Attenuating candidate live virus vaccines by incorporating unfavoured codon pairs to reduce translation efficiency is actually mediated though changes in frequencies of CpG and UpA dinucleotides, which make viruses more visible to the innate immune system.
The functional relevance of stem cell niche perturbation in sarcomagenesis is defined and the mouse model presented provides a rationale for the use of combination therapy for the treatment of genetically heterogeneous sarcomas.
Genetic and biochemical approaches identify a new component of the cellular signaling machinery driving migration of limb muscle precursor cells during mouse embryogenesis and reveal the underlying molecular mechanism.
The IGF2 mRNA binding protein-2/IMP2, overexpressed in many common cancers, drives cancer cell proliferation by increasing the abundance of IGF2 and the oncogene HMGA1, which controls a network of effectors that enhance IGF2 action.
RNA virus replication is attenuated by an intrinsic restriction mechanism after introducing CpG/UpA dinucleotides into both non-translated and coding regions of viral genomes, which may be exploited in the design of attenuated virus vaccines.
The basic helix-loop-helix transcription factor, HES3, acts downstream of the PAX3-FOXO1 fusion oncogene to impair muscle differentiation and promote tumorigenesis in rhabdomyosarcoma, a childhood muscle cancer.