Special Issue "EGFR in Cancer: Innovative Insights into Signalling, Mutation and Therapeutic Targeting"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 31 December 2019

Special Issue Editor

Guest Editor
Prof. Terrance G. Johns

Telethon Kids Cancer Centre, Telethon Kids Institute, Nedlands, WA 6009, Australia
Website | E-Mail
Interests: glioma; EGFR; antibody therapeutics; OLIG2; pediatric brain cancer

Special Issue Information

Dear Colleagues,

The epidermal growth factor receptor (EGFR) is one of the most frequently dysregulated tyrosine kinases in cancer. The cancers impacted include glioma, lung cancer, head and neck cancer and colon cancer, along with many others. EGFR dysregulation is driven by diverse mechanisms, including gene amplification, mutation, overexpression, improper interactions with other members of the ErbB family and inappropriate autocrine signaling. Interestingly, the primary mechanism of EGFR activation is comparatively tumor specific; kinase domain mutations are predominantly restricted to lung cancer for example.

The central role of EGFR dysregulation in cancer development has led to the development of both small molecule tyrosine kinase inhibitors and therapeutic antibodies. In some cancers (e.g., lung cancer) these have proven to be effective therapeutic strategies, but in other cancers (e.g., glioma) targeting EGFR has been ineffectual.

In this Special Issue, we will publish reviews and original research that provide new insights into the role of EGFR in cancer and how it can be targeted therapeutically. Novel insights into EGFR mutation and gene amplification will be particularly welcomed.

Prof. Terrance G. Johns
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • EGFR mutation
  • EGFR signalling
  • tyrosine kinase inhibitors
  • antibody therapeutics
  • imaging
  • EGFR gene amplification
  • therapeutic resistance
  • ErbB family

Published Papers (1 paper)

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Research

Open AccessArticle CX Chemokine Receptor 7 Contributes to Survival of KRAS-Mutant Non-Small Cell Lung Cancer upon Loss of Epidermal Growth Factor Receptor
Cancers 2019, 11(4), 455; https://doi.org/10.3390/cancers11040455
Received: 14 February 2019 / Revised: 25 March 2019 / Accepted: 27 March 2019 / Published: 30 March 2019
PDF Full-text (3102 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
KRAS-driven non-small cell lung cancer (NSCLC) patients have no effective targeted treatment. In this study, we aimed to investigate targeting epidermal growth factor receptor (EGFR) as a therapeutic approach in KRAS-driven lung cancer cells. We show that ablation of EGFR significantly [...] Read more.
KRAS-driven non-small cell lung cancer (NSCLC) patients have no effective targeted treatment. In this study, we aimed to investigate targeting epidermal growth factor receptor (EGFR) as a therapeutic approach in KRAS-driven lung cancer cells. We show that ablation of EGFR significantly suppressed tumor growth in KRAS-dependent cells and induced significantly higher expression of CX chemokine receptor 7 (CXCR7) and activation of MAPK (ERK1/2). Conversely, rescue of EGFR led to CXCR7 downregulation in EGFR−/− cells. Dual EGFR and CXCR7 inhibition led to substantial reduction of MAPK (pERK) and synergistic inhibition of cell growth. Analysis of two additional EGFR knockout NSCLC cell lines using CRISPR/Cas9 revealed genotype dependency of CXCR7 expression. In addition, treatment of different cells with gefitinib increased CXCR7 expression in EGFRwt but decreased it in EGFRmut cells. CXCR7 protein expression was detected in all NSCLC patient samples, with higher levels in adenocarcinoma as compared to squamous cell lung carcinoma and healthy control cases. In conclusion, EGFR and CXCR7 have a crucial interaction in NSCLC, and dual inhibition may be a potential therapeutic option for NSCLC patients. Full article
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