Poster 146: Development of Regenerative Therapy for the Tooth Using Cell Lines Derived From Tooth Germs: Transplantation of Ameloblast-Lineage Cells Into Subcutaneous Tissue of Nude Mouse

2007 ◽  
Vol 65 (9) ◽  
pp. 43.e85-43.e86
Author(s):  
Akira Nakata
Keyword(s):  
Cell Lines ◽  
Nude Mouse ◽  
Subcutaneous Tissue ◽  
Regenerative Therapy ◽  
Tooth Germs

Root development of rat tooth germs implanted in the tooth socket and in the subcutaneous tissue

Oral Diseases ◽  
2008 ◽  
Vol 14 (7) ◽  
pp. 644-651 ◽  
Author(s):  
Y Ina ◽  
Y Sasano ◽  
N Akiba ◽  
K Hatori ◽  
T Honma ◽  
...  
Keyword(s):  
Root Development ◽  
Subcutaneous Tissue ◽  
Tooth Socket ◽  
Tooth Germs

scholarly journals Recombinant RFB4 Immunotoxins Exhibit Potent Cytotoxic Activity for CD22-Bearing Cells and Tumors

Blood ◽  
1997 ◽  
Vol 90 (5) ◽  
pp. 2020-2026 ◽  
Author(s):  
Elizabeth Mansfield ◽  
Peter Amlot ◽  
Ira Pastan ◽  
David J. FitzGerald
Keyword(s):  
Antitumor Activity ◽  
B Cell ◽  
Cytotoxic Activity ◽  
Cell Lines ◽  
Nude Mouse ◽  
Binding Activity ◽  
Nude Mouse Model ◽  
Binding Characteristics ◽  
Cytotoxicity Activity ◽  
Recombinant Immunotoxin

Abstract Many B-cell malignancies express the CD22 antigen on their cell surface. To kill cells expressing this antigen, the RFB4 monoclonal antibody (MoAb) has been linked chemically with either deglycosylated ricin A chain or truncated versions of Pseudomonas exotoxin. These immunotoxins exhibited selective cytotoxic activity for CD22+ cells and antitumor activity in nude mouse models bearing human B-cell lymphomas. To construct a recombinant immunotoxin targeted to CD22, we first cloned the variable portions of the heavy and light chains of RFB4. The cloned Fv fragments were joined by a newly created disulfide bond to form a disulfide stabilized (ds) construct. The RFB4 construct was combined by gene fusion with PE38, a truncated version of PE. The recombinant immunotoxin was then expressed in Escherichia coli, purified by column chromatography and tested for cytotoxicity activity. RFB4(dsFv)PE38 retained its binding activity for CD22, was very stable at 37°C and exhibited selective cytotoxic activity for CD22+-cultured cell lines. Because of its favorable binding characteristics and potency for CD22-positive cell lines, RFB4(dsFv)PE38 was tested for antitumor activity in a nude mouse model of human lymphoma. CA46 cells were injected subcutaneously and then treated with the RFB4(dsFv)PE38 immunotoxin. Antitumor activity was dose responsive and was not evident when an irrelevant immunotoxin was administered on the same schedule.

scholarly journals Feline Mammary Cancer

2016 ◽  
Vol 54 (1) ◽  
pp. 32-43 ◽  
Author(s):  
B. B. Hassan ◽  
S. M. Elshafae ◽  
W. Supsavhad ◽  
J. K. Simmons ◽  
W. P. Dirksen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Nude Mouse ◽  
Human Breast Cancer ◽  
Age Of Onset ◽  
Biological Behavior ◽  
Human Breast ◽  
Nude Mouse Model ◽  
Primary Tumors ◽  
Highly Expressed Genes

Feline mammary carcinoma (FMC) is similar to human breast cancer in the late age of onset, incidence, histopathologic features, biological behavior, and pattern of metastasis. Therefore, FMC has been proposed as a relevant model for aggressive human breast cancer. The goals of this study were to develop a nude mouse model of FMC tumor growth and metastasis and to measure the expression of genes responsible for lymphangiogenesis, angiogenesis, tumor progression, and lymph node metastasis in FMC tissues and cell lines. Two primary FMC tissues were injected subcutaneously, and 6 FMC cell lines were injected into 3 sites (subcutaneous, intratibial, and intracardiac) in nude mice. Tumors and metastases were monitored using bioluminescent imaging and characterized by gross necropsy, radiology, and histopathology. Molecular characterization of invasion and metastasis genes in FMC was conducted using quantitative real-time reverse transcription polymerase chain reaction in 6 primary FMC tissues, 2 subcutaneous FMC xenografts, and 6 FMC cell lines. The histologic appearance of the subcutaneous xenografts resembled the primary tumors. No metastasis was evident following subcutaneous injection of tumor tissues and cell lines, whereas lung, brain, liver, kidney, eye, and bone metastases were confirmed following intratibial and intracardiac injection of FMC cell lines. Finally, 15 genes were differentially expressed in the FMC tissues and cell lines. The highly expressed genes in all samples were PDGFA, PDGFB, PDGFC, FGF2, EGFR, ERBB2, ERBB3, VEGFD, VEGFR3, and MYOF. Three genes ( PDGFD, ANGPT2, and VEGFC) were confirmed to be of stromal origin. This investigation demonstrated the usefulness of nude mouse models of experimental FMC and identified molecular targets of FMC progression and metastasis.

scholarly journals Measurement of proliferation nuclear and membrane markers in tumor cells by flow cytometry.

1991 ◽  
Vol 39 (8) ◽  
pp. 1125-1130 ◽  
Author(s):  
T E Kute ◽  
Y Quadri
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Line ◽  
Cell Lines ◽  
Nude Mouse ◽  
Solid Tumor ◽  
Athymic Nude Mouse ◽  
A431 Cells ◽  
Ki 67 ◽  
Membrane Markers

Nuclear and membrane markers that have been related to proliferative activity were measured by flow cytometry. The markers studied were transferrin receptor (TR), Ki-67 antigen, and epidermal growth factor receptor (EGFR). Two-color analysis for DNA via propidium iodide binding and for antigen expression via either a direct or indirect immunofluorescence assay was performed on three different cell lines and a solid human tumor model. The three cell lines tested were MCF-7 (breast), K-562 (leukemia), and A431 (a squamous cell). The solid tumor was obtained by subcutaneous injection of A431 cells into an athymic nude mouse. Our results demonstrate that TR are cell-cycle specific and can be readily measured in the cell lines. Ki-67 antigen is also cell-cycle specific in the cell lines tested, but the mean channel specific fluorescence uptake varies in the cell types. Finally, the EGFR was observed only in the A431 cell line, with most cells equally expressing this receptor. A bimodal distribution of EGFR was observed in A431 cells obtained from a solid tumor grown in an athymic nude mouse system. This suggests that cell line analysis may not always represent what might be observed under in vivo conditions. There are advantages to flow cytometry measurements of these factors which might be useful in predicting how patients should be treated and possibly the prognosis of cancer patients.

scholarly journals Knockdown of hsa_circ_0074298 suppressed the progression of pancreatic cancer by targeting the miR-519/SMOC2 axis

2020 ◽  
Author(s):  
Hong Chen ◽  
Dafang Xu ◽  
Lishan Wang ◽  
Jiahua Zhou
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Nude Mouse ◽  
Regulatory Mechanism ◽  
Malignant Tumors ◽  
Tumor Promoter ◽  
Luciferase Reporter ◽  
Aberrant Expression ◽  
Fast Progression

Abstract BACKGROUND: Pancreatic cancer (PC) is among the most malignant tumors in digestive system because of its fast progression, metastasis as well as resistance to chemotherapy. Former studies found that circRNAs that differentially expressed were correlated to progression and gemcitabine (GEM)-resistance in PC, and hsa_circ_0074298 aberrant expression played a role in PC progression, but the regulatory mechanism was unclear. METHODS: Rt-qPCR was used to detect hsa_circ_0074298 expression in PC cell lines. The CCK8, colony formation, and Transwell assays were used to evaluate the effect of hsa_circ_0074298 on PC cell migration and proliferation. Bioinformatics and luciferase reporter experiments were used to study the regulatory mechanism. Nude mouse xenografts were generated to examine the effect of hsa_circ_0074298 on tumor growth. RESULTS: The present study showed that hsa_circ_0074298 expression increased significantly in both PC cell lines and PC tissues. Downregulation of hsa_circ_0074298 caused a significant decrease in PC cell proliferation and in nude mouse xenograft growth. Hsa_circ_0074298 silencing also increased chemotherapy sensitivity to GEM. Bioinformatics analysis indicated that hsa_circ_0074298 was a miR-519 sponge and that the SMOC2 gene was a miR-519 target. MiR-519 downregulation or SMOC2 overexpression restored cell proliferation, migration, and chemoresistance after hsa_circ_0074298 silencing. The dual luciferase reporter assay showed that hsa_circ_0074298 interacted with miR-519, and miR-519 binding to the SMOC2 3′-UTR, then suppressed posttranscriptional SMOC2 expression. CONCLUSIONS: Taken together, hsa_circ_0074298 functioned as a tumor promoter through novel miR-519/SMOC2 axis, highlighting its possibility as a potential therapy for PC.

scholarly journals Knockdown of hsa_circ_0074298 suppressed the progression of pancreatic cancer by targeting the miR-519/SMOC2 axis

2020 ◽  
Author(s):  
Hong Chen ◽  
Dafang Xu ◽  
Lishan Wang ◽  
Jiahua Zhou
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Nude Mouse ◽  
Regulatory Mechanism ◽  
Malignant Tumors ◽  
Tumor Promoter ◽  
Luciferase Reporter ◽  
Aberrant Expression ◽  
Fast Progression

Abstract BACKGROUND: Pancreatic cancer (PC) is among the most malignant tumors in digestive system because of its fast progression, metastasis, as well as its resistance to chemotherapy. Former studies found that circRNAs that were differentially expressed were correlated with progression and gemcitabine (GEM)-resistance in PC, and hsa_circ_0074298 aberrant expression played a role in PC progression, but the regulatory mechanism was unclear. METHODS: The RT-qPCR was used to detect hsa_circ_0074298 expression in PC cell lines. The CCK8, colony formation, and Transwell assays were used to evaluate the effect of hsa_circ_0074298 on PC cell migration and proliferation. Bioinformatics and luciferase reporter experiments were used to characterize the regulatory mechanism. Nude mouse xenografts were generated to examine the effect of hsa_circ_0074298 on tumor growth. RESULTS: The present study showed that hsa_circ_0074298 expression increased significantly in both PC cell lines and PC tissues. Downregulation of hsa_circ_0074298 caused a significant decrease in PC cell proliferation and in nude mouse xenograft growth. Hsa_circ_0074298 silencing also increased chemotherapy sensitivity to GEM. Bioinformatics analysis indicated that hsa_circ_0074298 was a miR-519 sponge and that the SMOC2 gene was a miR-519 target. MiR-519 downregulation or SMOC2 overexpression restored cell proliferation, migration, and chemoresistance after hsa_circ_0074298 silencing. The dual luciferase reporter assay showed that hsa_circ_0074298 interacted with miR-519, and miR-519 binding to the SMOC2 3′-UTR, then suppressed posttranscriptional SMOC2 expression. CONCLUSIONS: Taken together, hsa_circ_0074298 functioned as a tumor promoter through a novel miR-519/SMOC2 axis, highlighting its possibility as a potential therapy for PC.

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