Results 201 to 210 of about 250,617 (285)

DMAP1 Deficiency Suppresses Lung Cancer Progression by Destabilizing Replication Fork and Activating IFN Signaling‐Mediated Anti‐tumor Immunity

open access: yesAdvanced Science, EarlyView.
Lung cancer remains the leading cause of cancer‐related death. We investigated the role of the epigenetic regulator DMAP1 in NSCLC and found that its loss induces replication stress and DNA damage. This in turn activates type I IFN signaling via the cGAS–STING pathway and transcriptional ISG de‐repression, enhancing anti‐tumor immune responses ...
Kan Huang   +10 more
wiley   +1 more source

Bibliometric analysis of ovarian cancer immune evasion research from 2015 to 2024. [PDF]

open access: yesFront Oncol
Wang X   +7 more
europepmc   +1 more source

Delivery of Pleckstrin‐Homology Domains Suppresses PI3K/Akt Signaling and Breast Cancer Metastasis

open access: yesAdvanced Science, EarlyView.
Current therapies curb tumor growth but not metastasis. Obscurin, a giant metastasis suppressor lost in breast cancer, restrains PI3K/Akt signaling but is impractical to restore. We deploy a mini‐obscurin, comprising the obscurin‐PH‐domain, which sequesters PI3K‐p85, potently suppressing invasion and metastasis.
Matthew Eason   +12 more
wiley   +1 more source

The AUTACE That Degrades KRAS and Engages CD8+ T Cells for the Treatment of KRAS/TP53 Co‐Mutant Tumors

open access: yesAdvanced Science, EarlyView.
AUTACE is a bifunctional nanoplatform that integrates tumor targeting, immune engagement, and on‐demand KRAS degradation. It targets KRAS/TP53 co‐mutant tumors via TP53‐specific TCRs, elicits antitumor CD8+ T‐cell responses through surface anti‐CD3 antibodies, and uses low‐intensity focused ultrasound (LIFU) to trigger controlled release of the KRAS ...
Luo Li   +6 more
wiley   +1 more source

Influence of USP15 and its derived-peptide on non-small cell lung cancer immune evasion via regulating PD-L1 stability. [PDF]

open access: yesJ Immunother Cancer
Wu D   +13 more
europepmc   +1 more source

Decoding IGLL5 Mutation‐Mediated BCR Signaling: A Novel Mechanism of CD8+ T Cell Exhaustion and Ocular MALT Lymphoma Progression

open access: yesAdvanced Science, EarlyView.
OAML harbors recurrent IGLL5 mutations that reinforce CD79A/CD79B‐associated BCR signaling. Mechanistic analysis of the S47G and A54G variants reveals induction of CXCL10/CXCL11, enhanced CD8+ T‐cell recruitment, and exhaustion‐associated dysfunction, supporting an immune‐tolerant niche.
Andi Zhao   +12 more
wiley   +1 more source

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