Binang gurri: turning a deaf ear to indigenous hearing loss

Objective: This paper asks whether Indigenous health policies might be improved if governments listened to Indigenous voices, both Australian and those who drafted the Declaration on the Rights of Indigenous Peoples, 2007. Methods: A fundamental tenet of the Declaration, which Australia endorsed in 2009, is respect for Indigenous knowledge and voice. The author analyses legal, cultural and historical sources for evidence of this respect. The metaphorical and empirical framework of the analysis is the epidemic of otitis media among Indigenous children. Results: A survey of Indigenous advice about health clearly demonstrates that access to their land and respect for the diversity of Indigenous cultures should inform health policies. Despite, however, claiming to consult Indigenous peoples, policy-makers have not been listening. In many Indigenous languages not listening, or ‘bad ears’, has connotations of disrespect. Conclusions: By turning a deaf ear to Indigenous knowledge governments are undermining any respect Indigenous peoples may have for them and their policies. A new approach is needed. Implications: The Declaration on the Rights of Indigenous Peoples can provide federal, state and territory governments with benchmarks against which health policy can be developed and implemented. Authentic consultation could restore Indigenous confidence in government policies.

Loss-of-function fibroblast growth factor receptor-2 mutations in melanoma

We report that 10% of melanoma tumors and cell lines harbor mutations in the fibroblast growth factor receptor 2 (FGFR2) gene. These novel mutations include three truncating mutations and 20 missense mutations occurring at evolutionary conserved residues in FGFR2 as well as among all four FGFRs. The mutation spectrum is characteristic of those induced by UV radiation. Mapping of these mutations onto the known crystal structures of FGFR2 followed by in vitro and in vivo studies show that these mutations result in receptor loss of function through several distinct mechanisms, including loss of ligand binding affinity, impaired receptor dimerization, destabilization of the extracellular domains, and reduced kinase activity. To our knowledge, this is the first demonstration of loss-of-function mutations in a class IV receptor tyrosine kinase in cancer. Taken into account with our recent discovery of activating FGFR2 mutations in endometrial cancer, we suggest that FGFR2 may join the list of genes that play context-dependent opposing roles in cancer.