CDKN2A expression

The released CCL13 enhances the infiltration of T cells within the tumor, potentially contributing to the improved prognosis observed in patients with high p16INK4A expression. These findings suggest that tumor cells with a senescence phenotype in GBM, through the secretion of chemokines such as CCL13, may augment immune cell infiltration and potentially enhance patient outcomes by creating a more immunologically active tumor microenvironment.

While this study observes trends suggesting that low p16 protein expression is associated with longer DFS and advanced TNM stage in laryngeal cancer, the multivariate analysis did not establish p16 as an independent prognostic factor. These findings suggest that while p16 may have a biological role in tumor progression, its utility as a standalone prognostic marker in clinical outcomes requires further validation.

It is hypothesised that the balance of this signal is also dependent on the ability of cells to moderate the TF, and therefore on the level of damage. However, prolonged exposure of cells for example due to inflammation, leads to the dysregulation of the G1/S checkpoint by the tumour suppressors, leading to aberrant growth.

In high-risk HPV-positive CC patients, HPV seems to play a role in recurrent disease. Our findings support ongoing research on targeting HPV oncogenes in CC, also in metastatic disease.

The inducible expression of p16Ink4a imposes MC senescence, providing a model for tracking the autonomous changes that occur in MCs during ageing. These changes include both morphological and functional alterations. In particular, the increased release of small EVs by senescent MCs suggests an enhanced ability to modulate neighbouring cells.

A significant linear correlation (p=0.000) is found between the p16INK4A and MPPED2 proteins. Conclusion It may support the therapeutic application of MPPED2 protein to prevent cervical carcinoma progression in the near future.

We identified age-increased p16/Cdkn2a-expressing OPCs enriched for senescence-related pathways and distinct senescence signatures between hippocampus and fimbria. Aged brain OPC populations differ in microenvironment properties and responses to senescence-directed intervention.

However, the role of PKD3 was elusive in some cancers. Our findings suggest that testing for PKD isotypes with immunohistochemistry may support the diagnostic estimation of tumor progression and prognosis in HNSCC with a potential therapeutic relevance.

Our findings indicate that there is a negative feedback loop between P16INK4A and RB1 expression and that disruption of this loop may partially rescue the biological outcomes of P16INK4A loss. We also revealed a hitherto unknown function for P16 INK4A in regulating proteome-scale ubiquitination by inhibiting cell proliferation, which may be useful for the development of anticancer drugs.

p16INK4a expression was higher in those who were frail, older than 60, and with higher expression in frail vs. fit patients who are 18-59 years. Our study highlights the high prevalence of frailty in survivors with detrimental effects on physical and overall wellbeing, and supports an association between frailty and the senescence marker p16INK4a.

Samples of metastatic tumors exhibited a higher proportion of elevated PD-L1 expression, a greater number of pathway alterations, and a higher occurrence of CDKN2A copy number deletions than primary samples. This highlights the importance of reinforcing the clinical management and follow-up of patients with CDKN2A deficiency, particularly within the subset of stage I lung adenocarcinoma.

P1/2, N=110, Recruiting, Antiva Biosciences | N=29 --> 110 | Trial completion date: May 2024 --> Jun 2025 | Trial primary completion date: Apr 2024 --> Jun 2025