Meixia Bi

TL;DR: It is demonstrated that cells cultured under hypoxic/anoxic conditions and transformed cells in hypoxic areas of tumors activate a translational control program known as the integrated stress response (ISR), which adapts cells to endoplasmic reticulum (ER) stress and suggests that this pathway is an attractive target for antitumor modalities.

TL;DR: It is shown that a subset of transcripts are preferentially translated during hypoxia, including activating transcription factor 4 (ATF4), an important mediator of the unfolded protein response, and an important integrated response between ER signaling and the cellular adaptation to hypoxic stress.

TL;DR: A role for UPR is established as an enhancer of c-Myc-induced transformation and suggest that UPR inhibition may be particularly effective against malignancies characterized by c- myc overexpression.

TL;DR: Hockel and Vaupel as discussed by the authors delineated the mechanisms by which hypoxia affects tumor physiology at both cellular and molecular levels for better understanding of tumor development and metastasis and designing better antitumor modalities.

TL;DR: It is demonstrated that treatment of tumor cells with small molecule inhibitors that target two different domains in FAS, orlistat and cerulenin, triggers activation of all three arms of the endoplasmic reticulum (ER) stress response, supporting the idea that ER stress is an upstream event in the cell death cascade.