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Another good year for biomarkers
Identification of a systemic molecular signature facilitating early diagnosis and enabling targeted therapy is the Holy Grail for the investigators of many pulmonary diseases, particularly those with heterogeneous presentation such as chronic obstruction pulmonary disease (COPD) or idiopathic pulmonary fibrosis (IPF). Genome-wide gene expression profiling of large groups of patients has revealed a clear gene signature for elastogenesis during COPD and identified fibulin-5 as a potential molecular target.1 Genetic regulation of gene expression patterns was investigated by integrative genomics which identified cystatin C (CST3) and CD22 as causal genes for airflow obstruction.2 The fact that these gene expression patterns in COPD are dynamic during treatment, reflecting disease severity, highlights the potential of this approach for the development of molecular phenotype-driven therapy for COPD.3 Similarly, a coordinated approach was used to assess the relationship between gene expression patterns, pathological features and systemic biomarkers to identify indicators of disease severity in patients with IPF. MMP3 and CXCL13 emerged as systemic biomarkers that reflect brochiolisation and lymphoid aggregates and are predicted to be of clinical value as prognostic or surrogate markers of disease severity in these patients.4 An alternative method of predicting cancer risk in patients presenting with endobronchial squamous metaplasia is the identification of DNA copy number aberration. This technique has proved a highly accurate biomarker for assessment of disease progression and could assist in deciding which patients with endobronchial lesions may benefit from more aggressive treatment or closer surveillance.5
Smoking and steroids
Further evidence that smoking is bad for you—and your immune system—stems from a series of papers examining the effect of cigarette smoke on innate immune function. Tobacco smoke blunted secretion of key innate cytokines such as interferon γ and tumour necrosis factor α and impaired the ability of macrophages derived from peripheral blood or the airways to …
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.
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