Matrigel Augments Xenograft Transplantation of Meningioma Cells into Athymic Mice

Jensen, Randy L.; Leppla, David C.; Rokosz, Norman; Wurster, Robert D.

doi:10.1097/00006123-199801000-00027

Cited by 38 publications

(18 citation statements)

References 29 publications

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“…In addition to the cellular suspension, we also added basement membrane extract to the injection cocktail as it has been reported to support the growth of solid tumors in this model. 40 As described throughout this report, we found that tumor growth occurred from all injected cell lines except for those expressing full-length Jagged1 over the course of the study. In addition, considerable differences in tumor phenotype from each cell line were observed.…”

Section: Ligand Expression Alters the Complement Of Notch Receptors Asupporting

confidence: 61%

Soluble Forms of the Notch Ligands Delta1 and Jagged1 Promote in Vivo Tumorigenicity in NIH3T3 Fibroblasts with Distinct Phenotypes

Urs

Roudabush

O’Neill

et al. 2008

The American Journal of Pathology

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We previously found that soluble forms of the Notch ligands Jagged1 and Delta1 induced fibroblast growth factor receptor-dependent cell transformation in NIH3T3 fibroblasts. However, the phenotypes of these lines differed, indicating distinct functional differences among these Notch ligands. In the present study, we used allografts to test the hypothesis that NIH3T3 fibroblasts that express soluble forms of Delta1 and Jagged1 accelerate tumorigenicity in vivo. With the exception of the full-length Jagged1 transfectant, all other cell lines, including the control, generated tumors when injected subcutaneously in athymic mice. Suppression of Notch signaling by the soluble ligands significantly increased tumor onset and growth, whereas full-length Jagged1 completely suppressed tumor development. In addition, there were striking differences in tumor pathology with respect to growth kinetics, vascularization, collagen content, size and number of necrotic foci, and invasiveness into the underlying tissue. Further, the production of angiogenic factors, including vascular endothelial growth factor, also differed among the tumor types. Lastly, both Jagged1-and Delta1-derived tumors contained phenotypically distinct populations of lipid-filled cells that corresponded with increased expression of adipocyte markers. The divergence of tumor phenotype may be attributed to ligand-specific alterations in Notch receptor responses in exogenous and endogenous cell populations within the allographs. Our findings demonstrate distinct functional properties for these Notch ligands in the promotion of tumorigenicity in vivo.

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Section: Ligand Expression Alters the Complement Of Notch Receptors Asupporting

confidence: 61%

Soluble Forms of the Notch Ligands Delta1 and Jagged1 Promote in Vivo Tumorigenicity in NIH3T3 Fibroblasts with Distinct Phenotypes

Urs

Roudabush

O’Neill

et al. 2008

The American Journal of Pathology

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“…Subcutaneous meningioma flank tumors were implanted as described previously. 18 Briefly, cells were grown to approximately 80% confluence in T-175 flasks. All steps were carried out on ice.…”

Section: Meningioma Mouse Xenograft Flank Modelmentioning

confidence: 99%

Celecoxib inhibits meningioma tumor growth in a mouse xenograft model

Ragel

Jensen

Gillespie

et al. 2006

Cancer

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BACKGROUND.Treatments for recurrent meningiomas are limited. We previously demonstrated universal expression of COX‐2 in meningiomas and dose‐dependent growth inhibition in vitro with celecoxib, a COX‐2 inhibitor. We therefore tested the effects of celecoxib on meningioma growth in a mouse xenograft model.METHODS.Meningioma cell lines (IOMM‐Lee, CH157‐MN, WHO grade I primary cultured tumor) were transplanted into flanks of nude mice fed mouse chow with celecoxib at varying concentrations (0, 500, 1000, 1500 ppm) ad libitum. Tumors were measured biweekly and processed for MIB‐1, Factor VIII, COX‐2, and VEGF, and assayed with transferase‐mediated dUTP‐biotin nick‐end labeling (TUNEL).RESULTS.Celecoxib reduced growth of mean tumor volume by 66% (P < .05), 25% (P > .05), and 65% (P < .05) compared with untreated controls in IOMM‐Lee, CH157‐MN, and benign tumors, respectively. IOMM‐Lee tumors removed from celecoxib treatment regained a growth rate similar to the control. Blood vessel density decreased and apoptotic cells increased in treated flank tumors. Diminished COX‐2 expression and VEGF were observed in treated IOMM‐Lee tumors. Mean plasma celecoxib levels were 845, 1540, and 2869 ng/mL, for low‐, medium‐, and high‐dose celecoxib, respectively.CONCLUSIONS.Celecoxib inhibits meningioma growth in vivo at plasma levels achievable in humans. Celecoxib‐treated tumors were less vascular with increased apoptosis. IOMM‐Lee tumors treated with celecoxib showed decreased COX‐2 and VEGF expression. COX‐2 inhibitors may have a role in the treatment of recurrent meningiomas. Cancer 2007;109:588–597. © 2006 American Cancer Society.

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“…Recent efforts to establish a benign meningioma in vivo model have employed implantation of tissue blocks or cell suspensions directly from patients' biopsy material into nude mice. [32][33][34] Specifically, subdural injection of 10 6 primary cells derived from benign meningiomas produced tumors in athymic mice, and no animal harboring a tumor died within 90 days of implantation; histologically these tumors were consistent with meningioma and commonly showed a whorling pattern and no signs of atypia or malignancy. 34 The major problem with these approaches is the heterogeneous, nonstandardized nature of primary cells.…”

Section: Ben-men-1 As a New Meningioma Modelmentioning

confidence: 99%

Establishment of a benign meningioma cell line by hTERT-mediated immortalization

Püttmann

Senner

Braune

et al. 2005

Laboratory Investigation

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Meningioma represents the most common intracranial tumor, but well-characterized cell lines derived from benign meningiomas are not available. A major reason for the lack of benign tumor cell lines is senescence of nonmalignant cells in vitro, while malignant cells are often immortal. We have developed a meningioma cell line by retrovirally transducing primary cells derived from a human WHO grade I meningothelial meningioma with the human telomerase reverse transcriptase (hTERT) gene, which enables bypassing cellular senescence. Five clones have been cultured for more than 21 months so far, while corresponding nontransfected cells ceased proliferation within 3 months. Quantitative RT-PCR and a telomeric repeat amplification protocol (TRAP) assay revealed high hTERT mRNA levels and high telomerase activity in all transduced populations, while nontransduced cells were negative. The average telomere size of transduced cells was considerably longer than that of parental cells and the biopsy specimen. One clone, designated Ben-Men-1, was characterized in more detail, and exhibited typical cytological, immunocytochemical, ultrastructural and genetical features of meningioma, including whorl formation, expression of epithelial membrane antigen, desmosomes and interdigitating cell processes, as well as À22q. Following subdural transplantation into nude mice, tumor tissue with typical histological features of meningothelial meningioma was found. We conclude that Ben-Men-1 represents an immortalized yet differentiated cell line useful for biological and therapeutical studies on meningioma.

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Matrigel Augments Xenograft Transplantation of Meningioma Cells into Athymic Mice

Cited by 38 publications

References 29 publications

Soluble Forms of the Notch Ligands Delta1 and Jagged1 Promote in Vivo Tumorigenicity in NIH3T3 Fibroblasts with Distinct Phenotypes

Soluble Forms of the Notch Ligands Delta1 and Jagged1 Promote in Vivo Tumorigenicity in NIH3T3 Fibroblasts with Distinct Phenotypes

Celecoxib inhibits meningioma tumor growth in a mouse xenograft model

Establishment of a benign meningioma cell line by hTERT-mediated immortalization

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