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• W2412430443 abstract "Interstitial lung diseases (ILDs) comprise a heterogeneous group of rare respiratory disorders characterised by diffuse pulmonary infiltrates and destruction of lung parenchyma [1]. With growing evidence that mutations in genes encoding proteins that participate in critical regulatory pathways have roles in the pathogenesis of some forms of ILD, it appears that some diseases under the ILD umbrella may be neoplastic and associated with the presence of cancer-like cells, not found in healthy individuals [2]. For example, lymphangioleiomyomatosis (LAM) results from the proliferation of LAM cells with mutation of tuberous sclerosis ( TSC ) 1 and TSC2 genes. LAM can be sporadic or occur in association with TSC, an autosomal dominant disorder [3]. TSC2 mutations were detected in seven (50%) out of 14 and a TSC1 mutation in one (7.1%) out of 14 TSC-LAM patients [4]. Sporadic LAM appears to be driven by TSC2 mutation [5]. The proteins encoded by TSC1 and TSC2 are upstream of the mammalian target of rapamycin pathway, which has been targeted in LAM treatment (Multicenter International Lymphangioleiomyomatosis Efficacy and Safety of Sirolimus (MILES) trial) [6].Identifying new therapeutic targets of interstitial lung disease from genetic studies" @default.
• W2412430443 created "2016-06-24" @default.
• W2412430443 creator A5048042168 @default.
• W2412430443 creator A5066716873 @default.
• W2412430443 date "2016-05-31" @default.
• W2412430443 modified "2023-09-24" @default.
• W2412430443 title "Genetic studies yield clues to the pathogenesis of Langerhans cell histiocytosis" @default.
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• W2412430443 doi "https://doi.org/10.1183/13993003.00568-2016" @default.
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