CDKN2C (Cyclin Dependent Kinase Inhibitor 2C)

This study revealed uterine leiomyoma subtypes to have distinct chromosomal aberration landscapes. Our large sample collection, detailed subclassification and extensive expression data integration enabled the identification of rare aberrations and subtype-specificity not previously feasible. Further research is implicated in studying the recurrently aberrant regions to identify the specific targets. This study shows, once again, the benefits for accurate subtype information in leiomyoma research and provides a new framework for further studies - towards comprehensive knowledge on the tumorigenesis and potential subtype-specific diagnostic and therapeutic strategies.

In 10 patients with paired, pre- and post-venetoclax treatment samples, post-venetoclax progression was recurrently driven by the selection of genomic events in BCL2/MCL1 and RAS pathways and of high-risk features (e.g., loss of TP53 and CDKN2C). Overall, our study shows that comprehensive genomic profiling can identify most mechanisms underlying resistance to BCL2 inhibition in t(11;14)(CCND1;IGH) MM.

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.

Furthermore, the proliferation, migration, invasion, and tube-forming capacities of HRMVECs were significantly suppressed following treatment with the STAT5 inhibitor. Our findings demonstrate that STAT5 signaling promotes RNV progression by enhancing endothelial cell survival and angiogenic functions.

GSVA confirmed an inverse correlation between C2CD4A expression and E2F pathway activity, with CDKN2C as a co-expressed functional gene. The T2D-related variant rs4502156 in C2CD4A independently predicts a lower risk of BCR, potentially via suppression of the E2F pathway, and may serve as a germline biomarker for postoperative risk stratification.

P2, N=120, Recruiting, Nationwide Children's Hospital | Trial primary completion date: Aug 2028 --> Aug 2029

Deletions and mutations were detected in TNFRSF17 encoding BCMA in patients treated with anti-BCMA regimens, and the information was used to change the treatment of the patients. Targeted sequencing of multiple myeloma patient diagnostic samples can be used for risk stratification and also to monitor and adjust treatments as resistance mechanisms evolve.

We analyze the molecular mechanisms by which p18INK4c regulates the cell cycle and how its dysregulation promotes cancer progression. Additionally, we highlight potential strategies aimed at enhancing p18INK4c activity, underscoring its promise as a target for reactivating tumor-suppressive pathways in cancer therapy.

Additionally, risk score was significantly higher in patients with advanced-stage and high-grade tumors. In conclusion, diagnostic biomarker candidates classifying HCC patients and healthy controls, and a novel prognostic gene signature predicting overall survival of HCC patients were identified by using machine learning approaches.

Moreover, further validation revealed that CDKN2C (one critical gene in the HBPS) deficiency was associated with immuno-cold tumor microenvironment and enhanced HR + HER2- breast cancer cells aggressiveness. Overall, the study's biological insights, crucial for comprehending and tackling drug resistance, hold the potential to inform precise drug treatments in HR+/HER2- BC patients.

To that end, nuclear expression of p18, one of the INK family proteins, was found to be positively associated with the GATA3 mutation, as well as a CDK4/6i treatment response. Therefore, our study suggests that a GATA3 gene mutation, collaborating with p18 protein expression in tumor nuclei, may have a predictive value for CDK4/6i therapy in breast carcinoma.