Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Epigenetic modifications such as histone acetylation play a central role in the transcriptional regulation of many oncogenic drivers. Accumulating evidence suggests that pharmacological modulation of certain key epigenetic reader proteins such as BRD2/3/4 may serve as an attractive strategy for treatment of many cancers, including tamoxifen-resistant breast cancer.
Last decade has seen quick developments in the understanding of a new type of T lymphocytes, Th17 cells. This information is benefiting the understanding and treatment of a variety of inflammatory diseases, as suggested by a recent paper in Immunity.
Triple negative breast cancers (TNBC) are clinically heterogeneous but mostly aggressive malignancies devoid of expression of the estrogen, progesterone and HER2 (ERBB2 or NEU) receptors. Recent evidence shows that basal endoplasmic reticulum stress (ERS) is typically activated in TNBC and cooperates with hypoxia signaling to promote tumor progression and relapse; ERS and hypoxia response may therefore be among the long-searched hallmarks of TNBC.
Slow-cycling BRAFV600E melanoma cells are notoriously resistant to standard chemotherapy or targeted therapy but the underlying mechanism remains elusive. Now a new study unlocks this mystery and offers novel insights into developing more effective therapeutic interventions.
Balancing inflammatory reactive oxygen species (ROS) production is essential for safely eliminating pathogenic microbes. The newly described protein Negative Regulator of ROS (NRROS) dampens ROS production by restricting NOX2 availability, and thus “cools-off” inflammation.
In a recent Cell paper, Kitambi and colleagues identify a small molecule (Vacquinol-1) that has beneficial effects on a glioblastoma multiforme mouse model by oral administration. In glioblastoma cells, Vacquinol-1 targets macropinocytosis, a cellular process that will not lead to cell death in normal cells.
