Overview:

p15INK4B protein acts as an important negative regulator of the cell cycle by inhibiting the activity of CDKs. p15INK4B protein is often inactivated by deletions, mutations, or hypermethylation in malignancy (1). Studies using methylation-specific PCR in patients with therapy-related myelodysplasia (t-MDS) or acute myeloid leukemia (t-AML), reveals the frequent loss of transcription of p15INK4B with promoter methylation. This appears not only in the advanced but also in the early stages of hepatocellular carcinoma suggesting that the epigenetic alteration of p15INK4B promoter is likely to be involved in hepatocarcinogenesis(2).

Gene Aliases:

CDKN2B, P15, MTS2, TP15, CDK4I, INK4B

Genbank Number:

NM_004936

References:

1. Fukai, K. et al. Methylation status of p14ARF, p15INK4b, and p16INK4a genes in human hepatocellular carcinoma. Liver International, 2005;25,6: pp. 1209-1216(8).

2. Christiansen D.H. et al: Methylation of p15INK4B is common, is associated with deletion of genes on chromosome arm 7q and predicts a poor prognosis in therapy-related myelodysplasia and acute myeloid leukemia. Leukemia,2003; 17, 1813–1819