Results 81 to 90 of about 1,757,011 (294)

Chemoresistome mapping in individual breast cancer patients unravels diversity in dynamic transcriptional adaptation

open access: yesMolecular 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

Tonic signaling of the B‐cell antigen‐specific receptor is a common functional hallmark in chronic lymphocytic leukemia cell phosphoproteomes at early disease stages

open access: yesMolecular 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

Expression and DNA methylation of 20S proteasome subunits as prognostic and resistance markers in cancer

open access: yesMolecular Oncology, EarlyView.
Comprehensive analysis of genomic mutations, gene expression, DNA methylation, and pathway analysis of TCGA data was carried out to define cancer types in which proteasome subunits expression is associated with worse survival. Albeit the effect of specific proteasome subunits on cellular function, the main role of the proteasome is better evaluated ...
Ruba Al‐Abdulla   +5 more
wiley   +1 more source

Early metastasis is characterized by Gr1+ cell dysregulation and is inhibited by immunomodulatory nanoparticles

open access: yesMolecular Oncology, EarlyView.
Breast cancer metastasis is associated with myeloid cell dysregulation and the lung‐specific accumulation of tumor‐supportive Gr1+ cells. Gr1+ cells support metastasis, in part, through a CHI3L1‐mediated mechanism, which can be targeted and inhibited with cargo‐free, polymeric nanoparticles.
Jeffrey A. Ma   +9 more
wiley   +1 more source

Riccati equations as a scale-relativistic gateway to quantum mechanics

open access: yes, 2019
Applying the resolution-scale relativity principle to develop a mechanics of non-differentiable dynamical paths, we find that, in one dimension, stationary motion corresponds to an Ito process driven by the solutions of a Riccati equation. We verify that
Al-Rashid, Saeed Naif Turki   +2 more
core  

MicroRNA 196a contributes to the aggressiveness of esophageal adenocarcinoma through the MYC/TERT/NFκB axis

open access: yesMolecular Oncology, EarlyView.
mir‐196a promotes Esophagus Adenocarcinoma aggressiveness. On one hand, mir‐196a targets the valosin‐containing protein (VCP) mRNA, causing the accumulation of c‐MYC protein that leads to high amounts of TERT. On the other hand, mir‐196a targets the inhibitor of NFκB (NFKBIA).
Jesús García‐Castillo   +8 more
wiley   +1 more source

Algorithms for computing the multivariable stability margin [PDF]

open access: yes
Stability margin for multiloop flight control systems has become a critical issue, especially in highly maneuverable aircraft designs where there are inherent strong cross-couplings between the various feedback control loops.
Chiang, Richard Y.   +2 more
core   +1 more source

The subcellular distribution of phosphorylated Y‐box‐binding protein‐1 at S102 in colorectal cancer patients, stratified by KRAS mutational status and clinicopathological features

open access: yesMolecular Oncology, EarlyView.
This study identifies nuclear YB‐1 S102 phosphorylation as a marker associated with KRAS and FBXW7 mutations in colorectal cancer. Mutated KRAS correlates specifically with nuclear, not cytoplasmic, S102 YB‐1. These findings provide the first ex vivo evidence of this link in CRC and suggest future studies should assess the prognostic and therapeutic ...
Konstanze Lettau   +9 more
wiley   +1 more source

Simultaneous inhibition of TRIM24 and TRIM28 sensitises prostate cancer cells to antiandrogen therapy, decreasing VEGF signalling and angiogenesis

open access: yesMolecular Oncology, EarlyView.
TRIM24 and TRIM28 are androgen receptor (AR) coregulators which exhibit increased expression with cancer progression. Both TRIM24 and TRIM28 combine to influence the response of castrate‐resistant prostate cancer (CRPC) cells to AR inhibitors by mediating AR signalling, regulation of MYC and upregulating VEGF to promote angiogenesis. Castrate‐resistant
Damien A. Leach   +8 more
wiley   +1 more source

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