ArticleBioMed research international2015
Anti-EGFR antibody reduces lung nodules by inhibition of EGFR-pathway in a model of lymphangioleiomyomatosis.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Novel treatment strategies for lymphangioleiomyomatosis: a narrative review.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Activation of mTOR signaling in adult lung microvascular progenitor cells accelerates lung aging.The Journal of clinical investigation · 2023Article
- Article
- Primary TSC2International journal of molecular sciences · 2022Article
- LAM Cells as Potential Drivers of Senescence in Lymphangioleiomyomatosis Microenvironment.International journal of molecular sciences · 2022Article
- Soluble Immune-Related Proteins as New Candidate Serum Biomarkers for the Diagnosis and Progression of Lymphangioleiomyomatosis.Frontiers in immunology · 2022Article
- RUNX1/EGFR pathway contributes to STAT3 activation and tumor growth caused by hyperactivated mTORC1.Molecular therapy oncolytics · 2021Article
- Article
- Article
- Possible Novel Therapeutic Targets in Lymphangioleiomyomatosis Treatment.Frontiers in medicine · 2020Review
- Potential lymphangiogenesis therapies: Learning from current antiangiogenesis therapies-A review.Medicinal research reviews · 2018Review
- NK cell activating receptor ligand expression in lymphangioleiomyomatosis is associated with lung function decline.JCI insight · 2016Article
- Estrogen maintains myometrial tumors in a lymphangioleiomyomatosis model.Endocrine-related cancer · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EGFR belongs to the HER/ErbB family of tyrosine kinase receptors and its activation in cancer cells has been linked with increased proliferation, angiogenesis, and metastasis. Lymphangioleiomyomatosis (LAM) is a rare, low-grade neoplasm that occurs sporadically or in association with tuberous sclerosis complex (TSC), a genetic, multisystem disorder characterized by hamartomas in several organs. From chylous of a LAM/TSC patient, we previously isolated smooth muscle-like LAM/TSC cells whose proliferation depends on EGF and monoclonal anti-EGFR antibodies reduced proliferation and caused cell death. We demonstrated that the dependency from EGF was caused by the absence of tuberin. To study the role of EGFR pathway in vivo, we developed a mouse model by administration of LAM/TSC cells to female nude mice. LAM/TSC cells caused pulmonary airspace enlargement and, after 30 weeks, nodule formation which express EGFR. Anti-EGFR antibody decreased the number and dimension of lung nodules likely for the inhibition of Erk and S6 signaling, reversed the pulmonary alterations, and reduced lymphatic and blood vessels. Moreover, in pulmonary nodules anti-EGFR antibody reduced the positivity to estrogen and progesterone receptors which enhance survival of LAM cells and Snail expression. These results suggest that the inhibition of EGFR signalling has a potential in treatment of LAM/TSC lung alterations.
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