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Differential Gene Expression in Erlotinib-Treated Fibroblasts
Karen E Wickersham1, Theresa K Hodges, Martin J Edelman
1Karen E. Wickersham, PhD, RN, was Assistant Professor, School of Nursing, University of Maryland, Baltimore; now Assistant Professor, University of South Carolina, College of Nursing, Columbia, South Carolina. Theresa K. Hodges, PhD, is Bioinformatics Analyst I, Institute for Genome Sciences, School of Medicine, University of Maryland, Baltimore, Maryland. Martin J. Edelman, MD, was Director, Medical Thoracic Oncology, University of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore, Maryland; now Professor and Chair, Department of Hematology/Oncology; Deputy Director, Cancer Center for Clinical Research; and G. Morris Dorrance Jr. Chair in Medical Oncology, Fox Chase Cancer Center, Philadelphia, Pennsylvania. Yang Song, PhD, is Bioinformatics Analyst II, Institute for Genome Sciences, School of Medicine, University of Maryland, Baltimore, Maryland. Mintong Nan, BS, was Laboratory Research Technician, Department of Pain and Translational Symptom Science, University of Maryland, Baltimore, School of Nursing, Baltimore, Maryland. Susan G. Dorsey, PhD, RN, FAAN, is Professor and Chair, Department of Pain and Translational Symptom Science, University of Maryland, Baltimore, School of Nursing, Baltimore, Maryland; and PhD Student at the University of Maryland.
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy for non-small cell lung cancer can cause severe skin rash. This study identified specific genes in dermal fibroblasts altered by erlotinib, potentially predicting rash development.
Area of Science:
- Dermatology
- Oncology
- Molecular Biology
Background:
- Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapies are crucial for non-small cell lung cancer (NSCLC) treatment.
- A common and debilitating side effect of EGFR-TKI therapy is a painful skin rash, making prediction and management challenging.
Purpose of the Study:
- To investigate the transcriptomic changes in dermal fibroblasts induced by erlotinib, an EGFR-TKI.
- To identify potential biomarkers for predicting EGFR-TKI-induced rash in NSCLC patients.
Main Methods:
- Dermal fibroblasts were treated with varying concentrations of erlotinib or vehicle control.
- Gene expression profiling was performed using Affymetrix arrays.
- Differentially expressed genes were analyzed using Ingenuity Pathway Analysis.
Main Results:
- Erlotinib treatment altered the expression of several genes in dermal fibroblasts.
- Key genes related to wound healing, inflammation, and cancer progression were identified.
- Four genes (MMP12, CCL2, CDC6, and SLC7A11) were validated using Western blot and qPCR.
Conclusions:
- The identified gene expression changes may serve as predictive markers for EGFR-TKI-induced rash.
- Findings could lead to better patient risk stratification and personalized treatment strategies.
- Potential for developing targeted interventions to manage rash and improve treatment adherence.
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