Genetic Polymorphism and Gene Expression of Pi3k Gene in Ameloblastoma

Urs, Aadithya B; Singh, Hanspal; Verma, Mahesh

doi:10.1016/j.oooo.2019.02.228

Cited by 2 publications

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“…The mechanisms underlying ameloblastoma's local invasiveness is still unknown, although their genes and signaling pathways, including Patch, Sonic Hedgehog (SHH), Smoothened (SMO), Akt, mTOR (mammalian target of rapamycin), and others, were reported to be involved in the pathogenesis. (6,18) Tumor biology can take on two distinct forms, with antiapoptotic proliferating sites on the periphery and proapoptotic differentiation sites in the center. ( 19) The tumor's peripheral cells that have chosen cell survival mode are believed to be the cause of disease progression that results in an expansile jaw lesion.…”

Section: Akt Signaling In Ameloblastomamentioning

confidence: 99%

Mechanism and Potential Therapy in Ameloblastoma: Akt Signaling Pathway

2022

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BACKGROUND: Ameloblastoma is the most common benign aggressive tumor. They are more prevalent in the mandible than in the maxilla, mostly observed on the posterior of the jaw. Ameloblastoma can arise at any age, however it most usually affect patients between the ages of 20 and 40. Numerous efforts have been made to develop molecular targeted therapies to treat cancers, such as Akt inhibitors. However, these drugs have not been tested for treating ameloblastoma yet, since underlying molecular factors have yet to be identified. This study was carried out to delineate possible molecular mechanisms related to the Akt signaling pathway in ameloblastoma and potential drugs for ameloblastoma treatment. CONTENT: Akt signaling pathway in ameloblastoma has been implicated in the formation and progression of tumors. Akt signaling is involved in various cellular mechanisms, such as cell cycle, apoptosis, and cytoskeletal rearrangement, which includes Phosphatidyl Inositol 3 Kinase (PI3K)-Akt signaling, Akt-Nuclear Factor (NF)-κB signaling, Akt-Mammalian Target of Rapamycin (mTOR) signaling, Akt-B-cell Lymphoma (Bcl)-2 Family signaling, Akt-Survivin signaling. Potential ways of treatments using chemical compounds and micro RNA (miRNA), and Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) were explored as well.SUMMARY: The present review highlights various Akt signaling involved in ameloblastoma and its potential pathways for treatments, while the gold standard of ameloblastoma treatment is still surgery to remove the tumor, there are many potential agents through various means of inhibition for ameloblastoma. Therefore, understanding the underlying signaling on ameloblastoma is necessary to induce inhibition on ameloblastoma. More research in potential ways to inhibit Akt signaling in ameloblastoma will lead to a better management of ameloblastoma in the future. KEYWORDS: ameloblastoma, Akt, PI3K, NFkB, mTOR, Bcl-2, miRNA, CRISPR

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Section: Akt Signaling In Ameloblastomamentioning

confidence: 99%

Mechanism and Potential Therapy in Ameloblastoma: Akt Signaling Pathway

2022

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Ameloblastoma uniquístico con patrón plexiforme. Revisión de la literatura a propósito de un caso clínico.

Román¹,

Pamatz²

2023

RRevista De La Asociación Dental Mexicana

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RESUMENEn 1827 el médico James William Cusack describió una lesión tumoral expansiva con características clínicas similares al ameloblastoma. Para el 2017 la Organización Mundial de la Salud lo clasificó como un tumor odontogénico benigno de origen epitelial. En la actualidad hemos aceptado la teoría de su etiología asociada con una mutación en el biomarcador BRAF-V600E, donde se presentan claras heterogeneidades extra/intratumorales en el metabolismo de la tumorogénesis; la mutación en BRAF genera cambios en la regulación de la odontogénesis, en conjunto con el gen CDC73 presente en el cromosoma 1 q25-q32, lo que produce un cambio en la proteína parafibromina que inhibe la proliferación celular durante el crecimiento y la división celular, esto afecta en conjunto al gen p53 y su homólogo p63 presentes en el cromosoma 17, por lo que se tiene como resultado la expresión de quistes y tumores dentales como el ameloblastoma. La presente obra muestra el caso clínico de un paciente femenino de 11 años de edad con aumento de volumen en la región submandibular izquierda de 7 × 4 cm, con seis años de evolución; de tal manera que fue diagnosticado con ameloblastoma uniquístico y tratado de forma conservadora mediante enucleación, posteriormente fue valorada anualmente hasta que la paciente cumplió los 18 años de edad.

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Genetic Polymorphism and Gene Expression of Pi3k Gene in Ameloblastoma

Cited by 2 publications

References 0 publications

Mechanism and Potential Therapy in Ameloblastoma: Akt Signaling Pathway

Mechanism and Potential Therapy in Ameloblastoma: Akt Signaling Pathway

Ameloblastoma uniquístico con patrón plexiforme. Revisión de la literatura a propósito de un caso clínico.

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