CDKN1C (Cyclin Dependent Kinase Inhibitor 1C)

Mechanistically, YTHDF2 enhanced the PCa progression and metastasis by modulating the m6A methylation of CDKN1C mRNA. Together, these findings suggest that Fbxo2 axis may serve as a potential prognostic marker and therapeutic target in PCa.

Rescue assays validated that CDKN1C mediates the pro-tumorigenic effects of FBXL6 on LUAD cell proliferation and metastasis. Collectively, our findings reveal that FBXL6 drives LUAD progression by ubiquitinating and degrading CDKN1C, highlighting its potential as a therapeutic target for LUAD.

Despite this progress, further studies are needed to resolve context-dependent functional discrepancies, validate biomarker utility, and develop cell-specific delivery systems. This review provides a framework to understand its pathophysiologcial roles and potential application as a biomarker and therapeutic target.

The induction of TNBC cell migration and expression of programmed death-ligand 1 (PD-L1) by a recombinant LIF, along with attenuation by EC359, a LIF inhibitor, were investigated using Transwell assay and flow cytometry...FAP-positive CAFs overexpress genes like LIF, which promotes cell migration and PD-L1 expression. LIF inhibition reduces these effects, suggesting LIF as a potential therapeutic target in TB-associated TNBC progression and immunotherapy.

From precursor to fully developed tumors, notable changes include the up-regulation of UCHL1 and MBD3L2, as well as the significant down-regulation of cell-cycle inhibitory genes, CDKN1A, CDKN1C, and CDKN2B, which play roles in cell survival and tumorigenesis. The current study provides insight into SI-NET initiation and progression, offering potential advancements in diagnosis, prevention, and treatment.

The transition to adult care remains underexplored, though recommendations include attention to residual pediatric complications, fertility, and potential long-term risks. This review reinforces the importance of a multidisciplinary and personalized approach to BWSp across the lifespan, calling for further research to refine diagnostics, long-term outcomes, and transition models.

These findings identify a STAT1-GBP1 axis that enhances postpartum epithelial proliferation by repressing CDKI expression. This mechanism may help to explain the heightened vulnerability observed after childbirth and highlights potential biomarkers or early intervention targets in postpartum breast tissues.

Histologically, ancillary techniques might not be sufficient to confirm the diagnosis of a hydatidiform mole, especially if the tissue available is scarce. In this case, STR has been demonstrated an effective tool in defining the chromosomal asset, even in paraffin-embedded samples.

This study revealed that FBXO42 promotes the malignancy of HCC through FBXO42-mediated p57Kip2 ubiquitination and degradation. Our findings underscore the possibility of FBXO42 as a potential therapeutic target for HCC.

Early diagnosis, standardized management, and tumor surveillance are crucial for improving prognosis in children with BWS. Ultrasonography enables early detection of tumors and informs clinical decision-making regarding intervention.

The central role of referral centers is also emphasized, not only in facilitating timely treatment and access to chemotherapy, but also in implementing standardized post-molar follow-up protocols that reduce progression to GTN and maternal mortality. By focusing on both advanced diagnostic strategies and the organization of care through referral centers, this review offers a comprehensive, practice-oriented perspective to optimize patient outcomes in GTD and address persistent care gaps in high-burden regions.

Given the presence of androgenetic elements and our institutional experience with gestational trophoblastic neoplasia development in a similar case, we recommend that such cases be managed according to complete hydatidiform mole surveillance protocols. This case highlights the diagnostic challenges posed by monozygotic androgenetic/biparental mosaic mechanisms and emphasizes the importance of molecular genetic analysis for the accurate diagnosis and appropriate clinical management of atypical hydatidiform moles.