akt/p27kip1 pathway is not involved in human insulinoma tumorigenesis

Clics: 136
ID: 250694
2018
PDF Gratuito
Metricas de Calidad y Rendimiento del Articulo
Calidad General
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
Evaluacion de Calidad por IA
No analizado
Readership in this journal
Emerging

Ranked #123 of 149 articles by views in zhonghua wei zhong bing ji jiu yi xue

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 149 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Resumen
Insulinomas are pancreatic neuroendocrine tumors (pNET), usually benign. Akt/p27kip1 is an intracellular pathway overexpressed in many pNET. There are no data regarding its expression in human insulinomas. We aimed to investigate the expression of Akt and p27kip1 in 24 human insulinomas and to compare them to their expression in normal surrounding islets. Staining was performed on embedded paraffin tissue using polyclonal antibodies against total Akt, p-Akt, p27kip1, and pp27kip1. p-Akt was the predominant form in insulinomas; they presented lower Akt and p-Akt expression than normal islets in 83.3% and 87.5% of tumors, respectively. p27kip1 and pp27kip1 were mainly cytoplasmic in both insulinomas and normal tissue. Cytoplasmic pp27kip1 staining was higher in insulinomas and surprisingly nearly half of the insulinomas also presented nuclear p27kip1 (p=0.029). No differences were observed in the subcellular localization of p27kip1 and activation of Akt between benign and malignant insulinomas. The low expression of Akt seen in insulinomas might explain the usual benign behavior of this type of pNET. Cytoplasmic p27kip1 in both insulinomas and normal islet cells could reflect the low rate of replication of beta cells, while nuclear p27kip1 would seem to indicate stabilization and nuclear anchoring of the cyclin D-Cdk4 complex. Our data seem to suggest that the Akt pathway is not involved in human insulinoma tumorigenesis.
Clave de Referencia
daz2018internationalakt/p27kip1 Use esta clave para autocitar en el manuscrito mientras usa SciMatic Manuscript Manager o Thesis Manager
Autores ;Adriana Graciela Díaz;Andrea Paes de Lima;Paula Garibaldi;Maria de los Milagros Rubio;Florencia García;Marta Kral;Oscar D. Bruno
Revista zhonghua wei zhong bing ji jiu yi xue
Ano 2018
DOI
10.1155/2018/7865072
URL
http://dx.doi.org/10.1155/2018/7865072
Palabras Clave
clinical endocrinology diseases of the endocrine glands

Citas

No se encontraron citas. Para agregar una cita, contacte al administrador en info@scimatic.org

Comentarios

Aun no hay comentarios. Sea el primero en comentar este articulo.