Results 101 to 110 of about 389,388 (249)

Root Cause Analysis of Specimen Rejection for Hematology Testing.

open access: yesJournal of Health Science and Medical Research (JHSMR), 2010
Objectives: Using root cause analysis to evaluate and improve the specimen collection process in order to reduce the sample rejection rate for hematology testing.
Meena Perkliang   +4 more
doaj  

Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2‐COL3A1 axis

open access: yesMolecular Oncology, EarlyView.
CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak   +10 more
wiley   +1 more source

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

ESR1 methylation and ESR1 mutations in circulating tumor cells (CTCs) and paired plasma‐cfDNA of advanced breast cancer patients: A feasibility proof‐of‐concept study

open access: yesMolecular Oncology, EarlyView.
Circulating tumor cells (CTCs) and plasma cell‐free DNA (cfDNA) were analyzed to detect ESR1 mutations and methylation in patients with advanced breast cancer. CTC‐derived DNA showed higher sensitivity for mutation detection and revealed complementary genetic and epigenetic alterations, highlighting the added value of CTC analysis for understanding ...
Dimitra Stergiopoulou   +12 more
wiley   +1 more source

Interpreting the effects of DNA polymerase variants at the structural level

open access: yesMolecular Oncology, EarlyView.
Using MAVISp and molecular dynamics simulations, we analyzed over 60 000 missense variants in POLE and POLD1 from ClinVar, COSMIC, cBioPortal, and saturation mutagenesis. Identified mechanistic indicators, including stability, binding, and long‐range, enable structural interpretation, providing ACMG‐like evidence for possible reclassification of VUS ...
Matteo Arnaudi   +7 more
wiley   +1 more source

DNA methylation and expression of MAPRE3 affect overall survival of early‐stage non‐small cell lung cancer patients

open access: yesMolecular Oncology, EarlyView.
Both cg12821679MAPRE3 methylation and MAPRE3 expression are significantly associated with overall survival (OS) of non‐small cell lung cancer. Meanwhile, MAPRE3 expression significantly modified the effect of smoking cessation on OS. Smoking cessation benefits OS merely for patients with high MAPRE3 expression.
Chao Chen   +14 more
wiley   +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

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

Root-cause analysis for clot in blood bag

open access: yesAsian Journal of Transfusion Science, 2016
Shamee Shastry, Soumya Das
doaj   +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