Establishment of ameloblastoma cell line, AM‐1

Harada, Hidemitsu; Mitsuyasu, Takeshi; Nakamura, Norifumi; Higuchi, Yoshinori; Toyoshima, Kuniaki; Taniguchi, Akiyoshi; Yasumoto, Shigeru

doi:10.1111/j.1600-0714.1998.tb01943.x

Cited by 57 publications

(57 citation statements)

References 16 publications

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“…The AM-1 ameloblastoma cell line was obtained from the laboratory of Dr. Hidemitsu Harada at Iwate Medical University (8). SK-MEL-28 (BRAF V600E-positive) and MCF7 (BRAF wild-type) cells were obtained from the American Type Culture Collection.…”

Section: Cell Linesmentioning

confidence: 99%

Activating FGFR2–RAS–BRAF Mutations in Ameloblastoma

Brown¹,

Rolland²,

McHugh³

et al. 2014

Clinical Cancer Research

232

367

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Purpose: Ameloblastoma is an odontogenic neoplasm whose overall mutational landscape has not been well characterized. We sought to characterize pathogenic mutations in ameloblastoma and their clinical and functional significance with an emphasis on the mitogen-activated protein kinase (MAPK) pathway.Experimental Design: A total of 84 ameloblastomas and 40 non-ameloblastoma odontogenic tumors were evaluated with a combination of BRAF V600E allele-specific PCR, VE1 immunohistochemistry, the Ion AmpliSeq Cancer Hotspot Panel, and Sanger sequencing. Efficacy of a BRAF inhibitor was evaluated in an ameloblastoma-derived cell line.Results: Somatic, activating, and mutually exclusive RAS-BRAF and FGFR2 mutations were identified in 88% of cases. Somatic mutations in SMO, CTNNB1, PIK3CA, and SMARCB1 were also identified. BRAF V600E was the most common mutation, found in 62% of ameloblastomas and in ameloblastic fibromas/ fibrodentinomas but not in other odontogenic tumors. This mutation was associated with a younger age of onset, whereas BRAF wild-type cases arose more frequently in the maxilla and showed earlier recurrences. One hundred percent concordance was observed between VE1 immunohistochemistry and molecular detection of BRAF V600E mutations. Ameloblastoma cells demonstrated constitutive MAPK pathway activation in vitro. Proliferation and MAPK activation were potently inhibited by the BRAF inhibitor vemurafenib.Conclusions: Our findings suggest that activating FGFR2-RAS-BRAF mutations play a critical role in the pathogenesis of most cases of ameloblastoma. Somatic mutations in SMO, CTNNB1, PIK3CA, and SMARCB1 may function as secondary mutations. BRAF V600E mutations have both diagnostic and prognostic implications. In vitro response of ameloblastoma to a BRAF inhibitor suggests a potential role for targeted therapy. Clin Cancer Res; 20(21); 5517-26. Ó2014 AACR.

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Section: Cell Linesmentioning

confidence: 99%

Activating FGFR2–RAS–BRAF Mutations in Ameloblastoma

Brown¹,

Rolland²,

McHugh³

et al. 2014

Clinical Cancer Research

232

367

View full text Add to dashboard Cite

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mentioning

confidence: 99%

“…Primary-cultured ameloblastoma cells are not suitable for long-term experiments 6 because these cells can generally not be maintained for longer than 3 months. In a previous study, we established immortalized plexiform-type ameloblastoma cells, AM-1, 6 and normal oral epithelial cells, MOE1b. 7 Ameloblastoma has been proposed to stem from odontogenic epithelium 1 and signaling molecules including Wnt, sonic hedgehog, and bone morphogenetic proteins, which are related to the odontogenic epithelialmesenchymal interaction in tooth morphogenesis.…”

mentioning

confidence: 99%

A novel ameloblastoma cell line (AM-3) secretes MMP-9 in response to Wnt-3a and induces osteoclastogenesis

Kibe

Fuchigami

Kishida

et al. 2013

Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology

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“…For cell line sample preparation, AM-1 cells [16,17] were cultured in Keratinocyte-SFM (Gibco, Grand Island, N.Y., USA), penicillin-streptomycin (Gibco), fungizone amphotericin B (Gibco) and supplemented with bovine pituitary extract (Gibco).…”

Section: Tissue Sample Selection and Cell Culturementioning

confidence: 99%

TRAIL Cleaves Caspase-8, -9 and -3 of AM-1 Cells: A Possible Pathway for TRAIL to Induce Apoptosis in Ameloblastoma

Sandra¹,

Hendarmin²,

Yu³

et al. 2005

Tumor Biol

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Tumor-necrosis-factor-related apoptosis-inducing ligand (TRAIL/Apo-2L), a potent ligand in inducing apoptosis, has recently emerged as a novel anticancer agent based on its ability to induce apoptosis in tumor cells, while exhibiting no toxicity in most normal cells. Since no potent apoptosis-inducing factor has been found yet in ameloblastoma, the present study was conducted. In the present study, expressions of TRAIL receptors, death receptor 4 (DR4) and DR5, were detected in all ameloblastoma tissues by immunohistochemistry as well as in AM-1 cells by immunofluorescence. By applying TRAIL in AM-1 cells, ameloblastoma cell line, for 24 h, we found that TRAIL cleaved caspase-8, -9 and –3, and lowered mitochondrial membrane potential (Δψm), and markedly induced apoptosis in AM-1 cells (46%). These results suggested that TRAIL is a potent apoptosis-inducing ligand in ameloblastoma.

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Establishment of ameloblastoma cell line, AM‐1

Cited by 57 publications

References 16 publications

Activating FGFR2–RAS–BRAF Mutations in Ameloblastoma

Activating FGFR2–RAS–BRAF Mutations in Ameloblastoma

A novel ameloblastoma cell line (AM-3) secretes MMP-9 in response to Wnt-3a and induces osteoclastogenesis

TRAIL Cleaves Caspase-8, -9 and -3 of AM-1 Cells: A Possible Pathway for TRAIL to Induce Apoptosis in Ameloblastoma

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