Integrative analysis revealed positive correlations between gene copy number and mRNA expression suggesting Met, Yap1, and Cdkn2a/b may serve as potential drivers that promote tumor recurrence.
As CDKN2A is a key tumor suppressor gene involved in cell cycle control, we investigated whether CDKN2A alterations may be involved in tumor recurrence.
The aim here was to investigate stage T1 tumors regarding MDM2 promoter SNP309 polymorphism, mutations in the p53 gene, and expression of p53 and p16 measured by immunohistochemistry, and subsequently relate these changes to tumor recurrence and progression.
While even advanced stages of gliomas may remain dependent upon KRas signaling for maintenance and growth, our findings demonstrate that loss of Ink4a/Arf facilitates the acquisition of oncogene independence and tumor recurrence.
One month after surgery, in the patients with recurrence of tumor, a dramatic increase in p16(INK4a) MS was observed, while in the disease-free patients no methylation was seen continuously.
The promoter methylation status of the DNA repair gene MGMT and the tumor suppressor genes CDKN2A and RASSF1 were evaluated by methylation-specific PCR in 88 primary oral and pharyngeal tumors and correlated with survival and tumor recurrence.
In the present study, we evaluated a series of 31 dural HPCs (including 3 pairs of primary and recurrent tumor) and 26 meningiomas for alterations in the cell-cycle regulatory genes CDKN2/p16 and p53.