Hypermethylation-associated inactivation indicates a tumor suppressor role for p15INK4B

摘要: Abstract The recently identified cyclin-dependent kinase inhibitor p15INK4B is localized to a region on chromosome 9p21 frequently deleted in human tumors. Previous evidence has pointed related gene, p16INK4A, as the principal target of this deletion. We report that gliomas and, striking degree, leukemias, p15 gene commonly inactivated association with promoter hypermethylation involving multiple sites 5′-CpG island. In some and all primary event occurs without alteration adjacent p16INK4A. other tumors, including lung, head neck, breast, prostate, colon cancer, inactivation p16INK4B only rarely concomitant p16. Aberrant methylation associated transcriptional loss gene. Treatment demethylating agent 5-aza-2′-deoxycytidine leads re-expression mRNA. selected leukemia cell lines, correlates known resistance growth-suppressive effects transforming growth factor-β. These results suggest selectively leukemias seems constitute an important tumor suppressor these neoplasms.