LMNA (Lamin A/C)

Moreover, 9 transcription factors (TFs) (like STAT1), 69 key microRNAs (miRNAs) (like hsa-miR-361-3p), and 78 long non-coding RNAs (lncRNAs) (like NEAT1) were found to have relationships with potential biomarkers, and potential biomarkers had stable binding affinity with adenosine diphosphate (ADP) and lonafarnib...Importantly, RT-qPCR confirmed higher expression of HSPA8, LMNA and SERPINH1 in CS patients. The findings suggested that HSPA8, LMNA and SERPINH1 might offer novel insights for the development of targeted therapies for CS associated with angiogenesis and ISR.

P=N/A, N=81, Not yet recruiting, Assistance Publique - Hôpitaux de Paris

Collectively, our findings suggested that the downregulation of RB1 significantly influences the morphology of LUAD by facilitating EMT and nuclear abnormalities through HDAC1-mediated deacetylation of lamin A/C. Future research should prioritize the development of targeted therapies aimed at restoring RB1 function or inhibiting HDAC1 to mitigate cancer progression, thereby enhancing patient stratification and treatment strategies in TKI-resistant LUAD.

It can be concluded that, down-regulation of MAPK3 and KIT and up-regulation of BMP4 which are the consequence of microsecond PEF treatment inhibit medulloblastoma. The results exhibited the significant role of MAPK3 in response to microsecond PEF treatment.

These cells, forming irregularly shaped spheroids post-migration, display nuclear shape deformation and downregulated VIM and LMNA genes linked to cell and nuclear stiffness. The findings highlight the heterogeneity of cancer cell migration in confined environments and the subsequent growth of tumor spheroids.

PCDH10 restoration antagonizes tumorigenesis by dual blockade of Wnt/β-catenin and Akt signaling pathways through interactions with GSK-3β, β-catenin, and LMNA, as a scaffold protein. Our findings reveal a novel PCDH10-dependent tumor-suppressive axis and highlight its potential as a therapeutic target and biomarker in breast cancer.

This integrated computational study identifies a set of candidate genes through which OTA may potentially interact with HCC-associated molecular networks. The robust binding predicted between OTA and the core targets provides a structural basis for these interactions. These findings offer a prioritized list of targets and a theoretical framework for subsequent experimental validation and investigation into OTA's toxicological role in HCC.

Concurrent comprehensive genome profiling (FoundationOne® CDx) confirmed the LMNA-NTRK1 fusion, and treatment with the TRK inhibitor larotrectinib was started. With larotrectinib treatment, the tumor shrank in size at an early stage, and the response has been maintained for > 2 years.

Notably, cg20370568, a cis-expression quantitative trait methylation site for ANTXR2, mediates 20% of the effect of body-trunk-radiotherapy on abnormal glucose. These findings suggest that prior genotoxic cancer treatments may become biologically embedded through DNAm variations that could contribute to cardiometabolic dysfunction and highlight candidate biomarkers for refining risk stratification and guiding intervention strategies in survivorship care.

Our study established that ECM stiffness drives NB cell migration through a lamin A/C/E2F4/PLK1 axis, governing post-mitotic NPC assembly and transport function. Targeting NPC-mediated transport may represent a promising therapeutic strategy for NB.

NRG1 fusions are oncogenic drivers in non-small cell lung cancer (NSCLC), with therapeutic relevance highlighted by the FDA's designation of Zenocutuzumab for NRG1 fusion-positive cases...No significant difference in progression-free survival was seen following first-line EGFR TKI therapy between uncommon and wild-type groups. Our findings highlight the heterogeneity of NRG1 fusions in NSCLC, revealing novel fusions, unique pathway enrichments, and expression profiles that may inform future personalized treatment strategies.

This protocol combines the advantages of individual compounds, producing cells that closely mimic primary neutrophils in both phenotype and function. The authors provide an improved method to differentiate HL60 cells into neutrophil-like cells that faithfully recapitulates the morphology and functionality of mature human neutrophils.