Dead Cells: Return to Castlevania is coming to Xbox in March. Dracula better watch his back...
Grab your stakes, because you'll be able to hunt Death and Dracula on March 6th, when the Return to Castlevania DLC launches on Xbox Series X|S and Xbox One forDead Cells: Return to Castlevania gameplay trailer. Still, Motion Twin has decided to treat us nonetheless, with crossover DLC with the timeless Castlevania series. In Dead Cells: Return to Castlevania, The Beheaded will take on vampires, skeletons, werewolves, and more as they attempt to stop Dracula and Death and save humanity.
If that's not enough Dead Cells news for you, how about a new game to play during games night? Dead Cells: The Rogue-Lite Board Game is heading to this spring, promising a cooperative roguelite Metoidvania-inspired experience. The game will feature an 'ever-changing' island, just like the game, so expect to be challenged at every turn.More Dead Cells stories:
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Dual mTORC1/2 inhibition synergistically enhances AML cell death in combination with the BCL2 antagonist venetoclaxAbstract. Purpose: Acute myeloid leukemia (AML) is an aggressive disease with a poor outcome. We investigated mechanisms by which the anti-AML activity of ABT-199 (venetoclax) could be potentiated by dual mTORC1/TORC2 inhibition. Methods: Venetoclax/INK128 synergism was assessed in various AML cell lines and primary patient AML samples in vitro. AML cells over-expressing MCL-1, constitutively active AKT, BAK and/or BAX knock-out, and acquired venetoclax resistance were investigated to define mechanisms underlying interactions. The antileukemic efficacy of this regimen was also examined in xenograft and patient-derived xenograft (PDX) models. Results: Combination treatment with venetoclax and INK128 (but not the mTORC1 inhibitor Rapamycin) dramatically enhanced cell death in AML cell lines. Synergism was associated with p-AKT and p-4EBP1 down-regulation and dependent upon MCL-1 downregulation and BAK/BAX up-regulation as MCL-1 overexpression and BAX/BAK knock out abrogated cell death. Constitutive AKT activation opposed synergism between venetoclax and PI3K or AKT inhibitors, but not INK128. Combination treatment also synergistically induced cell death in venetoclax- resistant AML cells. Similar events occurred in primary patient-derived leukemia samples but not normal CD34+ cells. Finally, venetoclax and INK128 co-treatment displayed increased anti-leukemia effects in in vivo xenograft and PDX models. Conclusions: The venetoclax/INK128 regimen exerts significant anti-leukemic activity in various preclinical models through mechanisms involving MCL-1 down-regulation and BAK/BAX activation, and offers potential advantages over PI3K or AKT inhibitors in cells with constitutive AKT activation. This regimen is active against primary and venetoclax resistant AML cells, and in in vivoAML models. Further investigation of this strategy appears warranted.
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Queen Elizabeth Prize: Solar team wins prestigious engineering awardFour pioneers behind silicon solar cells win this year's Queen Elizabeth Prize for Engineering.
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