Results 151 to 160 of about 861,022 (290)

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

open access: yesMolecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala   +15 more
wiley   +1 more source

Peroxidasin enables melanoma immune escape by inhibiting natural killer cell cytotoxicity

open access: yesMolecular Oncology, EarlyView.
Peroxidasin (PXDN) is secreted by melanoma cells and binds the NK cell receptor NKG2D, thereby suppressing NK cell activation and cytotoxicity. PXDN depletion restores NKG2D signaling and enables effective NK cell–mediated melanoma killing. These findings identify PXDN as a previously unrecognized immune evasion factor and a potential target to improve
Hsu‐Min Sung   +17 more
wiley   +1 more source

Phenotypic and genotypic characterization of single circulating tumor cells in the follow‐up of high‐grade serous ovarian cancer

open access: yesMolecular Oncology, EarlyView.
Single circulating tumor cells (sCTCs) from high‐grade serous ovarian cancer patients were enriched, imaged, and genomically profiled using WGA and NGS at different time points during treatment. sCTCs revealed enrichment of alterations in Chromosomes 2, 7, and 12 as well as persistent or emerging oncogenic CNAs, supporting sCTC identity.
Carolin Salmon   +9 more
wiley   +1 more source

Redox regulation meets metabolism: targeting PRDX2 to prevent hepatocellular carcinoma

open access: yesMolecular Oncology, EarlyView.
PRDX2 acts as a central redox hub linking metabolic dysfunction‐associated steatohepatitis (MASH) to hepatocellular carcinoma (HCC). In normal hepatocytes, PRDX2 maintains redox balance and metabolic homeostasis under oxidative stress. In contrast, during malignant transformation, PRDX2 promotes oncogenic signaling, stemness, and tumor initiation ...
Naroa Goikoetxea‐Usandizaga   +2 more
wiley   +1 more source

Tumor mutational burden as a determinant of metastatic dissemination patterns

open access: yesMolecular Oncology, EarlyView.
This study performed a comprehensive analysis of genomic data to elucidate whether metastasis in certain organs share genetic characteristics regardless of cancer type. No robust mutational patterns were identified across different metastatic locations and cancer types.
Eduardo Candeal   +4 more
wiley   +1 more source

TRAIL‐PEG‐Apt‐PLGA nanosystem as an aptamer‐targeted drug delivery system potential for triple‐negative breast cancer therapy using in vivo mouse model

open access: yesMolecular Oncology, EarlyView.
Aptamers are used both therapeutically and as targeting agents in cancer treatment. We developed an aptamer‐targeted PLGA–TRAIL nanosystem that exhibited superior therapeutic efficacy in NOD/SCID breast cancer models. This nanosystem represents a novel biotechnological drug candidate for suppressing resistance development in breast cancer.
Gulen Melike Demirbolat   +8 more
wiley   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

Basroparib inhibits YAP‐driven cancers by stabilizing angiomotin

open access: yesMolecular Oncology, EarlyView.
Basroparib, a selective tankyrase inhibitor, suppresses Wnt signaling and attenuates YAP‐driven oncogenic programs by stabilizing angiomotin. It promotes AMOT–YAP complex formation, enforces cytoplasmic YAP sequestration, inhibits YAP/TEAD transcription, and sensitizes YAP‐active cancers, including KRAS‐mutant colorectal cancer, to MEK inhibition.
Young‐Ju Kwon   +4 more
wiley   +1 more source

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