Results 91 to 100 of about 278,077 (263)

Transcriptional network analysis of PTEN‐protein‐deficient prostate tumors reveals robust stromal reprogramming and signs of senescent paracrine communication

open access: yesMolecular Oncology, EarlyView.
Combining PTEN protein assessment and transcriptomic profiling of prostate tumors, we uncovered a network enriched in senescence and extracellular matrix (ECM) programs associated with PTEN loss and conserved in a mouse model. We show that PTEN‐deficient cells trigger paracrine remodeling of the surrounding stroma and this information could help ...
Ivana Rondon‐Lorefice   +16 more
wiley   +1 more source

Mars Additive Difference [of the Equation of Anomaly] - Ptolemy's Almagest by Toomer (Gerald J.) (1984) | Type-B (ID n° 367)

open access: yes, 2021
This is a type B edition: A type-B edition corresponds to a critical edition of several table witnesses: it is based on several different editions, themselves based on tables from different primary sources. A type-B edition can be based on type-A, type-B or type-C editions.
openaire   +2 more sources

Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells

open access: yesMolecular Oncology, EarlyView.
We show that dabrafenib‐resistant melanoma cells undergo mitochondrial remodeling, leading to elevated respiration and ROS production balanced by stronger antioxidant defenses. This altered redox state promotes survival despite mitochondrial damage but renders resistant cells highly vulnerable to ROS‐inducing compounds such as PEITC, highlighting redox
Silvia Eller   +17 more
wiley   +1 more source

Cell surface interactome analysis identifies TSPAN4 as a negative regulator of PD‐L1 in melanoma

open access: yesMolecular Oncology, EarlyView.
Using cell surface proximity biotinylation, we identified tetraspanin TSPAN4 within the PD‐L1 interactome of melanoma cells. TSPAN4 negatively regulates PD‐L1 expression and lateral mobility by limiting its interaction with CMTM6 and promoting PD‐L1 degradation.
Guus A. Franken   +7 more
wiley   +1 more source

New Formulas of Feedback Capacity for AGN Channels with Memory: A Time-Domain Sufficient Statistic Approach

open access: yesEntropy
Recently, several papers identified technical issues related to equivalent time-domain and frequency-domain “characterization of the n–block or transmission” feedback capacity formula and its asymptotic limit, the feedback capacity, of additive Gaussian ...
Charalambos D. Charalambous   +2 more
doaj   +1 more source

PARP inhibition and pharmacological ascorbate demonstrate synergy in castration‐resistant prostate cancer

open access: yesMolecular Oncology, EarlyView.
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

LDAcoop: Integrating non‐linear population dynamics into the analysis of clonogenic growth in vitro

open access: yesMolecular Oncology, EarlyView.
Limiting dilution assays (LDAs) quantify clonogenic growth by seeding serial dilutions of cells and scoring wells for colony formation. The fraction of negative wells is plotted against cells seeded and analyzed using the non‐linear modeling of LDAcoop.
Nikko Brix   +13 more
wiley   +1 more source

Infrared laser sampling of low volumes combined with shotgun lipidomics reveals lipid markers in palatine tonsil carcinoma

open access: yesMolecular Oncology, EarlyView.
Nanosecond infrared laser (NIRL) low‐volume sampling combined with shotgun lipidomics uncovers distinct lipidome alterations in oropharyngeal squamous cell carcinoma (OPSCC) of the palatine tonsil. Several lipid species consistently differentiate tumor from healthy tissue, highlighting their potential as diagnostic markers.
Leonard Kerkhoff   +11 more
wiley   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

open access: yesMolecular Oncology, EarlyView.
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

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