Loss of P16, del(9p21)
Interstitial deletions of the chromosome 9p21 segment encoding the p16/CDKN2A tumor suppressor gene are frequently observed in a variety of human cancers. The loss of the 9p21 locus, del(9p21), is an early and widespread chromosomal abnormality in patients with Barrett’s esophagus predisposed to esophageal adenocarcinoma. Recent studies suggest that endogenous P16 inhibits colon tumor progression and tumor angiogenesis related to VEGF levels. These evidences seem to explain the correlation of aberrant P16 expression with malignant potential of esophageal adenocarcinoma. Although further studies will be required to explore the mechanism between p16 function and VEGF expression, restoration therapy of wild-type p16INK4a gene may be useful in addition to the selective modalities for inhibition of angiogenesis via VEGF suppression in patients with p16-negative esophageal adenocarcinoma.
References
- Martín-Ezquerra G, et al. (2010) Br. Assoc. Dermatol. 163: 1028–1035.
- Takeuchi H, et al. (2004) Int J Cancer. 109(4):483-90.
