Epidermal Growth Factor Is Associated with Loss of Mucosae Sealing and Peri-Implant Mucositis: A Pilot Study

This study aimed to evaluate the correlation between epidermal growth factor (EGF) and receptor (EGFR) levels in different clinical stages of dental implant rehabilitation and trace mucositis development’s biological profile. Thirty-six participants from the Specialization in Implant Dentistry, Universidade Federal Fluminense, Brazil, were included in the study and underwent sample collection: inside the alveolar socket, immediately before implant placement (Group 1, n = 10); at the peri-implant crevicular fluid (PICF) during reopening (Group 2, n = 10); PICF from healthy peri-implant in function (Group 3, n = 8); and PICF from mucositis sites (Group 4, n = 18). Quantitative polymerase chain reaction (PCR) evaluated EGF/EGFR gene expression using the SYBR Green Master Mix detection system. The results showed that EGF expression in the peri-implant crevicular fluid was statistically different. There was a higher EGF expression for group C (peri-implant health) (p = 0.04) than for the other groups. Regarding EGFR, there was no statistical difference among the groups (p = 0.56). It was concluded that low levels of EGF gene expression in the peri-implant crevicular fluid are related to the development of peri-implant mucositis and the absence of mucosae sealing. There was no correlation between EGFR gene expression with health or mucositis.

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Gene Expression Signature Associated With Combined Characteristics Of Female Non-smokers In Lung Adenocarcinomas Bearing Activating Epidermal Growth Factor Receptor (EGFR) Gene Mutations In Chinese

10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2069 ◽

2010 ◽

Author(s):

David Lam ◽

Luc Girard ◽

Alan D. Sihoe ◽

Lik-cheung CHENG ◽

Macy M. Lui ◽

...

Keyword(s):

Gene Expression ◽

Epidermal Growth Factor Receptor ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Growth Factor Receptor ◽

Gene Mutations ◽

Gene Expression Signature ◽

Egfr Gene ◽

Epidermal Growth ◽

Lung Adenocarcinomas

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Regulation of Epidermal Growth Factor Receptor Gene Expression by Retinoic Acid and Epidermal Growth Factor

Journal of Biological Chemistry ◽

10.1016/s0021-9258(18)94056-1 ◽

1989 ◽

Vol 264 (6) ◽

pp. 3230-3234 ◽

Cited By ~ 5

Author(s):

K L Thompson ◽

M R Rosner

Keyword(s):

Gene Expression ◽

Epidermal Growth Factor Receptor ◽

Retinoic Acid ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Receptor Gene ◽

Growth Factor Receptor ◽

Epidermal Growth ◽

Receptor Gene Expression

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Critical Update and Emerging Trends in Epidermal Growth Factor Receptor Targeting in Cancer

Journal of Clinical Oncology ◽

10.1200/jco.2005.11.890 ◽

2005 ◽

Vol 23 (11) ◽

pp. 2445-2459 ◽

Cited By ~ 505

Author(s):

José Baselga ◽

Carlos L. Arteaga

Keyword(s):

Epidermal Growth Factor Receptor ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Tyrosine Kinase ◽

Kinase Inhibitors ◽

Growth Factor Receptor ◽

Egfr Gene ◽

Epidermal Growth ◽

Egfr Tkis ◽

Receptor Family

The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase of the ErbB receptor family that is abnormally activated in many epithelial tumors. The aberrant activation of the EGFR leads to enhanced proliferation and other tumor-promoting activities, which provide a strong rationale to target this receptor family. There are two classes of anti-EGFR agents: monoclonal antibodies (MAbs) directed at the extracellular domain of the receptor and small molecule, adenosine triphosphate–competitive inhibitors of the receptor's tyrosine kinase. Anti-EGFR MAbs have shown antitumor activity in advanced colorectal carcinoma, squamous cell carcinomas of the head and neck, non–small-cell lung cancer (NSCLC) and renal cell carcinomas. The tyrosine kinase inhibitors (TKIs) have a partially different activity profile. They are active against NSCLC, and a specific EGFR inhibitor has shown improvement in survival. Recently, mutations and amplifications of the EGFR gene have been identified in NSCLC and predict for enhanced sensitivity to anti-EGFR TKIs. In addition to specific anti-EGFR TKIs, there are broader acting inhibitors such as dual EGFR HER-2 inhibitors and combined anti-pan-ErbB and antivascular endothelial growth factor receptor inhibitors. Current research efforts are directed at selecting the optimal dose and schedule and identifying predictive factors of response and resistance beyond EGFR gene mutations and/or amplifications. Finally, there is a need for improved strategies to integrate anti-EGFR agents with conventional therapies and to explore combinations with other molecular targeted approaches including other antireceptor therapies, receptor-downstream signaling transduction inhibitors, and targeted approaches interfering with other essential drivers of cancer, such as angiogenesis.

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