Reduced levels of miR-34a in neuroblastoma are not caused by mutations in the TP53 binding site

Galina Feinberg-Gorenshtein, Smadar Avigad, Marta Jeison, Gili Halevy-Berco, Jacques Mardoukh, Drorit Luria, Shifra Ash, Ran Steinberg, Avraham Weizman, Isaac Yaniv

Research output: Contribution to journalArticlepeer-review

Abstract

Neuroblastoma (NB) is the most common extracranial solid tumor in children below the age of 5 years. miR-34a, located in chromosome band 1p36, has been recently implicated as a tumor suppressor gene in NB. In addition, it has been shown that miR-34a is activated by TP53 by binding to a TP53 binding site upstream to the mature miR-34a. We studied NB tumors from 57 patients for miR-34a expression levels, 1p status, mutations in the TP53 coding region and mutations of the TP53 binding site. Reduced expression levels of miR-34a were identified in tumors harboring 1p36.3 Loss (P = 0.028). No mutations were identified in the coding region of TP53, or in the TP53 binding site. Thus, mutations in the binding site are not an additional mechanism for the inactivation of miR-34a in NB. Other regulatory mechanisms controlling miR-34a expression and its relationship to TP53 should be further explored.

Original languageEnglish
Pages (from-to)539-543
Number of pages5
JournalGenes Chromosomes and Cancer
Volume48
Issue number7
DOIs
StatePublished - Jul 2009

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