BRD4 has a pro-tumorigenic role but non-cell-autonomous mechanisms of BRD4 activation need to be elucidated. Here the authors unravel a mechanism by which CAFs activate BRD4 and induce resistance to BET inhibitors in cancer cells through IL6/IL8 signaling.

Our study demonstrates that tertiary lymphoid structures (TLS) can form in human glioma, and that agonistic CD40 therapy (αCD40) promotes the formation of TLS in murine glioma models. However, αCD40 also impairs T cell function through the induction of regulatory B cells in the tumor.

We are seeking two cancer research experts to join our cancer team; one role is for a permanent team member, the second role is for a locum - or a temporary position.

Fan Yang, & Yi Fan Department of Radiation Oncology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA 19104

Glioblastomas (GBM) are frequently resistant to immunotherapy. We showed that targeting regulatory T cells (Tregs) with an agonistic anti-GITR antibody reprograms tumor-infiltrating Tregs to effector cells, overcoming response to PD1 blockade in preclinical models of GBM.

The presence of drug efflux pumps that prevent drug accumulation in chemoresistant cancer cells is a cause of cancer treatment failure. We show that these drug pumps need mitochondrial ATP as fuel and that blocking mitochondrial ATP production with novel MCJ mimetics overcomes cancer chemoresistance