Results 151 to 160 of about 6,872,930 (361)

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

Ovarian cancer screening in the general population.

open access: yes, 2007
Despite significant improvements in therapy, ovarian cancer continues to be a leading cause of death amongst women with gynaecological malignancies. Advanced stage at diagnosis is thought to be a major contributor to mortality.
Menon, U., Menon, Usha Dr
core  

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

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

open access: yesMolecular Oncology, EarlyView.
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

Cardiovascular screening of athletes [PDF]

open access: yesVojnosanitetski Pregled, 2009
Stajić Zoran, Mijailović Zdravko M.
doaj   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

open access: yesMolecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu   +13 more
wiley   +1 more source

Weakening the nuclear envelope: Lamin B receptor in melanoma metastasis

open access: yesMolecular Oncology, EarlyView.
LBR‐driven nuclear fragility supports melanoma invasion. A: Melanocyte presents low LBR (Lamin B Receptor) levels, maintaining nuclear integrity and lamina‐chromatin tethering. B: During malignant progression, upregulation of LBR clusters at the INM (Inner Nuclear Membrane) during confined migration causes local lamina weakening and cholesterol ...
Francesca Lorenzini   +1 more
wiley   +1 more source

Spatial Localization of Vitamin D Metabolites in Mouse Kidney by Mass Spectrometry Imaging

open access: yesACS Omega, 2020
Karl W. Smith   +6 more
doaj   +1 more source

A Study of Maternal Patients Diagnosed with Inborn Errors of Metabolism Due to Positive Newborn Mass Screening in Their Newborns. [PDF]

open access: yesChildren (Basel), 2023
Onuki T   +6 more
europepmc   +1 more source

Patient therapy outcome modeling in cancer organoids is improved by cancer‐associated fibroblasts and organoid assembly convolution

open access: yesMolecular Oncology, EarlyView.
Patient‐derived organoids (PDOs) from pancreatic, colorectal, and gastric cancers were used to evaluate standard and experimental therapies. Incorporating cancer‐associated fibroblasts (CAFs) into organoid cultures improved patient therapy outcome prediction.
Marcin Grochowski   +12 more
wiley   +1 more source

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