MAN1A1 (Mannosidase Alpha Class 1A Member 1)

In our pilot study, MAN1A1 protein expression is a significant actor in progression along the metastatic path, supporting further study into MAN1A1 as driver of breast cancer patient survival.

Mechanistic investigations reveal that MAN1A1 exerts its pro-metastatic effects by significantly prolonging the TGFBR2 protein half-life. Together, our work identifies MAN1A1 as both a prognostic biomarker and a promising therapeutic target, highlighting the critical role of glycan remodeling in the metastatic progression of colorectal cancer.

While the exact roles of these molecular pathways in the progression from MGUS to MM remain unclear, the identified protein differences may serve as biomarkers and therapeutic targets, warranting further validation and functional studies for clinical application. In addition, the differential expression of PRKDC in AA patients suggests potential population-specific vulnerabilities. Validation of these findings in additional cohorts will help assess the potential usefulness of these biomarkers in predicting transition from MGUS to MM.

Additionally, the patient's intracranial metastatic lesion reduced in size from 19 mm to 8 mm, leading to an improvement in her headache symptoms. It is worth further exploring whether patients carrying IGR fusions can receive targeted therapy.

Moreover, semaglutide could significantly increase the expression of Man1a1 and Ntn4 in the kidneys of mice, while the high-expression of Man1a1 and Ntn4 in KIRC population had a better overall survival rate. Semaglutide could regulate the development of KIRC by up-adjusting the expression of Man1a1 and Ntn4.

In a mouse xenograft and glioma model, penfluridol enhanced the anti-tumor effect of the anti-PD-L1 antibody in vivo. Overall, these findings revealed an important biological activity of the antipsychotic drug penfluridol as an inhibitor of glycan processing and proposed a repurposed use of penfluridol in anti-tumor therapy through activation of T-cell immunity.

Our results highlight transcriptomic similarities and differences in ET patients according to the degree of maturation of the malignant clone and the type of mutation. The genes and processes altered in both CD34 + cells and mature neutrophils may reveal altered sustained processes that could be studied as future therapeutic targets for ET patients.

Elimination of the CD133-DNMT1 interaction by a cell-penetrating peptide or MAN1A1 overexpression inhibits the tumorigenesis of GSCs and increases the sensitivity of GSCs to temozolomide. Analysis of glioma samples reveals that the levels of high-mannose type N-glycan are correlated with glioma recurrence. Collectively, the high mannose CD133-DNMT1 interaction maintains the slow-cycling state and tumorigenic potential of GSC, providing a potential strategy to eliminate quiescent GSCs.