Logging and indigenous hunting impacts on persistence of large Neotropical animals

Areas allocated for industrial logging and community-owned forests account for over 50% of all remaining tropical forests. Landscapescale conservation strategies that include these forests are expected to have substantial benefits for biodiversity, especially for large mammals and birds that require extensive habitat but that are susceptible to extirpation due to synergies between logging and hunting. In addition, their responses to logging alone are poorly understood due to their cryptic behavior and low densities. In this study, we assessed the effects of logging and hunting on detection and occupancy rates of large vertebrates in a multiple- use forest on the Guiana Shield. Our study site was certified as being responsibly managed for timber production and indigenous communities are legally guaranteed use-rights to the forest. We coupled camera-trap data for wildlife detection with a spatially explicit dataset on indigenous hunting. A multi-species occupancy model found a weak positive effect of logging on occupancy and detection rates, while hunting had a weak negative effect. Model predictions of species richness were also higher in logged forest sites compared to unlogged forest sites. Density estimates for jaguars and ocelots in our multiple- use area were similar to estimates reported for fully protected areas. Involvement of local communities in forest management, control of forest access, and nesting production forests in a landscape that includes protected areas seemed important for these positive biodiversity outcomes. The maintenance of vertebrate species bodes well for both biodiversity and the humans that depend on multiple- use forests

Publisher Correction: Oncogenic hijacking of a developmental transcription factor evokes vulnerability toward oxidative stress in Ewing sarcoma (Nature Communications, (2020), 11, 1, (2423), 10.1038/s41467-020-16244-2)

The original version of this Article contained an error in Fig. 3b. In Fig. 3b the “<” symbol in the labelling for light grey circles was replaced by “>”. This has been corrected in both the PDF and HTML versions of the Article

Anaplastic thyroid carcinoma: from clinicopathology to genetics and advanced therapies

Anaplastic thyroid carcinoma (ATC) is a rare malignancy, accounting for 1-2% of all thyroid cancers. Although rare, ATC accounts for the majority of deaths from thyroid carcinoma. ATC often originates in a pre-existing thyroid cancer lesion, as suggested by the simultaneous presence of areas of differentiated or poorly differentiated thyroid carcinoma. ATC is characterized by the accumulation of several oncogenic alterations, and studies have shown that an increased number of oncogenic alterations equates to an increased level of dedifferentiation and aggressiveness. The clinical management of ATC requires a multidisciplinary approach; according to recent American Thyroid Association guidelines, surgery, radiotherapy and/or chemotherapy should be considered. In addition to conventional therapies, novel molecular targeted therapies are the most promising emerging treatment modalities. These drugs are often multiple receptor tyrosine kinase inhibitors, several of which have been tested in clinical trials with encouraging results so far. Accordingly, clinical trials are ongoing to evaluate the safety, efficacy and effectiveness of these new agents. This Review describes the updated clinical and pathological features of ATC and provides insight into the molecular biology of this disease. The most recent literature regarding conventional, newly available and future therapies for ATC is also discussed

Proportional Upregulation of CD97 Isoforms in Glioblastoma and Glioblastoma-Derived Brain Tumor Initiating Cells

CD97 is a novel glioma antigen that confers an invasive phenotype and poor survival in patients with glioblastoma (GBM), the most aggressive primary malignant brain tumor. The short isoform of CD97, known as EGF(1,2,5), has been shown to promote invasion and metastasis, but its role in gliomas and GBM-derived brain tumor initiating cells (BTICs) has not been studied. We sought to characterize CD97 expression among gliomas and identify the specific isoforms expressed. The short isoform of CD97 was identified in GBM and GBM-derived BTICs, but not low grade or anaplastic astrocytomas. All samples expressing the EGF(1,2,5) isoform were also found to express the EGF(1,2,3,5) isoform. These isoforms are believed to possess similar ligand binding patterns and interact with chondroitin sulfate, a component of the extracellular matrix, and the integrin α5β1. Using data acquired from the Cancer Genome Atlas (TCGA), we show that CD97 is upregulated among the classical and mesenchymal subtypes of GBM and significantly decreased among IDH1 mutant GBMs. Given its proven roles in tumor invasion, expression among aggressive genetic subtypes of GBM, and association with overall survival, CD97 is an attractive therapeutic target for patients with GBM