Results 151 to 160 of about 3,841,010 (347)
Molecular Oncology, EarlyView.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
Errata: Spin Density Matrices for Paramagnetic Molecules [PDF]
, 1959 Harden M. McConnell
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Molecular Oncology, EarlyView.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
Simple Equation for Estimating the Dipole Moment of a Molecule from Solution Data [PDF]
, 1959 Satish C. Srivastava, P. Charandas
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Molecular Oncology, EarlyView.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
The Quantization of the Rotational Motion of the Polyatomic Molecule by the New Wave Mechanics
, 1927 Enós E. Witmer
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The Magnetization of Iron, Nickel, and Cobalt by Rotation and Nature of the Magnetic Molecule [PDF]
, 1917 S. J. Barnett
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Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours?
Molecular Oncology, EarlyView.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
Molecular Oncology, EarlyView.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