MAD1L1 (Mitotic Arrest Deficient 1 Like 1)

Additionally, halofuginone decreased hepcidin expression in mice subjected to acute inflammation. These findings establish halofuginone as a potential therapeutic for mitigating hepcidin-driven iron restriction in anemic disorders.

Survival analysis revealed that hypomethylation of four specific CpGs-cg01052776 (RNH1), cg20747787, cg05001671, and cg01767116 (FBXL22)-was significantly associated with an increased risk of relapse, highlighting their potential as prognostic biomarkers. This study underscores the importance of epigenetic mechanisms in pediatric ALL.

Mechanistically, MAD1 ectopic condensates trap the diffusive pool of MAD2, weakening the MAD2 conversion cycle needed for a robust checkpoint. Our work highlights a loss of function caused by ectopic condensates in cancer cells.

This Method paper outlines the AMP workflow, including troubleshooting strategies and quality control criteria, and demonstrates its applicability to clinical samples. Our findings support the utility of RNA-based fusion detection in driver-negative melanomas and the potential of fusion genes as actionable targets.

The 10-gene prognostic model can independently predict patients' prognosis. The great correlation between ZC3H12B and multiple feature genes and immune cells may be tightly linked to EC progression.

This study provides evidence for a genome-wide genetic link between dried fruit intake and BC risk, identifying several loci that may be shared between the traits. These findings may help improve our understanding of BC development and offer preliminary leads for future dietary prevention and personalized interventions, pending further experimental validation.

Mechanistically, the rs11204679 G > C and rs33924488 GA > G- variants attenuate HOXA6 and SOX15 binding at a distal enhancer, respectively, suppressing HORMAD1 expression via long-range chromatin interactions. These findings establish HORMAD1 as a critical mediator of tobacco-related DNA repair dysregulation and a potential biomarker for ESCC risk stratification and precision prevention.

This multi-level analysis reveals that astrocytic tumor progression involves epigenetic derepression and microRNA-mediated dysregulation of TGF-β signaling. Elevated expression of SMAD1, SMAD3, and SKIL emerged as strong prognostic indicators, underscoring their potential as biomarkers and therapeutic targets in astrocytic tumors.

Mechanistically, the MAD1 ectopic condensate traps the diffusive pool of MAD2, an interaction partner of MAD1, thereby weakening the MAD2 conversion cycle necessary for a robust mitotic checkpoint. Our work illustrates a loss of function caused by ectopic condensates in MAD1-overexpressed cancer cells.

Moreover, breast cancer patient samples show a significant negative correlation between REST and MAD1L1 mRNA expression. These results support a model in which an altered transcriptional program downstream of loss of the tumor suppressor REST, which normally represses MAD1L1 transcription by recruiting HDAC1-containing repressive complexes, contributes to MAD1 overexpression in breast cancer.

This research established an innovative TRG-based risk model to forecast the survival outcomes and immune landscape of individuals with HNSCC. This reliable and validated prognostic indicator has the potential to inform and enhance the creation of innovative treatment approaches for individuals with HNSCC.

Moreover, in MV4-11 cells SMAD1 presence sensitized cells for TGF-β mediated G1-arrest. Overall, our data contributes to the understanding of the role of TGF-β signaling in acute myeloid leukemia with KMT2A::AFF1 by showing that SMAD1 loss can influence the growth dynamics and contribute to the pathogenic expression of disease driving factors.