Phenotypes to Genotypes: Breaking the Chains of EGFR Addiction in Lung Cancer
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".
Deadline for manuscript submissions: 31 March 2025 | Viewed by 71
Special Issue Editor
Interests: lung pathology; interstitial lung disease; idiopathic pulmonary fibrosis; molecular pathology
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The Special Issue "Phenotypes to Genotypes: Breaking the Chains of EGFR Addiction in Lung Cancer" seeks to explore the complex biology of EGFR mutations in non-small cell lung cancer (NSCLC) and the enduring challenge of acquired resistance to EGFR-targeted therapies. Although EGFR tyrosine kinase inhibitors (TKIs) have reshaped treatment outcomes for patients with EGFR-mutant NSCLC, resistance almost inevitably emerges, limiting the long-term effectiveness of these therapies. A deeper understanding of the molecular, genetic, and phenotypic changes driving this resistance is critical to overcoming these challenges.
A particularly compelling aspect of EGFR-mutant lung cancer is the correlation between specific histotypes, their morphological features, and the phenomenon of EGFR addiction. Certain histologic subtypes of NSCLC, such as adenocarcinoma with lepidic growth patterns, have been closely associated with EGFR mutations, showing a pronounced dependency on EGFR signaling for survival and growth. Morphologically distinct patterns, including solid, papillary, or micropapillary architecture, may offer insights into the tumor’s behavior, including its susceptibility to EGFR inhibitors and eventual progression to drug resistance. Examining these histologic characteristics in correlation with molecular alterations provides a deeper understanding of tumor evolution and may offer predictive value in assessing therapeutic responses and potential resistance mechanisms.
We aim to explore the mechanisms of resistance and progression, from well-characterized alterations like the EGFR T790M mutation and MET amplification to lesser-known pathways such as PIK3CA mutations, EGFR amplification, and epithelial-to-mesenchymal transition (EMT). In addition, it will address the growing recognition of tumor heterogeneity and the remarkable ability of NSCLC to transform into small cell lung cancer (SCLC), which presents both a therapeutic challenge and an opportunity. The evolving nature of resistance mechanisms—how they can be both acquired and lost under selective therapeutic pressure—highlights the need for innovative approaches to re-target resistant tumors.
The issue will also emphasize emerging therapeutic strategies aimed at "breaking the chains" of EGFR dependency in lung cancer, including combination therapies, sequential treatment protocols, and novel ways to target tumor plasticity. Additionally, the role of serial biopsies in tracking resistance evolution and guiding personalized treatment will be a key focus.
We invite submissions of scientific research articles, case reports, meta-analyses, and reviews that address the molecular and cellular mechanisms driving progression, and resistance in EGFR-mutant lung cancer as well as its histologic evolution,. We welcome contributions that offer new insights into the biology of EGFR-driven cancers and propose innovative therapeutic strategies to overcome drug resistance.
Dr. Massimiliano Mancini
Guest Editor
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Keywords
- EGFR-mutant lung cancer
- EGFR
- NSCLC
- tumor heterogeneity
- resistance mechanisms
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