Study on Functional Monoclonal Antibodies of Anti-Human Uterine Sarcoma Stem Cell-Like Cells

2020 ◽  
Author(s):  
Jingting Cai ◽  
Jiuping Gao ◽  
Beilei Zhang ◽  
Dihong Tang ◽  
Ting Gao ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Monoclonal Antibodies ◽  
Stem Cell ◽  
Cell Migration ◽  
Cell Line ◽  
Colony Formation ◽  
Formation Rate ◽  
Uterine Sarcoma ◽  
Spheroid Formation ◽  
Self Renewal

Abstract Background: To establish a functional monoclonal antibody library using Human Uterine Sarcoma Stem Cell-Like Cells (HUSSLCs) to screen and identify functional monoclonal antibodies that can recognize and inhibit HUSSLCs. Methods: B lymphocytes in proliferative state were prepared by using the second generation CD133+spheroid cells of SK-UT-1 cell line, i.e. HUSSLCs, as antigens; Spheroid formation, agar colony formation, wound healing, flow cytometry, and Western blotting were adopted to detect the effect of monoclonal antibodies with varied dilution ratios on HUSSLCs spheroid formation, agar colony formation, cell migration, CD133 expression, and expression of CD44, ABCG2, Bmi1, Nanog, Oct4 and ALDH1. Results: Myeloma cells of SP2/0 cell line can achieve 85% degrees of fusion and results of 1-2F monoclonal cell supernatants with different dilution ratios reduced HUSSLCs spheroid formation rate, agar colony formation rate, cell migration rate, CD133 positive cell expression and protein expression levels of CD44, ABCG2, Bmi1, Nanog, Oct4, and ALDH1 in concentration-dependent manner (P <0.05). Conclusion: The antibody valence produced by HUSSLCs-immunized mice reached the requirement for preparation of monoclonal antibody. Anti-HUSSLCs monoclonal antibodies feature functions of inhibiting the self-renewal, unrestricted proliferation, migration, invasion and multidrug resistance of HUSSLCs and functions characterized by tumor stem cells. Key words: uterine leiomyosarcoma; tumor stem cell; monoclonal antibody; self-renewal ability; infinite multiplication; drug resistance

Study on Functional Monoclonal Antibodies of Anti-Human Uterine Sarcoma Stem Cell-Like CellsStudy on Functional Monoclonal Antibodies of Anti-Human Uterine Sarcoma Stem Cell-Like Cells

2020 ◽  
Author(s):  
Jiuping Gao ◽  
Beilei Zhang ◽  
Dihong Tang ◽  
Ting Gao ◽  
Qiuhui Lin ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Monoclonal Antibodies ◽  
Stem Cell ◽  
Cell Migration ◽  
Cell Line ◽  
Colony Formation ◽  
Formation Rate ◽  
Uterine Sarcoma ◽  
Dependent Manner ◽  
Spheroid Formation

Abstract Background: To establish a functional monoclonal antibody library using Human Uterine Sarcoma Stem Cell-Like Cells (HUSSLCs) to screen and identify functional monoclonal antibodies that can recognize and inhibit HUSSLCs.Methods: B lymphocytes in proliferative state were prepared by using the second generation CD133+spheroid cells of SK-UT-1 cell line, i.e. HUSSLCs, as antigens; Spheroid formation, agar colony formation, wound healing, flow cytometry, and Western blotting were adopted to detect the effect of monoclonal antibodies with varied dilution ratios on HUSSLCs spheroid formation, agar colony formation, cell migration, CD133 expression, and expression of CD44, ABCG2, Bmi1, Nanog, Oct4 and ALDH1.Results: Myeloma cells of SP2/0 cell line can achieve 85% degrees of fusion and results of 1-2F monoclonal cell supernatants with different dilution ratios reduced HUSSLCs spheroid formation rate, agar colony formation rate, cell migration rate, CD133 positive cell expression and protein expression levels of CD44, ABCG2, Bmi1, Nanog, Oct4, and ALDH1 in concentration-dependent manner (P <0.05).Conclusion: The antibody valence produced by HUSSLCs-immunized mice reached the requirement for preparation of monoclonal antibody. Anti-HUSSLCs monoclonal antibodies feature functions of inhibiting the self-renewal, unrestricted proliferation, migration, invasion and multidrug resistance of HUSSLCs and functions characterized by tumor stem cells.

scholarly journals Multi-CSF-dependent colony formation by cells of a murine hemopoietic cell line: specificity and action of multi-CSF

Blood ◽  
1985 ◽  
Vol 65 (2) ◽  
pp. 357-362 ◽  
Author(s):  
D Metcalf
Keyword(s):  
Cell Cycle ◽  
Cell Line ◽  
High Frequency ◽  
Colony Formation ◽  
Hemopoietic Cell ◽  
Self Renewal ◽  
Cell Cycles ◽  
Cell Numbers ◽  
Gm Csf ◽  
Complete Cell

Abstract Cells of the Multi-CSF (IL-3)-dependent hemopoietic cell line 32D c13 formed colonies of varying size in agar cultures stimulated by Multi- CSF. Colony formation was linear with respect to cultured cell numbers; colony numbers and size increased with increasing concentrations of Multi-CSF, and 32D colonies themselves contained a high frequency of clonogenic cells. Clonogenic 32D cells died in the absence of Multi-CSF (half-life six hours), and most were unable to complete cell cycles in progress at the time of withdrawal of Multi-CSF. The concentration of Multi-CSF directly influenced the length of the cell cycle of dividing 32D cells. Purified GM-CSF, G-CSF, or M-CSF had no capacity to support the survival or proliferation of 32D cells. Colonies formed by 32D cells appear to offer a useful model for analyzing the action of Multi- CSF in controlling self-renewal by clonogenic hemopoietic cells.

scholarly journals Abalone Collagen Extracts Potentiate Stem Cell Properties of Human Epidermal Keratinocytes

Marine Drugs ◽  
2019 ◽  
Vol 17 (7) ◽  
pp. 424
Author(s):  
Sajee Thaweekitphathanaphakdee ◽  
Pithi Chanvorachote ◽  
Sagaw Prateepchinda ◽  
Mattaka Khongkow ◽  
Apirada Sucontphunt
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Stem Cell ◽  
Cell Migration ◽  
Expression Level ◽  
Epidermal Keratinocytes ◽  
Stem Cell Markers ◽  
Spheroid Formation ◽  
Human Epidermal Keratinocytes ◽  
Cell Markers

Stem cell activities in human tissues are critical for tissue integrity and function. Maintaining keratinocyte stem cells (KSCs) stemness helps sustain healthy skin by supporting keratinocyte renewal, involving the formation of epidermal barriers. In this study, abalone collagen (AC) extracts with molecular weights of 3 kDa (AC 1) and 300 kDa (AC 2) were compared to the epidermal growth factor (EGF) for their effects on cell proliferation, cell migration (wound healing), spheroid formation, and the expression level of stem cell markers on human keratinocytes (HaCaT cells). Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and cell proliferation was quantified by ATP and DNA content analysis and Sulforhodamine B (SRB) assays. Cell migration assay was determined using the scratch wound healing test. Spheroid formation was evaluated and the expression level of stem cell markers was investigated by western blot analysis. The results showed that AC 1 at the concentration of 100 µg/mL could stimulate HaCaT cell proliferation, migration, spheroid formation, and the expression level of stem cell markers (keratin 19, β-catenin, ALDH1A1) compared to the control. In conclusion, a smaller molecular weight of abalone collagen extract exhibits a better effect on keratinocytes proliferation, migration, and stemness, which could be a potential active ingredient in cosmeceutical products.

MiR-29a Maintains Hematopoietic Stem Cell Self-Renewal and Is Required For Myeloid Leukemogenesis

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1190-1190
Author(s):  
Wenhuo Hu ◽  
James Dooley ◽  
Stephen S. Chung ◽  
Safak Yalcin ◽  
Yu Sup Shin ◽  
...  
Keyword(s):  
Stem Cell ◽  
Colony Formation ◽  
Target Genes ◽  
Conflicts Of Interest ◽  
Ectopic Expression ◽  
Null Mouse ◽  
Cell Cycle Regulators ◽  
Self Renewal ◽  
Hematopoietic Stem

Abstract microRNAs (miRNAs) are important regulators of both embryonic and adult tissue stem cell self-renewal. We previously showed that ectopic expression of miR-29a, a miRNA highly expressed in HSCs as well as in human acute myeloid leukemia (AML) stem cells, in immature mouse hematopoietic cells is sufficient to induce a myeloproliferative disorder that progresses to AML. During the early phase of this disease, miR-29a induces aberrant self-renewal of committed myeloid progenitors, strongly suggesting a role for miR-29a in regulating HSC self-renewal. In order to determine the role of miR-29a in HSC function, we have evaluated our recently described miR-29a/b1 null mouse. Homozygous deletion of miR-29a/b1 resulted in reduced bone marrow cellularity and reduced colony forming capacity of hematopoietic stem and progenitor cells (HSPCs). The phenotype was mediated specifically by miR-29a since miR-29b expression was not significantly altered in HSCs and reconstitution of miR-29a/b1 null HSPCs with miR-29a, but not miR-29b, rescued in vitro colony formation defects. Self-renewal defects were observed in miR-29a deficient HSCs in both competitive and non-competitive transplantation assays, and these deficits were associated with increased HSC cell cycling and apoptosis. Gene expression studies of miR-29a deficient HSCs demonstrated widespread gene dysregulation including a number of up-regulated miR-29a target genes including DNA methylation enzymes (Dnmt3a, -3b) and cell cycle regulators (e.g. Cdk6, Tcl1, Hbp1, Pten). Knockdown of one of these targets, Dnmt3a, in miR-29a deficient HSCs resulted in partial restoration of colony formation, providing functional validation that Dnmt3a mediates part of miR-29a null HSPCs functional defects. miR-29a loss also abrogated leukemogenesis in the MLL-AF9 retroviral AML model. Together, our results demonstrate that miR-29a positively regulates HSC self-renewal and is required for myeloid leukemogenesis. Disclosures: No relevant conflicts of interest to declare.

ID: 22: DIFFERENTIAL ACTIONS OF ESTROGEN RECEPTOR α AND β VIA NON-GENOMIC SIGNALING IN HUMAN PROSTATE STEM-PROGENITOR CELLS

2016 ◽  
Vol 64 (4) ◽  
pp. 933-933
Author(s):  
S Majumdar ◽  
JC Rinaldi ◽  
T Gauntner ◽  
L Xie ◽  
W Hu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Cell Line ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Mapk Pathway ◽  
Human Prostate ◽  
Stem Cell Markers ◽  
Self Renewal ◽  
Progenitor Cell Proliferation

Genomic signaling via estrogen receptors (ER) has been widely studied and implicated as the main ER signaling pathway in prostate development and carcinogenesis. Non-genomic ER signaling has also been reported in prostate epithelium although down-stream cascades have not been clarified. Our lab has recently identified ERs in human prostate epithelial stem/progenitor cells and shown that that 17β-estradiol (E2) can stimulate stem cell symmetric self-renewal and progenitor cell proliferation. In this study we interrogate non-genomic membrane initiated ER signaling in this prostate stem/progenitor cell population. Human prostate stem-progenitor cells were enriched from primary prostate epithelial cell cultures (PrEC) of young, disease-free donors using a 3D prostasphere (PS) model as previously described. Cells were labeled using ERα or ERβ antibodies along with prostate stem cell markers CD49f and TROP2 followed by triple channel FACS to quantify ERα+/ERβ+ cell numbers. To explore ERα, the benign human prostate stem cell line WPE with extremely low levels of ERα and ERβ, was stably transfected with a lentiviral-ERα expression vector. The human prostate cancer stem-like cell line HuSLC (ERβ++, ERα−) was utilized to interrogate ERb actions. Cells were exposed to 10 nM estradiol (E2) over a 15 to 60 minute time course +/− ICI 182,870 (ICI), an ERα/β antagonist. FACS analysis of day 7 PS cells labeled for ERα or ERβ revealed 66% of day 7 PS cells as ERα+ and 40% as ERβ+. Among ERα or ERβ positive PS cells, 4% were Trop2+/CD49fhigh (stem-like cells) and 10–12% were Trop2+/CD49fmedium (early stage progenitor cells). PS exposed to 10 nM E2 showed sequential phosphorylation of Src, Erk1/2, p38, Akt and NFκB (p65) over 60 minutes. Phosphorylation of up-and downstream targets (EGFR, Jnk, GSK 3α/β, p70 S6 kinase, PRAS40, MSK1/2) was also seen using a phospho-kinase array. Furthermore, phosphorylation of ERα at S167 was noted over 60 min of E2 exposure enabling enhancement of genomic ERα transactivational activity in a feed-forward manner. ICI attenuated Akt and Erk1/2 phosphorylation, confirming membrane bound ERs are involved in downstream signaling. E2 treatment of HuSLCs showed phosphorylation of Erk1/2 but not Akt, indicating that ERβ signals exclusively through the MAPK pathway in these cells. Conversely, E2 treatment of WPE-stem cells overexpressing ERα resulted in robust phosphorylation of Akt but lower levels of Erk1/2 phosphorylation suggesting that Akt activation may be more reliant on ERα signaling. To identify pathway specific roles, specific inhibitors were added to PS cultures. PS treated with LY294002 (Akt inhibitor) for 7 days attenuated the E2-mediated increase in PS number and size. Inhibition of the NFκB downstream of the Akt pathway by IKK VII (IKK inhibitor) blocked p65 phosphorylation, abrogated the E2-induced increase in stem cell symmetric self-renewal and blunted E2 stimulation of progenitor cell proliferation. Analysis of PS cyclin mRNA levels revealed a G1 arrest of progenitor cells upon IKK inhibition suggesting an essential role of NFκB in progenitor cell amplification. MAPK pathway inhibition with U0126(Erk1/2 inhibitor) resulted in an attenuation of the E2-mediated increase in PS number and size and an increase stem cell symmetric self-renewal suggesting that MAPK pathway activation promotes commitment to stem and progenitor cell expansion. Taken together, the present findings reveal that human prostate stem-progenitor cells express both ERα and ERβ which differentially activate different signaling cascades originating at the membrane. These signaling events may lead to unique downstream actions that influence prostate stem-progenitor cell proliferation as well as lineage commitment decisions.

scholarly journals The RNA N6-Methyladenosine Methyltransferase METTL3 Promotes the Progression of Kidney Cancer via N6-Methyladenosine-Dependent Translational Enhancement of ABCD1

2021 ◽  
Vol 9 ◽  
Author(s):  
Yue Shi ◽  
Yanliang Dou ◽  
Jianye Zhang ◽  
Jie Qi ◽  
Zijuan Xin ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Kidney Cancer ◽  
Renal Cell ◽  
Xenograft Model ◽  
The Cancer Genome Atlas ◽  
Dependent Manner ◽  
Spheroid Formation

The role of N6-methyladenosine (m6A)-modifying proteins in cancer progression depends on the cell type and mRNA affected. However, the biological role and underlying mechanism of m6A in kidney cancer is limited. Here, we discovered the variability in m6A methyltransferase METTL3 expression was significantly increased in clear cell renal cell carcinoma (ccRCC) the most common subtype of renal cell carcinoma (RCC), and high METTL3 expression predicts poor prognosis in ccRCC patients using a dataset from The Cancer Genome Atlas (TCGA). Importantly, knockdown of METTL3 in ccRCC cell line impaired both cell migration capacity and tumor spheroid formation in soft fibrin gel, a mechanical method for selecting stem-cell-like tumorigenic cells. Consistently, overexpression of METTL3 but not methyltransferase activity mutant METTL3 can promote cell migration, spheroid formation in cell line and tumor growth in xenograft model. Transcriptional profiling of m6A in ccRCC tissues identified the aberrant m6A transcripts were enriched in cancer-related pathways. Further m6A-sequencing of METTL3 knockdown cells and functional studies confirmed that translation of ABCD1, an ATP-binding cassette (ABC) transporter of fatty acids, was inhibited by METTL3 in m6A-dependent manner. Moreover, knockdown of ABCD1 in ccRCC cells decreased cancer cell migration and spheroid formation, and upregulation of ABCD1 acts as an adverse prognosis factor of kidney cancer patients. In summary, our study identifies that METTL3 promotes ccRCC progression through m6A modification-mediated translation of ABCD1, providing an epitranscriptional insight into the molecular mechanism in kidney cancer.

scholarly journals Loss of Phospholipase C Gamma 1 (PLCG1) Impairs AML1-ETO Induced Leukemia Stem Cell Self-Renewal

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 531-531
Author(s):  
Tina M. Schnoeder ◽  
Adrian Schwarzer ◽  
Florian Perner ◽  
Joanna Kirkpatrick ◽  
Anna Dolnik ◽  
...  
Keyword(s):  
Stem Cell ◽  
Phospholipase C ◽  
Median Survival ◽  
Colony Formation ◽  
Cellular Functions ◽  
Self Renewal ◽  
Leukemia Stem Cell ◽  
Gene Sets ◽  
Disease Penetrance

Chromosomal translocations found in acute myeloid leukemia (AML) can generate oncogenic fusions with aberrant epigenetic and transcriptional functions. However, direct therapeutic targeting of leukemia fusion proteins has not been accomplished so far. Although high remission rates can be induced in patients diagnosed with AML1-ETO/t(8;21)-positive AML only half of them achieve long-term disease-free survival (Papaemmanuiel et al., NEJM, 2016). In the other half of these patients, the disease maintaining leukemia stem cell (LSC) clone is not eliminated by chemotherapy. A functional characteristic of LSCs is unlimited self-renewal capacity and several signaling pathways have been identified that maintain stem cell self-renewal. Targeting the oncogene induced self-renewal capacity of LSCs has great potential to eliminate the malignant clone and prevent relapse. To identify oncogenic cellular functions with relevance for LSC self-renewal, we performed global proteome profiling in murine AML1-ETO9a (AE) compared to MLL-AF9 (MA9) driven LSCs. Gene set enrichment analyses revealed a significant enrichment of calcium-dependent cellular functions and Phospholipase C (PLC)-signaling in AE LSCs. These data could be confirmed in sorted CD34+ blasts from AE-positive AML when compared to non-AE-AML. All PLC family members are regulators of Ca2+ homeostasis. However, when analyzing published AML gene expression datasets we found exclusively PLCG1 to be highly expressed in t(8;21) AML. Conditional activation of AE in embryonic stem cells resulted in induction of PLCG1 expression and PLCG1 was identified as a direct target of the AE fusion by ChIP-sequencing in AE-positive Kasumi-1 cells.Here, PLCG1 depletion resulted in reduced Ca2+ release, impaired proliferation and reduced colony formation in vitro. In a xenograft model, inactivation of PLCG1 resulted not only in delayed disease development (median survival shNT vs. shPLCG1: 135 days vs. not reached, p=0.02) but also in reduction of disease penetrance by 87%. Consistent with these results, transcriptome analysis revealed strong induction of gene sets related to myeloid differentiation and down-regulation of gene sets linked to proliferation, stemness and c-Myc targets. To confirm the functional role of PLCG1-signaling in AE-driven LSCs, we generated a new conditional knockout mouse model for Plcg1 and induced leukemia using the oncogenes AE and KRAS-G12D (AE/K). Genetic inactivation of Plcg1in vivo after engraftment of leukemic cells resulted in significant reduction of LSC numbers (p=0.04) and a reduction of disease penetrance by 67% in primary recipients. Isolated LSCs revealed induction of differentiation, loss of cell cycle activity and failed to re-establish disease in secondary recipients (Plcg1+/+ vs. Plcg1-/-: median survival 12 days vs. not reached; p=0.0001). In contrast, genetic deletion of Plcg1 appeared to be dispensable for normal murine HSC function during primary and secondary transplantation. Primary human t(8;21) AML cells (derived from 4 different donors) showed impaired colony forming capacity following PLCG1 inactivation in vitro irrespective of co-occurring mutations while colony formation of human CD34+ BM cells was not affected to a major extent. As Ca2+ signaling appeared deregulated in t(8;21) AML, we aimed to investigate the effects of pharmacologic Ca2+ inhibition as a tractable target downstream of PLCG1. To assess specifically for LSC function, we treated primary recipient mice with established AE/K-driven leukemia with the clinically approved calcineurin inhibitor ciclosporin (CsA), a compound that blocks intracellular Ca2+ release. CsA-treated animals showed reduction in total leukemic burden (spleen weight diluent vs. CsA, p=0.01) and LSC numbers (p=0.02). This resulted in increased survival of secondary recipient hosts (diluent vs. CsA: median 15 vs. 29 days, p=0.0002). These effects could not be observed for other oncogenes (e.g. MA9), confirming its specificity for AE-induced disease. Consistently, CsA treated primary human t(8;21)-positive AML blasts failed to form colonies in methylcellulose. In summary, our findings identified PLCG1-dependent Ca2+ signaling as a critical pathway for t(8;21) LSC maintenance and self-renewal. Most importantly, as PLCG1 is dispensable for maintenance of normal HSPCs, PLCG1 could serve as a novel therapeutic target in t(8;21) AML. Disclosures Döhner: Daiichi: Honoraria; Jazz: Honoraria; Novartis: Honoraria; Celgene: Honoraria; Janssen: Honoraria; CTI Biopharma: Consultancy, Honoraria. Bullinger:Novartis: Honoraria; Menarini: Honoraria; Jazz Pharmaceuticals: Honoraria; Abbvie: Honoraria; Astellas: Honoraria; Amgen: Honoraria; Seattle Genetics: Honoraria; Sanofi: Honoraria; Janssen: Honoraria; Hexal: Honoraria; Gilead: Honoraria; Daiichi Sankyo: Honoraria; Celgene: Honoraria; Bristol-Myers Squibb: Honoraria; Bayer: Other: Financing of scientific research; Pfizer: Honoraria.

scholarly journals Study on using the hybrid cell a6g11c9 to produce the anti-a monoclonal antibody that agglunating a antigen on the surface of red blood cells

2017 ◽  
Vol 40 (1) ◽  
pp. 25-31
Author(s):  
Nguyen Thi Trung ◽  
Truong Nam Hai
Keyword(s):  
Monoclonal Antibody ◽  
Monoclonal Antibodies ◽  
Red Blood Cells ◽  
Cell Line ◽  
Blood Cells ◽  
Culture Medium ◽  
Hybrid Cell ◽  
In Vitro Method ◽  
Antibody Solution

Almost of the ABO blood grouping reagents is being trading derive from  the monoclonal antibodies. There are two methods to produce the  monoclonal antibodies from hybridoma lines, which were in vitro method (hybridoma cultured in the medium) and in vivo method (hybridoma cultured in the mice intra-abdominal). In Vietnam, Nguyen Thi Trung and co-authors was succesfully screened in hybridoma cell line A6G11C9 which generating of the anti A monoclonal antibody agglutinated A antigen on the surface of red blood cells. The fusion of mouse lymohocyte B generated anti-A antibody with mouse myeloma sp2/0 is formed that hybrid cell lines. The anti-A monoclonal antibody is produced from hybridoma cell line A6G11C9 have been highly intensive confirmed. It is capability of growth and anti B monoclonal antibody producing stability through the generations. In this study, the process to produce large amounts of monoclonal antibodies from B4D10C9 hybridoma by in vitro method are published. Firstly, hybridoma cells are stored in liquid nitrogen to wake by culture in medium. Then, First, hybrid cells are stored frozen in liquid nitrogen to wake cultured cells. Then, they were first inoculated to produce enough biomass to serve a larger scale. Cell biomass continues to be second inoculated into DMEM containing 10% fetal bovin serum for 10 days. The culture medium contained anti-A monoclonal antibodies were collected by centrifugation to remove cells. The anti-A monoclonal antibody levels in culture medium was concentrated and remove phenol red indicator by the precipitation with NH4SO4 50% saturated. The anti-A monoclonal antibody solution at 5 times concentrated have been better agglutinated with erythrocytes containing A antigen than monoclonal antibody solution non-concentration. 150 ml of concentrated antibodies were produced. Antibody titer of the anti-A monoclonal antibodies in the concentrated 5 times solution was 1/512. The intensity of the reaction anti-A monclonal antibody with red blood cell containing A antigen was 4+.   Citation: Nguyen Thi Trung, Truong Nam Hai, 2018. Study on using the hybrid cell a6g11c9 to produce the anti-a monoclonal antibody that agglunating a antigen on the surface of red blood cells. Tap chi Sinh hoc, 40(1): x-xx. DOI: 10.15625/0866-7160/v40n1.9154. *Corresponding author: [email protected] Received 12 January 2017, accepted 20 December 2017 

scholarly journals Alemtuzumab and Natalizumab: The Monoclonal Antibody Story Continues

2006 ◽  
Vol 17 (6) ◽  
pp. 327-329 ◽  
Author(s):  
BL Johnston ◽  
JM Conly
Keyword(s):  
Monoclonal Antibody ◽  
Clinical Trials ◽  
Monoclonal Antibodies ◽  
Stem Cell ◽  
Hematopoietic Stem Cell Transplantation ◽  
Infectious Complications ◽  
Solid Organ ◽  
Infection Rates ◽  
Hematopoietic Stem ◽  
The Many

In the July/August 2006 issue of this journal, the infectious complications associated with the use of infliximab, etanercept and adalimumab were reviewed (1). These represent only three of the many monoclonal antibodies either licensed or in clinical trials for therapeutic use in cancer and autoimmune disease or to prevent rejection in both solid organ and hematopoietic stem cell transplantation. While most of these agents have not been associated with increased infection rates, alemtuzumab and natalizumab have gained particular attention related to either the frequency or type of infection seen in some individuals who have received them.

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