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Opposing consequences of signaling through EGF family members: Escape from CTLs could be a bait for NK cells
Oncogenes have been traditionally viewed as molecular drivers for tumor growth and survival. Recent evidence indicates that oncogenes may facilitate the escape of malignant cells from immune recognition and elimination. In this article, we discuss the implications of the overexpression of epidermal...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Landes Bioscience
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3494645/ https://www.ncbi.nlm.nih.gov/pubmed/23170279 http://dx.doi.org/10.4161/onci.20685 |
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author | Kiessling, Rolf Okita, Riki Mougiakakos, Dimitrios Mao, Yumeng Sarhan, Dhifaf Wennerberg, Erik Seliger, Barbara Lundqvist, Andreas Mimura, Kousaku Kono, Koji |
author_facet | Kiessling, Rolf Okita, Riki Mougiakakos, Dimitrios Mao, Yumeng Sarhan, Dhifaf Wennerberg, Erik Seliger, Barbara Lundqvist, Andreas Mimura, Kousaku Kono, Koji |
author_sort | Kiessling, Rolf |
collection | PubMed |
description | Oncogenes have been traditionally viewed as molecular drivers for tumor growth and survival. Recent evidence indicates that oncogenes may facilitate the escape of malignant cells from immune recognition and elimination. In this article, we discuss the implications of the overexpression of epidermal growth factor receptor (EGFR) family members on immune escape of tumors and immunotherapy. |
format | Online Article Text |
id | pubmed-3494645 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Landes Bioscience |
record_format | MEDLINE/PubMed |
spelling | pubmed-34946452012-11-20 Opposing consequences of signaling through EGF family members: Escape from CTLs could be a bait for NK cells Kiessling, Rolf Okita, Riki Mougiakakos, Dimitrios Mao, Yumeng Sarhan, Dhifaf Wennerberg, Erik Seliger, Barbara Lundqvist, Andreas Mimura, Kousaku Kono, Koji Oncoimmunology Author's View Oncogenes have been traditionally viewed as molecular drivers for tumor growth and survival. Recent evidence indicates that oncogenes may facilitate the escape of malignant cells from immune recognition and elimination. In this article, we discuss the implications of the overexpression of epidermal growth factor receptor (EGFR) family members on immune escape of tumors and immunotherapy. Landes Bioscience 2012-10-01 /pmc/articles/PMC3494645/ /pubmed/23170279 http://dx.doi.org/10.4161/onci.20685 Text en Copyright © 2012 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Author's View Kiessling, Rolf Okita, Riki Mougiakakos, Dimitrios Mao, Yumeng Sarhan, Dhifaf Wennerberg, Erik Seliger, Barbara Lundqvist, Andreas Mimura, Kousaku Kono, Koji Opposing consequences of signaling through EGF family members: Escape from CTLs could be a bait for NK cells |
title | Opposing consequences of signaling through EGF family members: Escape from CTLs could be a bait for NK cells |
title_full | Opposing consequences of signaling through EGF family members: Escape from CTLs could be a bait for NK cells |
title_fullStr | Opposing consequences of signaling through EGF family members: Escape from CTLs could be a bait for NK cells |
title_full_unstemmed | Opposing consequences of signaling through EGF family members: Escape from CTLs could be a bait for NK cells |
title_short | Opposing consequences of signaling through EGF family members: Escape from CTLs could be a bait for NK cells |
title_sort | opposing consequences of signaling through egf family members: escape from ctls could be a bait for nk cells |
topic | Author's View |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3494645/ https://www.ncbi.nlm.nih.gov/pubmed/23170279 http://dx.doi.org/10.4161/onci.20685 |
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