Results 101 to 110 of about 24,956 (275)

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

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
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

Longitudinal genome‐wide aneuploidy measurements in circulating cell‐free DNA to predict lack of benefit from pembrolizumab in patients with metastatic urothelial cancer

open access: yesMolecular Oncology, EarlyView.
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

Identification of targetable epigenetic vulnerabilities for uveal melanoma

open access: yesCell Death and Disease
Uveal melanoma (UM) is the most common adult primary intraocular malignancy, with a strong predilection for hepatic metastasis, occurring in approximately 50% of cases. Metastatic UM is highly resistant to therapy and is almost invariably fatal.
Gulum Yenisehirli   +18 more
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

Suppression of interferon β gene transcription by inhibitors of bromodomain and extra-terminal (BET) family members [PDF]

open access: yes, 2015
PLK (Polo-like kinase) inhibitors, such as BI-2536, have been reported to suppress IFNB (encoding IFNβ , interferon β ) gene transcription induced by ligands that activate TLR3 (Toll-like receptor 3) and TLR4.
Lopez-Pelaez, Marta   +8 more
core   +1 more source

Tumor B‐cell infiltration in platinum‐treated advanced muscle‐invasive urothelial carcinoma

open access: yesMolecular Oncology, EarlyView.
Bladder tumors with higher pretreatment memory B‐cell infiltration were linked to longer survival after cisplatin chemotherapy, but not carboplatin. These tumors also showed more organized immune structures (tertiary lymphoid structures) and a shared pro‐inflammatory B‐cell‐rich community, suggesting that memory B cells may help identify patients most ...
Konrad Stawiski   +10 more
wiley   +1 more source

BET bromodomain inhibition potentiates radiosensitivity in models of H3K27-altered diffuse midline glioma

open access: yesThe Journal of Clinical Investigation
Diffuse midline glioma (DMG) H3K27-altered is one of the most malignant childhood cancers. Radiation therapy remains the only effective treatment yet provides a 5-year survival rate of only 1%.
Jun Watanabe   +14 more
doaj   +1 more source

Epigenetic heterogeneity and plasticity in therapy‐induced tumor states through single‐cell multi‐omics

open access: yesMolecular Oncology, EarlyView.
Single‐cell multi‐omics reveals epigenetic heterogeneity across therapy‐adaptive tumor states, including quiescent/dormant, drug‐tolerant persister, and EMT‐like phenotypes. By linking regulatory features with state‐associated biomarkers, these approaches inform biomarker‐guided therapeutic strategies for evolving tumors.
Hee Jung Kim   +3 more
wiley   +1 more source

Opposing effects of cancer type-specific SPOP mutations on BET protein degradation and sensitivity to BET inhibitors

open access: yes, 2018
It is generally assumed that recurrent mutations within a given cancer driver gene elicit similar drug responses. Cancer genome studies have identified recurrent but divergent missense mutations in the substrate recognition domain of the ubiquitin ligase
Bellini, Elisa   +28 more
core   +1 more source

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