Results 141 to 150 of about 22,430,852 (308)

Chiral separation of chloroalkanes with the chromatographic column onboard Martian rovers

open access: yesFEBS Letters, EarlyView.
Computer image of the Rosalind Franklin Rover of ESA's ExoMars mission. ExoMars is scheduled to land on planet Mars in Oxia Planum in 2029. This area represents an interesting spot to look for biosignatures. Investigations of ExoMars include measurement on molecular chirality. We show that chiral chloroalkanes, that have been identified on Mars, can be
Asma Merzougui   +4 more
wiley   +1 more source

Artificial molecular machines and motors—Design and control of nanoscale motion

open access: yesFEBS Letters, EarlyView.
Molecules are constantly moving because of thermal fluctuations, but random motion alone cannot be exploited to perform directional tasks. Artificial molecular machines use chemical, electrical, or light energy to bias this motion. Molecular shuttles, rotary motors, and supramolecular pumps illustrate how nanoscale movement can be controlled and ...
Leonardo Andreoni, Alberto Credi
wiley   +1 more source

The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers

open access: yesMolecular Oncology, EarlyView.
The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce   +11 more
wiley   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

open access: yesMolecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska   +13 more
wiley   +1 more source

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

open access: yesMolecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura   +19 more
wiley   +1 more source

A time-scale representation of EEG Higuchi fractal dimension. [PDF]

open access: yesSci Rep
Masoumirad S   +3 more
europepmc   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Home - About - Disclaimer - Privacy