Results 131 to 140 of about 6,047,039 (310)
Annual Report - Marine Biological Laboratory, 1986
Annual report of the Marine Biological Laboratory in Woods Hole. 1986.
Marine Biological Laboratory (Woods Hole MA)
core
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
Annual Report - Marine Biological Laboratory, 1985
Annual report of the Marine Biological Laboratory in Woods Hole. 1985.
Marine Biological Laboratory (Woods Hole MA)
core
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
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
Annual Report - Marine Biological Laboratory, 1890
Annual report of the Marine Biological Laboratory in Woods Hole. 1890.
Marine Biological Laboratory (Woods Hole MA)
core
Pair‐wise comparison of the CellSearch and FETCH enrichment technologies for circulating tumor cells (CTCs) from metastatic breast, prostate, and small cell lung cancer patients shows an increased capture of CTCs using FETCH enrichment. The clinical implementation of circulating tumor cells (CTCs) as a predictive tool for therapy efficacy in the ...
Michiel Stevens +6 more
wiley +1 more source
Annual Report - Marine Biological Laboratory, 1903-1906
https://hdl.handle.net/1912/21944Marine Biological Laboratory.
Marine Biological Laboratory (Woods Hole MA)
core
Treatment of lichen sclerosus and hypertrophic scars with dupilumab
Danielle M. Peterson, MD +2 more
doaj +1 more source
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
Annual Report - Marine Biological Laboratory, 1984
Annual report of the Marine Biological Laboratory in Woods Hole. 1984.
Marine Biological Laboratory (Woods Hole MA)
core

