Results 151 to 160 of about 5,517,215 (329)
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska +13 more
wiley +1 more source
Annual; Began with Oct. 1, 2008.; Description based on: Oct. 1, 2008; tilte from PDF cover (publisher's web site, viewed May 21, 2009).; At head of title: State of Connecticut.; "An Act Concerning Hospital Acquired Infections."; Latest issue consulted ...
Healthcare Associated Infections Program (Conn.)
core
Drug resistance limits treatment success in a subset of lung cancers driven by ROS1 gene alterations. Using patient‐derived cells and computer simulations, we studied three key mutations and how they affect five targeted drugs. The mutations reduced drug effectiveness in different ways by altering protein structure and behavior.
Farhan Ul Haq +8 more
wiley +1 more source
Annual; Began with Oct. 1, 2008.; "An Act Concerning Hospital Acquired Infections."; At head of title: State of Connecticut.; Volume for Oct.
Healthcare Associated Infections Program (Conn.)
core
This study identifies somatostatin receptor 4 (Sstr4) as a critical tumor suppressor against skin and head/neck cancers (HNSCC, cSCC, and BCC). The loss of Sstr4 removes a check on cell growth, causing hyperactivation of the MAPK‐ERK signaling pathway (↑).
Ali Taqvi +6 more
wiley +1 more source
Annual; Began with Oct. 1, 2008.; "An Act Concerning Hospital Acquired Infections."; At head of title: State of Connecticut.; Volume for Oct.
Healthcare Associated Infections Program (Conn.)
core
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou +4 more
wiley +1 more source
Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim +7 more
wiley +1 more source
Study Design. A retrospective study of a consecutive series of all patients with pyogenic spinal infections treated at a single institution over a 10-year period.Objective.
Gana, Natalia +11 more
core +1 more source

