Eribulin prolongs survival in an orthotopic xenograft mouse model of malignant meningioma

Nakano, Tomoyuki; Fujimoto, Kenji; Tomiyama, Arata; Takahashi, Manabu; Achiha, Takamune; Arita, Hideyuki; Kawauchi, Daisuke; Yasukawa, Mami; Masutomi, Kenkichi; Kondo, Akihide; Narita, Yoshitaka; Maehara, Taketoshi; Ichimura, Koichi

doi:10.1111/cas.15221

Cited by 5 publications

(7 citation statements)

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“…(10 4 ) [ 49 ], (5 × 10 4 ) [ 60 , 66 , 83 ], (10 5 ) [ 50 , 62 , 67 , 78 , 82 ], (1.5 × 10 5 ) [ 58 ], (2 × 10 5 ) [ 85 ] (2.5 × 10 5 ) [ 47 , 53 , 54 , 59 , 61 , 79 , 83 , 84 ], (4 × 10 5 ) [ 45 ], (5 × 10 5 ) [ 66 – 68 , 70 , 75 ], (10 6 ) [ 24 , 44 , 74 , 77 , 81 ], (3 × 10 6 ) [ 66 ]/(0.5) [ 66 , 83 ], (1) [ 66 ], (2) [ 62 , 84 ]…”

Section: Resultsmentioning

confidence: 99%

“…SS (10) [ 60 , 66 ], (11) [ 85 ], (12) [ 66 ], (13) [ 77 ], (15) [ 53 ], (17) [ 47 , 66 ], (20) [ 66 , 79 ], (21) [ 49 , 84 ], (23) [ 50 ], (27) [ 45 ], 15–21 [ 83 ]…”

Section: Resultsunclassified

“…Histology [ 24 , 44 , 45 , 47 , 50 , 53 , 54 , 60 – 62 , 66 – 68 , 70 , 74 , 75 , 77 – 79 , 81 , 82 , 84 , 85 ]…”

Section: Resultsunclassified

“…(2 × 10 4 ) [ 46 ], (1.5 × 10 5 ) [ 58 ], (5 × 10 5 ) [ 20 , 46 , 72 ], (10 6 ) [ 57 , 63 , 71 , 73 , 76 ], (1.5 × 10 6 ) [ 20 ], (2 × 10 6 ) [ 45 , 86 , 88 ], (3 × 10 6 ) [ 59 , 61 , 62 , 83 ], (4 × 10 6 ) [ 64 ], (5 × 10 6 ) [ 48 , 49 , 52 , 65 , 75 , 84 ], (10 7 ) [ 22 , 55 , 56 , 87 ], (5 × 10 7 ) [ 51 ]/(3) [ 58 ]…”

Section: Resultsmentioning

confidence: 99%

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Meningioma animal models: a systematic review and meta-analysis

Andersen,

Kofoed,

Paludan-Müller

et al. 2023

J Transl Med

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Background Animal models are widely used to study pathological processes and drug (side) effects in a controlled environment. There is a wide variety of methods available for establishing animal models depending on the research question. Commonly used methods in tumor research include xenografting cells (established/commercially available or primary patient-derived) or whole tumor pieces either orthotopically or heterotopically and the more recent genetically engineered models—each type with their own advantages and disadvantages. The current systematic review aimed to investigate the meningioma model types used, perform a meta-analysis on tumor take rate (TTR), and perform critical appraisal of the included studies. The study also aimed to assess reproducibility, reliability, means of validation and verification of models, alongside pros and cons and uses of the model types. Methods We searched Medline, Embase, and Web of Science for all in vivo meningioma models. The primary outcome was tumor take rate. Meta-analysis was performed on tumor take rate followed by subgroup analyses on the number of cells and duration of incubation. The validity of the tumor models was assessed qualitatively. We performed critical appraisal of the methodological quality and quality of reporting for all included studies. Results We included 114 unique records (78 using established cell line models (ECLM), 21 using primary patient-derived tumor models (PTM), 10 using genetically engineered models (GEM), and 11 using uncategorized models). TTRs for ECLM were 94% (95% CI 92–96) for orthotopic and 95% (93–96) for heterotopic. PTM showed lower TTRs [orthotopic 53% (33–72) and heterotopic 82% (73–89)] and finally GEM revealed a TTR of 34% (26–43). Conclusion This systematic review shows high consistent TTRs in established cell line models and varying TTRs in primary patient-derived models and genetically engineered models. However, we identified several issues regarding the quality of reporting and the methodological approach that reduce the validity, transparency, and reproducibility of studies and suggest a high risk of publication bias. Finally, each tumor model type has specific roles in research based on their advantages (and disadvantages). Systematic review registration: PROSPERO-ID CRD42022308833.

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Section: Resultsmentioning

confidence: 99%

“…SS (10) [ 60 , 66 ], (11) [ 85 ], (12) [ 66 ], (13) [ 77 ], (15) [ 53 ], (17) [ 47 , 66 ], (20) [ 66 , 79 ], (21) [ 49 , 84 ], (23) [ 50 ], (27) [ 45 ], 15–21 [ 83 ]…”

Section: Resultsunclassified

“…Histology [ 24 , 44 , 45 , 47 , 50 , 53 , 54 , 60 – 62 , 66 – 68 , 70 , 74 , 75 , 77 – 79 , 81 , 82 , 84 , 85 ]…”

Section: Resultsunclassified

Section: Resultsmentioning

confidence: 99%

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Meningioma animal models: a systematic review and meta-analysis

Andersen,

Kofoed,

Paludan-Müller

et al. 2023

J Transl Med

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“…Furthermore, these cell lines accumulated additional genetic alterations during establishment and passage that are not part of meningioma pathology. Despite these drawbacks, these lines are convenient to use given the high proliferation rate and ability to grow as xenotransplants [ 8 , 9 ]. We developed a primary tumor-derived meningioma culture system which recapitulates the disease with high-fidelity [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of the epigenetically activated miR-483-5p/IGF-2 pathway results in rapid loss of meningioma tumor cell viability

et al. 2023

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Purpose Meningioma is the most common primary central nervous system tumor often causing serious complications, and presently no medical treatment is available. The goal of this study was to discover miRNAs dysregulated in meningioma, and explore miRNA-associated pathways amenable for therapeutic interventions. Methods Small RNA sequencing was performed on meningioma tumor samples to study grade-dependent changes in microRNA expression. Gene expression was analyzed by chromatin marks, qRT-PCR and western blot. miRNA modulation, anti-IGF-2 neutralizing antibodies, and inhibitors against IGF1R were evaluated in a tumor-derived primary cultures of meningioma cells. Results Meningioma tumor samples showed high, grade-dependent expression of miR-483-5p, associated with high mRNA and protein expression of its host gene IGF-2. Inhibition of miR-483-5p reduced the growth of cultured meningioma cells, whereas a miR-483 mimic increased cell proliferation. Similarly, inhibition of this pathway with anti-IGF-2 neutralizing antibodies reduced meningioma cell proliferation. Small molecule tyrosine kinase inhibitor blockade of the IGF-2 receptor (IGF1R) resulted in rapid loss of viability of cultured meningioma tumor-derived cells, suggesting that autocrine IGF-2 feedback is obligatory for meningioma tumor cell survival and growth. The observed IGF1R-inhibitory IC50 for GSK1838705A and ceritinib in cell-based assays along with the available pharmacokinetics data predicted that effective drug concentration could be achieved in vivo as a new medical treatment of meningioma. Conclusion Meningioma cell growth is critically dependent on autocrine miR-483/IGF-2 stimulation and the IGF-2 pathway provides a feasible meningioma treatment target.

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