Lifespan‐Regulated CAR‐Macrophages from Myeloid Progenitors for Enhanced Colorectal Cancer Therapy
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
Anti-tumor necrosis factor-alpha inhibitor-induced linear psoriasis: A case report. [PDF]
MacIntyre OC, Purdy K.
europepmc +1 more source
Treatment of ankylosing spondylitis by inhibition of tumor necrosis factor alpha.
Jennifer D. Gorman+2 more
semanticscholar +1 more source
Genome‐wide CRISPR/Cas9 based screening identified RELA as a key tumor suppressor in TP53R249S‐mutant HCC. Its loss promotes tumorigenesis and metastasis via DVL1‐mediated Wnt/β‐catenin activation, while its agonist betulinic acid suppresses tumor progression.
Zhiping Wu+17 more
wiley +1 more source
Correction: Recent Clinical Studies on the Effects of Tumor Necrosis Factor-Alpha (TNF-α) and Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) Antibody Therapies in Refractory Cutaneous Sarcoidosis: A Systematic Review. [PDF]
Toriola SL+9 more
europepmc +1 more source
P. Hart+5 more
semanticscholar +1 more source
Ultrathin Multi‐Doped Molybdenum Oxide Nanodots as a Tunable Selective Biocatalyst
This paper presents an advanced multi‐doped molybdenum oxide nanodots with tunable ammonium and proton doping, exhibiting strong ROS generation. The material demonstrates ultrafast and complete dye degradation and unique selective toxicity toward cancer cells, highlighting its promising potential for cancer therapy applications.
Bao Yue Zhang+19 more
wiley +1 more source
Resveratrol Mitigates Inflammation by Modulating Tumor Necrosis Factor-Alpha Receptors (TNFRs) in a 2,4,6-Trinitrobenzene Sulfonic Acid (TNBS)-Induced Rat Model of Colitis. [PDF]
Veszelka M+10 more
europepmc +1 more source
USP13 deficiency in intestinal epithelial cells aggravates DSS‐induced colitis by enhancing ER stress and apoptosis. USP13 interacts with GRP78 and reduces its K63‐linked ubiquitination to alleviate epithelial injury. Restoring USP13 expression or targeting the USP13‐GRP78 axis may represent a promising strategy for treating inflammatory bowel disease ...
Chenchen Qian+9 more
wiley +1 more source