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Berasain C, Ujue Latasa M, Urtasun R, et al. Epidermal Growth Factor Receptor (EGFR) Crosstalks in Liver Cancer. Cancers (Basel). 2011;3(2):2444-61doi: 10.3390/cancers3022444.
Berasain, C., Ujue Latasa, M., Urtasun, R., Goñi, S., Elizalde, M., Garcia-Irigoyen, O., Azcona, M., Prieto, J., & Avila, M. A. (2011). Epidermal Growth Factor Receptor (EGFR) Crosstalks in Liver Cancer. Cancers, 3(2), 2444-61. https://doi.org/10.3390/cancers3022444
Berasain, Carmen, et al. "Epidermal Growth Factor Receptor (EGFR) Crosstalks in Liver Cancer." Cancers vol. 3,2 (2011): 2444-61. doi: https://doi.org/10.3390/cancers3022444
Berasain C, Ujue Latasa M, Urtasun R, Goñi S, Elizalde M, Garcia-Irigoyen O, Azcona M, Prieto J, Avila MA. Epidermal Growth Factor Receptor (EGFR) Crosstalks in Liver Cancer. Cancers (Basel). 2011 May 18;3(2):2444-61. doi: 10.3390/cancers3022444. PMID: 24212818; PMCID: PMC3757426.
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Cancers (Basel). 2011 May 18;3(2):2444-61. doi: 10.3390/cancers3022444.

Epidermal Growth Factor Receptor (EGFR) Crosstalks in Liver Cancer.

Cancers

Carmen Berasain, María Ujue Latasa, Raquel Urtasun, Saioa Goñi, María Elizalde, Oihane Garcia-Irigoyen, María Azcona, Jesús Prieto, Matías A Avila

Affiliations

  1. Division of Hepatology and Gene Therapy, CIMA, University of Navarra, Pamplona 31008, Spain. [email protected].

PMID: 24212818 PMCID: PMC3757426 DOI: 10.3390/cancers3022444

Abstract

Hepatocarcinogenesis is a complex multistep process in which many different molecular pathways have been implicated. Hepatocellular carcinoma (HCC) is refractory to conventional chemotherapeutic agents, and the new targeted therapies are meeting with limited success. Interreceptor crosstalk and the positive feedback between different signaling systems are emerging as mechanisms of targeted therapy resistance. The identification of such interactions is therefore of particular relevance to improve therapeutic efficacy. Among the different signaling pathways activated in hepatocarcinogenesis the epidermal growth factor receptor (EGFR) system plays a prominent role, being recognized as a "signaling hub" where different extracellular growth and survival signals converge. EGFR can be transactivated in response to multiple heterologous ligands through the physical interaction with multiple receptors, the activity of intracellular kinases or the shedding of EGFR-ligands. In this article we review the crosstalk between the EGFR and other signaling pathways that could be relevant to liver cancer development and treatment.

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