Results 321 to 330 of about 2,599,480 (386)

Clotting and other plasma factors in septicemia [PDF]

open access: yes, 1980
Fritz, Hans   +4 more
core  

Okanin Suppresses the Growth of Colorectal Cancer Cells by Targeting at Peroxiredoxin 5

open access: yesAdvanced Science, EarlyView.
Okanin suppresses colorectal cancer growth by directly targeting PRDX5. This natural compound selectively binds peroxiredoxin 5 (PRDX5), inhibiting its activity and inducing WSB1‐mediated degradation. PRDX5 loss elevates ROS, suppresses GPX4 via SIAH2, and further triggers cell death (apoptosis and ferroptosis).
Ji Zhong Zhao   +9 more
wiley   +1 more source

A Comprehensive Review About the Use of Monoclonal Antibodies in Cancer Therapy. [PDF]

open access: yesAntibodies (Basel)
Justiz-Vaillant A   +4 more
europepmc   +1 more source

HERV‐K TM Subunit Elicits CD8+ T Cell Anergy and Tumor Immune Evasion via Targeting CD3 Coreceptor ε in AML and PDAC

open access: yesAdvanced Science, EarlyView.
Novel viral immune checkpoint K‐TM subunit is aberrantly expressed in CD8+ T cells and enriched in sera of cancer patients, inducing CD8+ T cell anergy and eliciting potent tumor immune escape in mouse model. Mechanistically, K‐TM directly targets and induces the phosphorylation of CD3ε receptor.
Mengyuan Li   +13 more
wiley   +1 more source

Lifespan‐Regulated CAR‐Macrophages from Myeloid Progenitors for Enhanced Colorectal Cancer Therapy

open access: yesAdvanced Science, EarlyView.
Using a tamoxifen‐inducible Hoxb8 system, proliferative bone marrow progenitors can be generated, which are subsequently engineered with an anti‐CEA CAR construct containing a suicide gene (iCas9) and differentiated into CAR‐macrophages. This method facilitates scale up the production of CAR‐macrophages.
Chuancheng Gao   +8 more
wiley   +1 more source

Targeting Intratumoral Copper Inhibits Tumor Progression via p62‐Mediated EZH2 Degradation and Potentiates Anti‐PD‐1 Immunotherapy in Oral Squamous Cell Carcinoma

open access: yesAdvanced Science, EarlyView.
The authors find that by targeting intratumoral copper, they can enhance p62‐mediated ubiquitination of EZH2 at the Ub‐K63 site by suppressing copper binding to SMURF2, an E3 ligase of EZH2, leading to its autophagic degradation. This mechanism suppressed OSCC progression and potentiated anti‐PD‐1 immunotherapy, highlighting a potential new therapeutic
Xiaohu Lin   +9 more
wiley   +1 more source

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