K‐<i>Ras</i> gene status and expression of Ras/mitogen‐activated protein kinase (MAPK) signaling molecules in ameloblastomas

Kumamoto, Hiroyuki; Takahashi, Nobuhiro; Ooya, Kiyoshi

doi:10.1111/j.1600-0714.2004.00141.x

Cited by 41 publications

(36 citation statements)

References 39 publications

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“…Strong reactivity was observed in inner dental epithelium, and weak to moderate staining was visible in outer dental epithelium, stratum intermedium and stellate reticulum [Kumamoto et al, 2004]. These results are in agreement with the expression pattern described for Map2k1 in the present study except for the localization within the stel-late reticulum and stratum intermedium sometimes difficult to assess.…”

Section: Discussionsupporting

confidence: 82%

From the Transcription of Genes Involved in Ectodermal Dysplasias to the Understanding of Associated Dental Anomalies

Laugel-Haushalter

Langer²,

Marrie³

et al. 2012

Mol Syndromol

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Orodental anomalies are one aspect of rare diseases and are increasingly identified as diagnostic and predictive traits. To understand the rationale behind gene expression during tooth or other ectodermal derivative development and the disruption of odontogenesis or hair and salivary gland formation in human syndromes we analyzed the expression patterns of a set of genes (Irf6, Nfkbia, Ercc3, Evc2, Map2k1) involved in human ectodermal dysplasias in mouse by in situ hybridization. The expression patterns of Nfkbia, Ercc3 and Evc2 during odontogenesis had never been reported previously. All genes were indeed transcribed in different tissues/organs of ectodermal origin. However, for Nfkbia, Ercc3, Evc2, and Map2k1, signals were also present in the ectomesenchymal components of the tooth germs. These expression patterns were consistent in timing and localization with the known dental anomalies (tooth agenesis, microdontia, conical shape, enamel hypoplasia) encountered in syndromes resulting from mutations in those genes. They could also explain the similar orodental anomalies encountered in some of the corresponding mutant mouse models. Translational approaches in development and medicine are relevant to gain understanding of the molecular events underlying clinical manifestations.

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Section: Discussionsupporting

confidence: 82%

From the Transcription of Genes Involved in Ectodermal Dysplasias to the Understanding of Associated Dental Anomalies

Laugel-Haushalter

Langer²,

Marrie³

et al. 2012

Mol Syndromol

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“…Distinct signalling pathways have been implicated in TIMP growth‐promoting activity, including ERK 1/2 30 . Furthermore, ERK 1/2 has been described in ameloblastoma 34,35 . These results suggest that ERK 1/2 transducer signals are generated by growth factors and TIMPs, probably increasing the proliferation rate in ameloblastoma.…”

Section: Discussionmentioning

confidence: 81%

Matrix metalloproteinases, TIMPs and growth factors regulating ameloblastoma behaviour

et al. 2010

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“…RhoA, RhoB, Cdc42, and Rac1 are considered crucial to the initiation and maintenance of neoplastic transformation by the Ras oncogene pathway (23); though, according to Kumamoto et al. (50), Ras oncogene plays a secondary role in ameloblastoma oncogenesis, because its immunohistochemical expression was detected in normal odontogenic epithelium and ameloblastoma neoplastic cells at similar levels.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical expression of Rho GTPases in ameloblastomas

Modolo

Biz

Sousa

et al. 2011

J Oral Pathology Medicine

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Rho GTPases are proteins that regulate cell cycle, shape, polarization, invasion, migration, and apoptosis, which are important characteristics of normal and neoplastic cells. Rho GTPases expression has been reported in normal tooth germ and several pathologies; however, it has not been evaluated in ameloblastomas. The aim of this study was to analyze the expression and distribution of RhoA, RhoB, Rac1, and Cdc42 Rho GTPases in solid and unicystic ameloblastomas. Three-micrometer sections from paraffin-embedded specimens were evaluated by using an avidin-biotin immunohistochemical method with antibodies against the proteins mentioned above. RhoA and RhoB staining was observed in a high number of cells (P < 0.05) and greater intensity in non-polarized ones. Rac1 was not observed, and Cdc42 did not show any statistical differences between the number of non-polarized and basal positive cells (P > 0.05). Upon comparing the studied ameloblastomas, a higher number of positive cells in the unicystic variant was observed than that in the solid one (P < 0,05). The results obtained suggest that these GTPases could play a role in the ameloblastoma neoplastic epithelial cell phenotype determination (polarized or non-polarized), as well as in variant (solid or unicystic) and subtype (follicular or plexiform) determination. Furthermore, they could participate in solid ameloblastoma invasion mechanisms.

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K‐Ras gene status and expression of Ras/mitogen‐activated protein kinase (MAPK) signaling molecules in ameloblastomas

Cited by 41 publications

References 39 publications

From the Transcription of Genes Involved in Ectodermal Dysplasias to the Understanding of Associated Dental Anomalies

From the Transcription of Genes Involved in Ectodermal Dysplasias to the Understanding of Associated Dental Anomalies

Matrix metalloproteinases, TIMPs and growth factors regulating ameloblastoma behaviour

Immunohistochemical expression of Rho GTPases in ameloblastomas

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