Results 201 to 210 of about 680,986 (338)

CRISPR targeting of FOXL2 c.402C>G mutation reduces malignant phenotype in granulosa tumor cells and identifies anti‐tumoral compounds

open access: yesMolecular Oncology, Volume 19, Issue 4, Page 1092-1116, April 2025.
FOXL2 c.402C>G mutation drives granulosa cell tumors. Using CRISPR technology, we selectively corrected this mutation, reducing malignancy and increasing sensitivity to dasatinib and ketoconazole. Transcriptomic changes revealed potential therapeutic targets, demonstrating CRISPR's promise for treating this rare ovarian cancer.
Sandra Amarilla‐Quintana   +17 more
wiley   +1 more source

Integration of single‐cell and bulk RNA‐sequencing data reveals the prognostic potential of epithelial gene markers for prostate cancer

open access: yesMolecular Oncology, EarlyView.
Prostate cancer is a leading malignancy with significant clinical heterogeneity in men. An 11‐gene signature derived from dysregulated epithelial cell markers effectively predicted biochemical recurrence‐free survival in patients who underwent radical surgery or radiotherapy.
Zhuofan Mou, Lorna W. Harries
wiley   +1 more source

MET variants with activating N‐lobe mutations identified in hereditary papillary renal cell carcinomas still require ligand stimulation

open access: yesMolecular Oncology, EarlyView.
MET variants in the N‐lobe of the kinase domain, found in hereditary papillary renal cell carcinoma, require ligand stimulation to promote cell transformation, in contrast to other RTK variants. This suggests that HGF expression in the microenvironment is important for tumor growth in such patients. Their sensitivity to MET inhibitors opens the way for
Célia Guérin   +14 more
wiley   +1 more source

Respiratory complex I‐mediated NAD+ regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21Cip1 expression by SIRT3 and SIRT7

open access: yesMolecular Oncology, EarlyView.
NAD+ regeneration by mitochondrial complex I NADH dehydrogenase is important for cancer cell proliferation. Specifically, NAD+ is necessary for the activities of NAD+‐dependent deacetylases SIRT3 and SIRT7, which suppress the expression of p21Cip1 cyclin‐dependent kinase inhibitor, an antiproliferative molecule, at the translational and transcriptional
Masato Higurashi   +5 more
wiley   +1 more source

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