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STAT 3 activation in head and neck squamous cell carcinomas is controlled by the EGFR.

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STAT 3 activation in head and neck squamous cell carcinomas is controlled by the EGFR. / Hambek, Markus; Baghi, Mehran; Strebhardt, Klaus; Strebhard, Klaus; May, Angelika; Adunka, Oliver; Gstöttner, Wolfgang; Knecht, Rainald.

in: ANTICANCER RES, Jahrgang 24, Nr. 6, 6, 2004, S. 3881-3886.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Hambek, M, Baghi, M, Strebhardt, K, Strebhard, K, May, A, Adunka, O, Gstöttner, W & Knecht, R 2004, 'STAT 3 activation in head and neck squamous cell carcinomas is controlled by the EGFR.', ANTICANCER RES, Jg. 24, Nr. 6, 6, S. 3881-3886. <http://www.ncbi.nlm.nih.gov/pubmed/15736426?dopt=Citation>

APA

Hambek, M., Baghi, M., Strebhardt, K., Strebhard, K., May, A., Adunka, O., Gstöttner, W., & Knecht, R. (2004). STAT 3 activation in head and neck squamous cell carcinomas is controlled by the EGFR. ANTICANCER RES, 24(6), 3881-3886. [6]. http://www.ncbi.nlm.nih.gov/pubmed/15736426?dopt=Citation

Vancouver

Hambek M, Baghi M, Strebhardt K, Strebhard K, May A, Adunka O et al. STAT 3 activation in head and neck squamous cell carcinomas is controlled by the EGFR. ANTICANCER RES. 2004;24(6):3881-3886. 6.

Bibtex

@article{c92803b615224da29300638bd6e27818,
title = "STAT 3 activation in head and neck squamous cell carcinomas is controlled by the EGFR.",
abstract = "Proliferation of squamous cell carcinoma of the head and neck (SCCHN) depends on epidermal growth factor receptor (EGFR) expression. As STAT 3 activation as well contributes to the cell growth in SCCHN, the interaction of STAT 3 and the EGFR is of great interest when considering treatment options through inhibition of STAT 3. We, therefore, evaluated the influence of blocking or activating the EGFR in human SCCHN cell lines and in vivo tumors on STAT 3 activation. We compared the effects on STAT 3 activation with the regulation of MAP Kinase under these conditions. We found that STAT 3 can be strongly inhibited via EGFR blocking in vitro as well as in vivo. However, the influence of EGFR regulation on the MAP Kinase pathway seemed to be very slight. These findings provide evidence that STAT 3 signal activity in head and neck carcinomas, which is partially responsible for proliferative activity, can be controlled via the EGFR.",
author = "Markus Hambek and Mehran Baghi and Klaus Strebhardt and Klaus Strebhard and Angelika May and Oliver Adunka and Wolfgang Gst{\"o}ttner and Rainald Knecht",
year = "2004",
language = "Deutsch",
volume = "24",
pages = "3881--3886",
journal = "ANTICANCER RES",
issn = "0250-7005",
publisher = "International Institute of Anticancer Research",
number = "6",

}

RIS

TY - JOUR

T1 - STAT 3 activation in head and neck squamous cell carcinomas is controlled by the EGFR.

AU - Hambek, Markus

AU - Baghi, Mehran

AU - Strebhardt, Klaus

AU - Strebhard, Klaus

AU - May, Angelika

AU - Adunka, Oliver

AU - Gstöttner, Wolfgang

AU - Knecht, Rainald

PY - 2004

Y1 - 2004

N2 - Proliferation of squamous cell carcinoma of the head and neck (SCCHN) depends on epidermal growth factor receptor (EGFR) expression. As STAT 3 activation as well contributes to the cell growth in SCCHN, the interaction of STAT 3 and the EGFR is of great interest when considering treatment options through inhibition of STAT 3. We, therefore, evaluated the influence of blocking or activating the EGFR in human SCCHN cell lines and in vivo tumors on STAT 3 activation. We compared the effects on STAT 3 activation with the regulation of MAP Kinase under these conditions. We found that STAT 3 can be strongly inhibited via EGFR blocking in vitro as well as in vivo. However, the influence of EGFR regulation on the MAP Kinase pathway seemed to be very slight. These findings provide evidence that STAT 3 signal activity in head and neck carcinomas, which is partially responsible for proliferative activity, can be controlled via the EGFR.

AB - Proliferation of squamous cell carcinoma of the head and neck (SCCHN) depends on epidermal growth factor receptor (EGFR) expression. As STAT 3 activation as well contributes to the cell growth in SCCHN, the interaction of STAT 3 and the EGFR is of great interest when considering treatment options through inhibition of STAT 3. We, therefore, evaluated the influence of blocking or activating the EGFR in human SCCHN cell lines and in vivo tumors on STAT 3 activation. We compared the effects on STAT 3 activation with the regulation of MAP Kinase under these conditions. We found that STAT 3 can be strongly inhibited via EGFR blocking in vitro as well as in vivo. However, the influence of EGFR regulation on the MAP Kinase pathway seemed to be very slight. These findings provide evidence that STAT 3 signal activity in head and neck carcinomas, which is partially responsible for proliferative activity, can be controlled via the EGFR.

M3 - SCORING: Zeitschriftenaufsatz

VL - 24

SP - 3881

EP - 3886

JO - ANTICANCER RES

JF - ANTICANCER RES

SN - 0250-7005

IS - 6

M1 - 6

ER -