Integration of tumor inflammation, cell proliferation, and traditional biomarkers improves prediction of immunotherapy resistance and response.

Background: Contemporary to the rapidly evolving landscape of cancer immunotherapy is the equally changing understanding of immune tumor microenvironments (TMEs) which is crucial to the success of these therapies. Their reliance on a robust host immune response necessitates clinical grade measurements of immune TMEs at diagnosis. In this study, we describe a stable tumor immunogenic profile describing immune TMEs in multiple tumor types with ability to predict clinical benefit from immune checkpoint inhibitors (ICIs).

Genome enablement of the notothenioidei: genome size estimates from 11 species and BAC libraries from 2 representative taxa.

The perciform suborder Notothenoidei provides a compelling opportunity to study the adaptive radiation of a marine species flock in the cold Southern Ocean surrounding Antarctica. To enable genome-level studies of these psychrophilic fishes, we estimated the sizes of the genomes of 11 Antarctic species and generated high-quality BAC libraries for 2, the notothen Notothenia coriiceps and the icefish Chaenocephalus aceratus. Our results indicate that evolution of phylogenetically derived notothenioid families, [e.

Complete HOX cluster characterization of the coelacanth provides further evidence for slow evolution of its genome.

The living coelacanth is a lobe-finned fish that represents an early evolutionary departure from the lineage that led to land vertebrates, and is of extreme interest scientifically. It has changed very little in appearance from fossilized coelacanths of the Cretaceous (150 to 65 million years ago), and is often referred to as a "living fossil." An important general question is whether long-term stasis in morphological evolution is associated with stasis in genome evolution.

Prevention of peripheral tolerance by a dendritic cell growth factor: flt3 ligand as an adjuvant.

Injections of soluble proteins are poorly immunogenic, and often elicit antigen-specific tolerance. The mechanism of this phenomenon has been an enduring puzzle, but it has been speculated that tolerance induction may be due to antigen presentation by poorly stimulatory, resting B cells, which lack specific immunoglobulin receptors for the protein. In contrast, adjuvants, or infectious agents, which cause the release of proinflammatory cytokines such as tumor necrosis factor alpha and interleukin 1beta in vivo are believed to recruit and activate professional antigen-presenting cells to the site(s) of infection, thereby eliciting immunity.