Results 101 to 110 of about 114,835 (256)
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
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
Finding novel vulnerabilities of hypomorphic BRCA1 alleles
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder +10 more
wiley +1 more source
Many patients with urothelial cancer do not benefit from treatment with pembrolizumab, while at risk of severe side effects. Changes in the levels of circulating tumor DNA early during treatment, measured by a simple and affordable assay that can be easily implemented in the clinic, can be used as a prognostic tool to identify these patients.
Youssra Salhi +14 more
wiley +1 more source
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka +9 more
wiley +1 more source
NUP155 and NDC1 interaction in NSCLC: a promising target for tumor progression
BackgroundNUP155 was reported to involve breast invasive carcinoma and hepatocellular carcinoma. We hypothesized that NUP155 and NDC1impacted the progression of NSCLC.MethodsThe dataset was analyzed to find differentially expressed genes.
Kai-Min Li +3 more
doaj +1 more source
ON THE OCTAGONALITY OF THE NUCLEAR PORE COMPLEX [PDF]
openaire +2 more sources
Drug resistance limits treatment success in a subset of lung cancers driven by ROS1 gene alterations. Using patient‐derived cells and computer simulations, we studied three key mutations and how they affect five targeted drugs. The mutations reduced drug effectiveness in different ways by altering protein structure and behavior.
Farhan Ul Haq +8 more
wiley +1 more source
The role of the nuclear pore complex in the stability of disease-related short tandem DNA repeats. [PDF]
Ollivaud S +7 more
europepmc +2 more sources
BCL9 and BCL9L drive bladder cancer progression by enhancing β‐catenin signaling, promoting proliferation, migration, invasion, and organoid growth. Genetic depletion of BCL9(L) suppresses malignant phenotypes, while pharmacological disruption of the β‐catenin/BCL9(L) complex with ZW4864 inhibits canonical Wnt signaling and tumor‐associated cellular ...
Roland Kotolloshi +11 more
wiley +1 more source

