Harun M. Said

TL;DR: Gen transfer of Smad7 inhibits experimental fibrogenesis in vivo and suggests that the underlying mechanisms involve inhibition of TGF-beta signaling and HSC transdifferentiation.

TL;DR: In conclusion, Id1 is identified as TGF‐β/ALK1/Smad1 target gene in HSCs and represents a critical mediator of transdifferentiation that might be involved in hepatic fibrogenesis.

TL;DR: YB-1 is the main target of interferon-γ signaling via Jak1 that exerts antifibrotic action by both interference with TGF-β signaling and direct down-regulation of collagen expression.

TL;DR: Classic approaches to normalize tumor oxygenation involve the breathing of modified gas mixtures and pharmacologic modification of blood flow as in the "accelerated radiotherapy, carbogen, nicotinamide" (ARCON) scheme and direct targeting of hypoxia-related molecules such as hypoxIA-inducible factor-1alpha, the central regulator of the hypoxic response in tumor cells, is an attractive approach currently tested in preclinical models.

TL;DR: Among a panel of known Hypoxia-inducible genes, OPN and CA9 emerge as most consistently induced by in vitro hypoxia in human GBM cell lines and most specifically expressed in patient GBM tumor tissue, rendering these two genes attractive targets for hypoxIA-directed treatment approaches.