A STAG2-PAXIP1/PAGR1 axis suppresses lung tumorigenesis.

The cohesin complex is a critical regulator of gene expression. STAG2 is the most frequently mutated cohesin subunit across several cancer types and is a key tumor suppressor in lung cancer. Here, we coupled somatic CRISPR-Cas9 genome editing and tumor barcoding with an autochthonous oncogenic KRAS-driven lung cancer model and showed that STAG2 is uniquely tumor-suppressive among all core and auxiliary cohesin components.

A high-resolution two-step evolution experiment in yeast reveals a shift from pleiotropic to modular adaptation.

Evolution by natural selection is expected to be a slow and gradual process. In particular, the mutations that drive evolution are predicted to be small and modular, incrementally improving a small number of traits. However, adaptive mutations identified early in microbial evolution experiments, cancer, and other systems often provide substantial fitness gains and pleiotropically improve multiple traits at once.

A Pipeline and Recommendations for Population and Individual Diagnostic SNP Selection in Non-Model Species.

Despite substantial reductions in the cost of sequencing over the last decade, genetic panels remain relevant due to their cost-effectiveness and flexibility across a variety of sample types. In particular, single nucleotide polymorphism (SNP) panels are increasingly favoured for conservation applications. SNP panels are often used because of their adaptability, effectiveness with low-quality samples, and cost-efficiency for population monitoring and forensics.

Navigated Osteosynthesis for Unstable Atlas Fractures: Technical Note and Case Series.

Objective: Fractures of the atlas are typically considered stable or unstable based on the integrity of the transverse ligament. Whereas stable Jefferson burst fractures can be treated nonoperatively, unstable fractures with disruption of the transverse ligament often require surgical intervention. Atlas osteosynthesis has been proposed as a motion-preserving alternative to atlantoaxial fusion.

Cancers adapt to their mutational load by buffering protein misfolding stress.

In asexual populations that don't undergo recombination, such as cancer, deleterious mutations are expected to accrue readily due to genome-wide linkage between mutations. Despite this mutational load of often thousands of deleterious mutations, many tumors thrive. How tumors survive the damaging consequences of this mutational load is not well understood.