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Researchers Nick Haining and Jernej Godec of Dana-Farber Cancer Institute, Harvard Medical School, and ӳý collaborated with ӳý and UC San Francisco computational biologists to build a collection of gene signatures from different immune cell types and perturbations. The collection, called , includes almost 5,000 new gene sets and has been added to . The additions are expected to greatly improve the use of Gene Set Enrichment Analysis for immunological studies; in a paper published by the journal , the team uses the collection to identify species-specific and shared aspects of the biology of the immune response to sepsis between mice and humans.

ӳý Genomic Services has partnered with Takeda Pharmaceutical Company Limited to perform genomic analysis on patient samples from a Phase 3 clinical trial of NINLARO® (ixazomib), an oral proteasome inhibitor that was recently approved by the U.S. Food and Drug Administration (FDA), indicated in combination with lenalidomide and dexamethasone, for the treatment of patients with multiple myeloma who have received at least one prior therapy.

Every day, every cell in the body picks up one or two genetic mutations. Luckily, cells have a whole battery of strategies for fixing these errors. But most of the time, even if a mutation doesn’t get fixed — or doesn’t get fixed properly — there are no obvious functional implications. That is, the mutation isn't known to impair the function of the cell. Some mutations, however — called “driver” mutations — do impair the cell, leading to cancer, aging, or other types of diseases.

Prion disease is the common name for a family of rare, progressive neurodegenerative disorders that can be caused by mutations in the prion protein gene (PRNP). These mutations produce misshapen proteins, which accumulate, destroying neurons and leaving the brain with sponge-like holes resulting in dementia, and ultimately death.