Results 241 to 250 of about 2,542,719 (338)
Alectinib resistance in ALK+ NSCLC depends on treatment sequence and EML4‐ALK variants. Variant 1 exhibited off‐target resistance after first‐line treatment, while variant 3 and later lines favored on‐target mutations. Early resistance involved off‐target alterations, like MET and NF2, while on‐target mutations emerged with prolonged therapy.
Jie Hu+11 more
wiley +1 more source
METHODS OF HANDLING INJURIES ON TRANSPORTATION SYSTEMS AND WOUND TREATMENT
KENNETH A. J. MACKENZIE
openalex +2 more sources
Practical Coal Production Mine Transportation and Market Preparation: Mine Transportation, Hoisting and Hoisting Equipment, Coal Preparation [PDF]
openalex +1 more source
This study used longitudinal transcriptomics and gene‐pattern classification to uncover patient‐specific mechanisms of chemotherapy resistance in breast cancer. Findings reveal preexisting drug‐tolerant states in primary tumors and diverse gene rewiring patterns across patients, converging on a few dysregulated functional modules. Despite receiving the
Maya Dadiani+14 more
wiley +1 more source
B‐cell chronic lymphocytic leukemia (B‐CLL) and monoclonal B‐cell lymphocytosis (MBL) show altered proteomes and phosphoproteomes, analyzed using mass spectrometry, protein microarrays, and western blotting. Identifying 2970 proteins and 316 phosphoproteins, including 55 novel phosphopeptides, we reveal BCR and NF‐kβ/STAT3 signaling in disease ...
Paula Díez+17 more
wiley +1 more source
Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours?
Current anticancer therapies are limited by the occurrence of resistance and undruggability of most proteins. Targeted protein degraders are novel, promising agents that trigger the selective degradation of previously undruggable proteins through the recruitment of the ubiquitin–proteasome machinery. Their mechanism of action raises exciting challenges,
Noé Herbel, Sophie Postel‐Vinay
wiley +1 more source
Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen+12 more
wiley +1 more source