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Inequalities are prevalent across the spectrum of cancer research and patient care, with destructive repercussions for people and society. We cannot ignore them and must act against the social injustices that perpetuate them.
KEAP1 is a tumor suppressor encoded by a gene commonly mutated in lung cancer. A systematic search for Keap1-mutant cancer vulnerabilities now reveals that Slc33a1 is a context-specific essential gene that represents a promising new anti-cancer target.
The pre-metastatic niche is a complex microenvironment formed by the influence of tumor-derived factors on stromal and immune cells at distant sites of disseminated tumor-cell colonization. Signaling through the kinase p38α and regulation of the type I interferon receptor are now linked to formation of the pre-metastatic niche.
Gui et al. report that tumor-cell-derived factors induce p38a activation in lung fibroblasts, leading to inactivation of type I interferon signaling, matrix remodeling and neutrophil infiltration, thereby generating a metastasis-permissive niche.
Van Loo and colleagues report that loss of the Zeb2 regulator of epithelial-to-mesenchymal transition from the intestinal epithelium leads to inflammation, increased intestinal permeability and colorectal cancer development, which is enhanced by the resident intestinal microbiome.
Alkallas et al. uncover new significantly mutated genes in a large cohort of cutaneous melanoma, including the RNA helicase DDX3X, through integrated analysis of genomic, transcriptomic and DNA methylation data.