent manner, but not the T lymphoma cell line Jurkat, suggesting that the cellular binding of MAb B7 was specific. Using this MAb, BLyS expression on two multiple myeloma cell lines (XG-7 and SKO-007) and two Burkitt's lymphoma cell lines (Daudi and Raji) was evaluated. MAb B7 did bind to XG- 7 and SKO-007 (66.84% and 79.38% positive cells, respectively). But MAb B7 did not bind Burkitt's lymphoma cell lines, Daudi and Raji (4.09% and 3.02% positive cells, respectively). It will be interesting to further analyze the expression of BLyS on B malignant cells of multiple myeloma and lymphoma patients, and to evaluate the correlation of its expression and patient prognosis.

Antibodies, Monoclonal↗