Results 181 to 190 of about 4,406,015 (337)

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

open access: yesMolecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura   +19 more
wiley   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Transition

open access: yesEcology and Society, 2021
Marco A. Janssen   +2 more
doaj   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober   +16 more
wiley   +1 more source

Artificial Intelligence (AI), Operations Research (OR), and Decision Support Systems (DSS): A conceptual framework [PDF]

open access: yes
In recent years there has been increasing interest in applying the computer based problem solving techniques of Artificial Intelligence (AI), Operations Research (OR), and Decision Support Systems (DSS) to analyze extremely complex problems. A conceptual
Parnell, Gregory S.   +2 more
core   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder   +10 more
wiley   +1 more source

Adaptive identification and control of structural dynamics systems using recursive lattice filters [PDF]

open access: yes
A new approach for adaptive identification and control of structural dynamic systems by using least squares lattice filters thar are widely used in the signal processing area is presented.
Montgomery, R. C.   +2 more
core   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

open access: yesMolecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu   +13 more
wiley   +1 more source

Weakening the nuclear envelope: Lamin B receptor in melanoma metastasis

open access: yesMolecular Oncology, EarlyView.
LBR‐driven nuclear fragility supports melanoma invasion. A: Melanocyte presents low LBR (Lamin B Receptor) levels, maintaining nuclear integrity and lamina‐chromatin tethering. B: During malignant progression, upregulation of LBR clusters at the INM (Inner Nuclear Membrane) during confined migration causes local lamina weakening and cholesterol ...
Francesca Lorenzini   +1 more
wiley   +1 more source

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