2 research outputs found

    Surgical polarimetric endoscopy for the detection of laryngeal cancer

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    The standard-of-care for the detection of laryngeal pathologies involves distinguishing suspicious lesions from surrounding healthy tissue via contrasts in colour and texture captured by white-light endoscopy. However, the technique is insufficiently sensitive and thus leads to unsatisfactory rates of false negatives. Here we show that laryngeal lesions can be better detected in real time by taking advantage of differences in the light-polarization properties of cancer and healthy tissues. By measuring differences in polarized-light retardance and depolarization, the technique, which we named 'surgical polarimetric endoscopy' (SPE), generates about one-order-of-magnitude greater contrast than white-light endoscopy, and hence allows for the better discrimination of cancerous lesions, as we show with patients diagnosed with squamous cell carcinoma. Polarimetric imaging of excised and stained slices of laryngeal tissue indicated that changes in the retardance of polarized light can be largely attributed to architectural features of the tissue. We also assessed SPE to aid routine transoral laser surgery for the removal of a cancerous lesion, indicating that SPE can complement white-light endoscopy for the detection of laryngeal cancer

    Lung adenocarcinoma promotion by air pollutants

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    A complete understanding of how exposure to environmental substances promotes cancer formation is lacking. More than 70 years ago, tumorigenesis was proposed to occur in a two-step process: an initiating step that induces mutations in healthy cells, followed by a promoter step that triggers cancer development1. Here we propose that environmental particulate matter measuring ≤2.5 μm (PM2.5), known to be associated with lung cancer risk, promotes lung cancer by acting on cells that harbour pre-existing oncogenic mutations in healthy lung tissue. Focusing on EGFR-driven lung cancer, which is more common in never-smokers or light smokers, we found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in four within-country cohorts. Functional mouse models revealed that air pollutants cause an influx of macrophages into the lung and release of interleukin-1β. This process results in a progenitor-like cell state within EGFR mutant lung alveolar type II epithelial cells that fuels tumorigenesis. Ultradeep mutational profiling of histologically normal lung tissue from 295 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively. These findings collectively support a tumour-promoting role for PM2.5 air pollutants and provide impetus for public health policy initiatives to address air pollution to reduce disease burden
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