Results 211 to 220 of about 1,355,306 (336)

Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy

open access: yesMolecular Oncology, EarlyView.
Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen   +9 more
wiley   +1 more source

Molecular cancer prevention: Intercepting disease

open access: yesMolecular Oncology, EarlyView.
Oncological practice must evolve, from treating established tumours to proactive cancer interception before clinical manifestation. This will require mechanistic insight into tumour initiation, validated biomarkers of early disease development and redesigned clinical trials, enabling cancer interception to become a core pillar of oncology with the ...
Charlotte Grieco   +2 more
wiley   +1 more source

Ultrasound Autofocusing: Common Midpoint Phase Error Optimization via Differentiable Beamforming. [PDF]

open access: yesIEEE Trans Med Imaging
Simson W   +5 more
europepmc   +1 more source

Circulating tumor cell viability during and after radiotherapy mirrors treatment response in cancer patients

open access: yesMolecular Oncology, EarlyView.
Radiotherapy (RT) response depends on the DNA repair capacity of tumor and host cells. We show that circulating tumor cell (CTC) counts and apoptosis rates before and after RT predict treatment response and outcome, which can be accessed via easily accessible liquid biopsy approaches. Created in BioRender. Wikman, H.
Yvonne Goy   +10 more
wiley   +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

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