ArticleCancer research2014
SRC kinase is a novel therapeutic target in lymphangioleiomyomatosis.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02737202 (Safety and Efficacy of Saracatinib In Subjects With Lymphangioleiomyomatosis), which is not on this map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Safety and Efficacy of Saracatinib In Subjects With Lymphangioleiomyomatosis
Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Current insight into the molecular mechanisms of lymphangioleiomyomatosis.American journal of respiratory cell and molecular biology · 2026Review
- Extracellular vesicles modulate integrin signaling and subcellular energetics to promote pulmonary lymphangioleiomyomatosis metastasis.Communications biology · 2025Article
- Novel treatment strategies for lymphangioleiomyomatosis: a narrative review.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- A multi‑omics study of diagnostic markers and the unique inflammatory tumor micro‑environment involved in tuberous sclerosis complex‑related renal angiomyolipoma.International journal of oncology · 2022Article
- Mechanisms of disease-modifying effect of saracatinib (AZD0530), a Src/Fyn tyrosine kinase inhibitor, in the rat kainate model of temporal lobe epilepsy.Neurobiology of disease · 2021Article
- Challenges and Opportunities for Drug Repositioning in Fibrodysplasia Ossificans Progressiva.Biomedicines · 2021Review
- Inhibitors of Src Family Kinases, Inducible Nitric Oxide Synthase, and NADPH Oxidase as Potential CNS Drug Targets for Neurological Diseases.CNS drugs · 2021Review
- Differential Impact of Severity and Duration ofFrontiers in cellular neuroscience · 2021Article
- Possible Novel Therapeutic Targets in Lymphangioleiomyomatosis Treatment.Frontiers in medicine · 2020Review
- Zoledronic acid inhibits TSC2-null cell tumor growth via RhoA/YAP signaling pathway in mouse models of lymphangioleiomyomatosis.Cancer cell international · 2020Article
- Drug repurposing: progress, challenges and recommendations.Nature reviews. Drug discovery · 2019Review
- The Importance of Tyrosine Phosphorylation Control of Cellular Signaling Pathways in Respiratory Disease: pY and pY Not.American journal of respiratory cell and molecular biology · 2018Review
- Reply to Yanagisawa: Treatment of Pulmonary Lymphangioleiomyomatosis during Pregnancy.American journal of respiratory and critical care medicine · 2018Article
- New insights in lymphangioleiomyomatosis and pulmonary Langerhans cell histiocytosis.European respiratory review : an official journal of the European Respiratory Society · 2017Review
- Aberrant SYK Kinase Signaling Is Essential for Tumorigenesis Induced by TSC2 Inactivation.Cancer research · 2017Article
- Minireview: Lymphangioleiomyomatosis (LAM): The "Other" Steroid-Sensitive Cancer.Endocrinology · 2016Review
- Evidence Supporting a Lymphatic Endothelium Origin for Angiomyolipoma, a TSC2(-) Tumor Related to Lymphangioleiomyomatosis.The American journal of pathology · 2016Article
- Therapeutic Strategies for Treatment of Pulmonary Lymphangioleiomyomatosis (LAM).Expert opinion on orphan drugs · 2014Article
- Management of lymphangioleiomyomatosis.F1000prime reports · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Lymphangioleiomyomatosis (LAM) is a progressive cystic lung disease affecting some women with tuberous sclerosis complex (TSC). Sporadic LAM can develop in women without TSC, owing to somatic mutations in the TSC2 gene. Accumulating evidence supports the view of LAM as a low-grade, destructive, metastasizing neoplasm. The mechanisms underlying the metastatic capability of LAM cells remain poorly understood. The observed behavior of LAM cells with respect to their infiltrative growth pattern, metastatic potential, and altered cell differentiation bears similarity to cells undergoing epithelial-mesenchymal transition. Here, we report increased levels of active Src kinase in LAM lungs and in TSC2(-/-) cells, caused by a reduction of autophagy. Furthermore, increased Src kinase activation promoted migration, invasion, and inhibition of E-cadherin expression in TSC2(-/-) cells by upregulating the transcription factor Snail. Notably, Src kinase inhibitors reduced migration and invasion properties of TSC2(-/-) cells and attenuated lung colonization of intravenously injected TSC2(-/-) cells in vivo to a greater extent than control TSC2(+/+) cells. Our results reveal mechanistic basis for the pathogenicity of LAM cells and they rationalize Src kinase as a novel therapeutic target for treatment of LAM and TSC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.