Putting the rights of nature on the map. A quantitative analysis of rights of nature initiatives across the world

The Rights of Nature (RoN) promote a new understanding of the human environment, where natural entities are conceived as subjects with intrinsic value independent of human interests. The implementation of this idea gained momentum in the United States in 2006. One decade and a half later, the idea has spread all over the world. Despite some efforts, a sophisticated geographical inventory of the movement is missing. Building on Kauffman (2020), we identified and analysed 409 initiatives in 39 countries, creating the most comprehensive database of RoN initiatives to date. We developed a taxonomy that may guide further research. We also present two detailed maps which can help policymakers, legislators, judges, researchers, and the public at large to evaluate and compare initiatives. The findings of this investigation directly help the UN Harmony with Nature Programme and have contributed to the launch of the Eco-Jurisprudence Monitor, an online database of RoN initiatives

The Rights of Nature as a Bridge between Land-Ownership Regimes: The Potential of Institutionalized Interplay in Post-Colonial Societies

Despite the growing prominence and use of Rights of Nature (RoN), doubts remain as to their tangible effect on environmental protection efforts. By analyzing two initiatives in post-colonial societies, we argue that they do influence the creation of institutionalized bridges between differing land-ownership regimes. Applying the methodology of inter-legality, we examine the Ecuadorian Constitution of 2008 and the Ugandan National Environment Act 2019. We identify five normative spheres that influence land-ownership regimes. We find that the established Ecuadorian RoN have an institutionalized effect on the nation's legal system. Their more recently established Ugandan counterpart shows potential to develop in the same direction

Comprehensive genomic profiles of small cell lung cancer

We have sequenced the genomes of 110 small cell lung cancers (SCLC), one of the deadliest human cancers. In nearly all the tumours analysed we found bi-allelic inactivation of TP53 and RB1, sometimes by complex genomic rearrangements. Two tumours with wild-type RB1 had evidence of chromothripsis leading to overexpression of cyclin D1 (encoded by the CCND1 gene), revealing an alternative mechanism of Rb1 deregulation. Thus, loss of the tumour suppressors TP53 and RB1 is obligatory in SCLC. We discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73Dex2/3. In rare cases, SCLC tumours exhibited kinase gene mutations, providing a possible therapeutic opportunity for individual patients. Finally, we observed inactivating mutations in NOTCH family genes in 25% of human SCLC. Accordingly, activation of Notch signalling in a pre-clinical SCLC mouse model strikingly reduced the number of tumours and extended the survival of the mutant mice. Furthermore, neuroendocrine gene expression was abrogated by Notch activity in SCLC cells. This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer

Comprehensive genomic profiles of small cell lung cancer

We have sequenced the genomes of 110 small cell lung cancers (SCLC), one of the deadliest human cancers. In nearly all the tumours analysed we found bi-allelic inactivation of TP53 and RB1, sometimes by complex genomic rearrangements. Two tumours with wild-type RB1 had evidence of chromothripsis leading to overexpression of cyclin D1 (encoded by the CCND1 gene), revealing an alternative mechanism of Rb1 deregulation. Thus, loss of the tumour suppressors TP53 and RB1 is obligatory in SCLC. We discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73Dex2/3. In rare cases, SCLC tumours exhibited kinase gene mutations, providing a possible therapeutic opportunity for individual patients. Finally, we observed inactivating mutations in NOTCH family genes in 25% of human SCLC. Accordingly, activation of Notch signalling in a pre-clinical SCLC mouse model strikingly reduced the number of tumours and extended the survival of the mutant mice. Furthermore, neuroendocrine gene expression was abrogated by Notch activity in SCLC cells. This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer