Results 191 to 200 of about 1,939,761 (391)

Intein‐based modular chimeric antigen receptor platform for specific CD19/CD20 co‐targeting

open access: yesMolecular Oncology, EarlyView.
CARtein is a modular CAR platform that uses split inteins to splice antigen‐recognition modules onto a universal signaling backbone, enabling precise, scarless assembly without re‐engineering signaling domains. Deployed here against CD19 and CD20 in B‐cell malignancies, the design supports flexible multi‐antigen targeting to boost T‐cell activation and
Pablo Gonzalez‐Garcia   +9 more
wiley   +1 more source

EFFECTS OF THE DIRECTION JUDGMENT OF THE USER BASED ON THE ARROW OF SIGN AT THE STATION

open access: diamond, 2019
Yusuke Nishijima   +4 more
openalex   +2 more sources

Improving PARP inhibitor efficacy in bladder cancer without genetic BRCAness by combination with PLX51107

open access: yesMolecular Oncology, EarlyView.
Clinical trials on PARP inhibitors in urothelial carcinoma (UC) showed limited efficacy and a lack of predictive biomarkers. We propose SLFN5, SLFN11, and OAS1 as UC‐specific response predictors. We suggest Talazoparib as the better PARP inhibitor for UC than Olaparib.
Jutta Schmitz   +15 more
wiley   +1 more source

Cytoplasmic p21 promotes stemness of colon cancer cells via activation of the NFκB pathway

open access: yesMolecular Oncology, EarlyView.
Cytoplasmic p21 promotes colorectal cancer stem cell (CSC) features by destabilizing the NFκB–IκB complex, activating NFκB signaling, and upregulating BCL‐xL and COX2. In contrast to nuclear p21, cytoplasmic p21 enhances spheroid formation and stemness transcription factor CD133.
Arnatchai Maiuthed   +10 more
wiley   +1 more source

Anterior lumbar hernia in a neonate. [PDF]

open access: yesBMJ Case Rep
Schmitt MK, Starks KM, Escobar MA.
europepmc   +1 more source

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

open access: yesMolecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto   +13 more
wiley   +1 more source

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