Results 211 to 220 of about 4,357,163 (359)
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
Development of therapies targeting cancer‐associated fibroblasts (CAFs) necessitates preclinical model systems that faithfully represent CAF–tumor biology. We established an in vitro coculture system of patient‐derived pancreatic CAFs and tumor cell lines and demonstrated its recapitulation of primary CAF–tumor biology with single‐cell transcriptomics ...
Elysia Saputra +10 more
wiley +1 more source
Managing Drug-Drug Interactions Involving the Non-Prescription Opioid Loperamide Through Physiologically Based Pharmacokinetic Modeling. [PDF]
Zhou Z +6 more
europepmc +1 more source
Effect of chemotherapy on passenger mutations in metastatic colorectal cancer
Changes in passenger mutation load and predicted immunotherapy response after chemotherapy treatment. Tumor cells rich with passenger mutations have increased sensitivity to chemotherapy. Correlation of passenger mutations with neoantigen load suggests highly mutated clones promote a more effective response to immunotherapy, and therefore, first‐line ...
Marium T. Siddiqui +6 more
wiley +1 more source
Comparative Risk of Serious Infections Associated With Treatment of Inflammatory Bowel Disease. [PDF]
Khan N +5 more
europepmc +1 more source
Association between the use of proton pump inhibitors and osteoporosis/fracture: nested case-control studies using a national health screening cohort [PDF]
Hyun Youk +7 more
openalex +1 more source
Identification of a New Class of Molecules, the Arachidonyl Amino Acids, and Characterization of One Member That Inhibits Pain [PDF]
Susan M. Huang +12 more
openalex +1 more source
Dual targeting of RET and SRC synergizes in RET fusion‐positive cancer cells
Despite the strong activity of selective RET tyrosine kinase inhibitors (TKIs), resistance of RET fusion‐positive (RET+) lung cancer and thyroid cancer frequently occurs and is mainly driven by RET‐independent bypass mechanisms. Son et al. show that SRC TKIs significantly inhibit PAK and AKT survival signaling and enhance the efficacy of RET TKIs in ...
Juhyeon Son +13 more
wiley +1 more source

