Results 211 to 220 of about 14,999,742 (341)
A subset of MMR‐proficient colon cancers responds to neoadjuvant immunotherapy
Tan et al. reveal that a distinct subset of early‐stage pMMR colon cancers can respond to neoadjuvant immunotherapy. In the NICHE‐2 trial, responders (26%) were characterized by chromosomal instability, TP53 mutations, and proliferative cell‐cycle programs, whereas nonresponders showed metabolic and stromal reprogramming with TGF‐β‐driven ...
Eleonora Piumatti +3 more
wiley +1 more source
Pleiotropy and the evolutionary stability of plastic phenotypes: a geometric framework. [PDF]
Wang CQ, DuBose JG.
europepmc +1 more source
The cancer problem is increasing globally with projections up to the year 2050 showing unfavourable outcomes in terms of incidence and cancer‐related deaths. The main challenges are prevention, improved therapeutics resulting in increased cure rates and enhanced health‐related quality of life.
Ulrik Ringborg +43 more
wiley +1 more source
Tissue-specific mutagenesis from endogenous guanine damage is suppressed by Polκ and DNA repair. [PDF]
Jiang Y +18 more
europepmc +1 more source
Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
Nicolas Gordon +13 more
wiley +1 more source
Tumors with mutations in chromatin regulators are associated with higher mutational burden and improved response to checkpoint immunotherapy. [PDF]
Gjorgjievska M +6 more
europepmc +1 more source
Plecstatin inhibits hepatocellular carcinoma tumorigenesis and invasion through cytolinker plectin
The ruthenium‐based metallodrug plecstatin exerts its anticancer effect in hepatocellular carcinoma (HCC) primarily through selective targeting of plectin. By disrupting plectin‐mediated cytoskeletal organization, plecstatin inhibits anchorage‐dependent growth, cell polarization, and tumor cell dissemination.
Zuzana Outla +10 more
wiley +1 more source
Intrapatient variation in PD-L1 expression and tumor mutational burden and implications for outcomes to immune checkpoint inhibitor therapy in patients with non-small-cell lung cancer. [PDF]
Li G +7 more
europepmc +1 more source
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala +15 more
wiley +1 more source

