Results 161 to 170 of about 1,861,365 (381)
Cellular senescence and senolytics: the path to the clinic
Selim Chaib, T. Tchkonia, J. Kirkland
semanticscholar +1 more source
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
Cellular Senescence: A Pathogenic Driver for Pulmonary Fibrosis
Pulmonary fibrosis is a life-threatening progressive lung disease characterized by increased fibrogenesis and decreased lung function. Pulmonary fibrosis has a poor prognosis and a low patient survival rate, with no effective treatments currently ...
Sihan Wang+8 more
doaj +1 more source
Cloning and expression of SAG: A novel marker of cellular senescence [PDF]
Cheryl Wistrom, Bryant Villeponteau
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
Cellular senescence in ageing: from mechanisms to therapeutic opportunities
R. Di Micco+3 more
semanticscholar +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
Background Cellular senescence is one of the key steps in the progression of pulmonary fibrosis, and the senescence of type II alveolar epithelial cells (AEC IIs) may potentially accelerate the progression of pulmonary fibrosis.
Junhui Ba+9 more
doaj +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
Senescent cells accumulate in most tissues with organismal aging, exposure to stressors, or disease progression. It is challenging to identify senescent cells because cellular senescence signatures and phenotypes vary widely across distinct cell types ...
Mark A. Sanborn+4 more
doaj +1 more source