Results 181 to 190 of about 319,103 (346)

The TET3/GATA6 Axis Drives Lipid Metabolism and Therapeutic Vulnerabilities in Pancreatic Ductal Adenocarcinoma

open access: yesAdvanced Science, EarlyView.
The DNA demethylase TET3 drives lipid metabolic reprogramming in pancreatic ductal adenocarcinoma via a non‐catalytic mechanism. TET3 recruits histone deacetylases to repress GATA6, sustaining lipogenic enzyme expression and ferroptosis resistance.
Shuai Liu   +8 more
wiley   +1 more source

Pharmacokinetics and Tolerance of Nicotinamide Combined with Radiation Therapy in Patients with Glioblastoma Multiforme [PDF]

open access: bronze, 1994
F. Cartei   +6 more
openalex   +1 more source

Bispecific Antibody Targeting VEGF/TGF‐β Synergizes with Local Radiotherapy: Turning Tumors from Cold to Inflamed and Amplifying Abscopal Effects

open access: yesAdvanced Science, EarlyView.
Y332D, a bispecific antibody that simultaneously blockades VEGF and TGF‐β, counteracted negative RT effects that are attributed to the upregulation of TGF‐β and VEGF, as well as further enhanced the immunostimulatory effects of RT, thereby reprograming the TME from immune “cold” to inflamed state and forming an effective in‐situ vaccine that eradicate ...
Lijuan Lyu   +13 more
wiley   +1 more source

Radiation Exposure Induced Blood–Brain Barrier Injury via Mitochondria‐Mediated Sterile Inflammation

open access: yesAdvanced Science, EarlyView.
This work describes a blood–brain barrier (BBB) microphysiological system (MPS) to explore the responses of BBB to radiation exposure. Following radiation exposure, obvious BBB comprise and brain endothelial injuries are detected. Mechanism study shows radiation induced significant sterile inflammation via mitochondrial dysfunction and cGAS‐STING ...
Peng Wang   +6 more
wiley   +1 more source

Activation of expression of genes coding for extracellular matrix proteins in Tat-producing glioblastoma cells. [PDF]

open access: green, 1992
J. Paul Taylor   +6 more
openalex   +1 more source

What is a glioblastoma?

open access: yesNeuro-Oncology, 2023
Andrew B Lassman, Martin J van den Bent
openaire   +3 more sources

Combining PIM‐2 and PARP1 Inhibitors Induces MICA Expression on Multiple Myeloma Cells to Activate NK Cells through NKG2D Binding

open access: yesAdvanced Science, EarlyView.
The findings suggest that the combination of PIM‐2 and PARP1 inhibitors can induce MICA expression on MM cells, thereby activating NK cells through NKG2D binding. This process may restore NK cell function and serve as a potential therapeutic approach for MM patients. Abstract While immunogenic death in tumor cells activates specific anti‐tumor T cells,
Zhaoyun Liu   +6 more
wiley   +1 more source

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