CCND1 (Cyclin D1)

Functionally, H4Q27dop acts as a transcriptional repressor in a neuroblastoma model, where it blocks CEBPD binding at the CCND1 promoter, leading to transcriptional downregulation of CCND1 and subsequent suppression of cell proliferation. Our findings provide both a valuable resource of dopaminylated substrate proteins and a distinct mechanistic insight into how dopamine regulates neuroblastoma cell growth.

Reduced postoperative expression of miR-184 and miR-206 may predict early recurrence in patients with HBV-related HCC. Their associated regulatory networks suggest possible mechanisms of recurrence and represent potential biomarkers for postoperative surveillance. Further studies are needed to validate their prognostic value.

P2, N=52, Not yet recruiting, Miltenyi Biomedicine GmbH

This finding expands the molecular spectrum of uterine mesenchymal neoplasms and defines a novel kinase-driven subset. The BRAF fusion indicates MAPK pathway activation and raises the possibility of a distinct entity or a novel pathogenetic pathway in HG-ESS, with potential therapeutic implications.

On confirmation of this rearrangement by comprehensive genomic profiling, the decision was made to utilize a venetoclax-based regimen...This case highlights a novel and targetable genomic subtype of MM and reinforces the importance of molecular diagnostics in guiding precision therapy. Trial Registration: The authors have confirmed clinical trial registration is not needed for this submission.

These findings indicate that γ-T3 inhibits HeLa cell proliferation, at least in part, via suppression of the PI3K/AKT/mTOR signaling pathway. This supports further evaluation of γ-T3 as a nutrition-relevant bioactive compound for cancer prevention research and as a potential adjunct to therapy.

PC3/Tis21/BTG2 and BTG1 bind and regulate multiple genes, including Id3, cyclin D1, PRMT1 and the chemokine Cxcl3. These interactions underscore the potential of these cofactors in controlling neurogenesis and tumorigenesis through multiple molecular pathways.

Remarkably, pronounced stereochemistry-dependent activity emerged against MDA-MB-231 cells: 6a displayed approximately 100-fold greater potency than 6b (β, β, α) and 6.6-fold superiority over gemcitabine. Mechanistic investigations revealed that 6a downregulates Cyclin D1, CDK4, and CDK6 expression, thereby inducing G0/G1 phase cell cycle arrest. These findings underscore the pivotal role of stereochemical configuration in modulating artemisinin trimer bioactivity and provide rational guidance for structure-based design of artemisinin-derived anticancer therapeutics.

Additionally, rPEDF treatment elevated intracellular ROS levels, triggering oxidative stress-mediated cytotoxicity in TNBC cells. Overall, our comprehensive findings establish rPEDF as a potent suppressor of EMT and Wnt-driven oncogenic signaling in TNBC, highlighting its promising potential as a recombinant protein to mitigate tumour metastasis and aggressiveness.

These findings support a rational therapeutic strategy that exploits oxidative genomic instability and synthetic lethality via HR pathway disruption, offering a promising combination therapy for managing mut/delp53 MCL.

We conclude that, in clear contrast to non-dysplastic HOL, Wnt/β-catenin activity is increased in non-dysplastic NHOL, which correlates with the expression of downstream proliferation markers. Additionally, both dysplastic NHOL and HOL present high Wnt/β-catenin activity, regardless of the dysplasia grade.