| Identifier | HPI102669 |
| Interaction | p16 <==> p53 |
| Role & State | --- |
| Interaction Type | IT:0000132,methylation; IT:0000071,induction; IT:0000025,associate; |
| Biological Process | BP:0006917,induction of apoptosis; BP:0016446,mutation; BP:0006915,apoptosis; BP:0040007,growth; |
| Biological Function | --- |
| Subcelluar Location | --- |
| Detection Method | --- |
| Reference | 12136424_8, Importantly, induction of apoptosis in vitro and reduction of tumor growth in vivo by p16 was p53- as well as bax-independent because identical results were obtained using cancer cells, either wild type or mutant for p53 or bax.
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| Reference | 12168936_3, We examined 40 pairs of HCCs/noncancerous liver tissues for homozygous deletions (HD), methylation and mutations of the INK4a/ARF locus and for mutations of p53, and analyzed their clinicopathological correlation. p16(INK4a), p53 and p14(ARF) were inactivated in 62.5% (25 out of 40), 42.5% (17 out of 40) and 20% (8 out of 40) of HCCs, respectively.
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| Reference | 18723830_10, Negative expression of p16 at a protein level was also associated with poor survival in recurrent stage I to II hepatocellular carcinomas, but p53 expression did not have a synergistic effect on the poor prognosis.
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