CDK4 overexpression

Our data strongly support investigation of the chemotherapy-free palbociclib and venetoclax combination as an innovative treatment strategy for post-ibrutinib MCL patients without RB1 deletion.

In addition, high CDK4 expression and cell cycle variability were observed in AM, with high immunogenicity in NAM. Overall, these findings provide further insights into the pathogenesis of melanoma and serve as a reference for future research on this major malignant disease.

P2, N=40, Recruiting, Grupo Espanol de Investigacion en Sarcomas | Trial completion date: Dec 2023 --> Sep 2024 | Trial primary completion date: Dec 2023 --> Sep 2024

This study suggests a relationship between CDK4 and immune infiltration and prognosis in HCC. Additionally, a CDK4 inhibitor may have anti-tumor properties against hepatocellular cancer.

Translational research showed a significant correlation between CDK4 mRNA and protein expression. Palbociclib was active in a variety of sarcoma subtypes, selected by CDK4/CDKN2A, and deserves further investigation in the sarcoma context.

In this study, the overexpression/knockdown CDK4 and negative control group were successfully constructed in H1339 and SW1271 cells, revealing the radiotherapy resistance of CDK4 alterations in vitro and in vivo experiment. And CDK4 alterations was shown to promote radiotherapy resistance through phosphorylation of MAPK/ERK signaling pathway in SCLC.

Importantly, the inhibitory effects of METTL1 knockdown on the proliferation of HNSC, esophageal cancer (ESCA), stomach adenocarcinoma (STAD), and colon adenocarcinoma (COAD) were significantly mitigated by over-expression of CDK4. Taken together, this study expands the understanding of epigenetic mechanisms involved in tumorigenesis and identifies the METTL1/CDK4 axis as a potential therapeutic target for digestive system tumors.

We identified overexpressers of CDK and cyclin genes among a heterogeneous sample of sarcoma patients. By setting a threshold of 2 SD above the mean of each gene we captured the top ~2% of expressers, and by considering subtypes with ≥ 25% of cases above that threshold we accurately identified known associations between CDK4/LPS and CCND1/Ewing sarcoma while also revealing new associations. The most notable overexpressers were chordoma (CDK7, CDK18), CCS (CDK2, CCNA1), RCS (CCND2), and RMS (CDK6, CDK8, CCND2, CCNE1).

Rescue function experiments corroborated that the anticancer activities of TFAP2A-AS1 deficient on the oncogenicity of NSCLC cells were reversed by downregulating miR-584-3p or overexpressing CDK4. To sum up, TFAP2A-AS1 exhibits cancer-promoting roles in NSCLC through the adjustment of miR-584-3p/CDK4 axis.

Sanguinarine inhibits the proliferation and invasion of HCC cells, and induces the apoptosis of HCC cells by regulating the expression of miR-497-5p/CDK4.