Results 101 to 110 of about 3,176,644 (267)

Pre- and Post-Treatment Quality of Life Among Patients with Advanced Stage Cervical Cancer at Tikur Anbessa Specialized Hospital, Ethiopia

open access: yesCancer Management and Research
Roza Teshome,1 Irene Yang,2 Edom Woldetsadik,3 Eshetu Girma,4 Melinda Higgins,2 Jessica Wells2 1Department of Midwifery, School of Nursing & Midwifery, College of Health Sciences, Addis Ababa University, Addis Ababa, Ethiopia; 2Nell Hodgson Woodruff ...
Teshome R   +5 more
doaj  

KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer

open access: yesMolecular Oncology, EarlyView.
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan   +16 more
wiley   +1 more source

Heterozygous loss‐of‐function alleles associate the conserved 3′‐5′ exoribonuclease EXOSC10 with hypersensitivity to the anticancer drug 5‐fluorouracil

open access: yesMolecular Oncology, EarlyView.
EXOSC10, an essential nuclear RNA exosome‐associated 3′‐5′ exoribonuclease, is inhibited by the anticancer drug 5‐fluorouracil (5‐FU), and EXOSC10 depletion increases 5‐FU sensitivity. The colon‐cancer variant EXOSC10S402T, located in a proteolysis motif, is stable and nuclear but nonfunctional in vivo.
Radhika Sain   +10 more
wiley   +1 more source

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

open access: yesMolecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu   +10 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

Proteasome inhibitor, ixazomib prevents topoisomerase‐I degradation and reverses irinotecan resistance in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata   +10 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

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

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