Crowdfunding in the Cultural Industries

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Crowdfunding in the Cultural Industries

Cultural production has stood at the forefront of crowdfunding adoption representing some of the first crowdfunding campaigns on record. This development emerged as part of comprehensive value chain reconfigurations in the cultural sector, which were triggered by the advent of digitalization on the one hand and the downsizing in public funds on the other. As a result, the emerging phenomenon here labelled as ‘cultural crowdfunding’ (CCF) has captured the imagination of researchers and practitioners. The study of CCF is of high relevance, as it presses creators to strike a balance between the commercial and the non-commercial, the economic and the cultural outcomes, as well as the authentic and independent versus the mass dictated and dependent. In this chapter we review earlier research on CCF and identify core themes and key studies representing such themes. Later, we outline an agenda for future research, while also suggesting some implications for practice

Lung adenocarcinoma promotion by air pollutants

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