Proviral insertion indicates a dominant oncogenic role for Runx1/AML-1 in T-cell lymphoma (original) (raw)

Wotton, Sandy, Stewart, Monica, Blyth, Karen ORCID: https://orcid.org/0000-0002-9304-439X, Vaillant, Francois, Kilbey, Anna, Neil, James C. ORCID: https://orcid.org/0000-0003-4447-8279 and Cameron, Ewan R. ORCID: https://orcid.org/0000-0001-8311-1491(2002) Proviral insertion indicates a dominant oncogenic role for Runx1/AML-1 in T-cell lymphoma.Cancer Research, 62(24), pp. 7181-7185. (PMID:12499254)

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Publisher's URL: https://cancerres.aacrjournals.org/content/62/24/7181

Abstract

The RUNX1/AML1 gene is a frequent target for chromosomal translocations in human leukemia. The biological properties of the resulting fusion products and the finding that haploinsufficiency increases the risk of developing leukemia (W-J. Song et al., Nat. Genet., 23: 166–175, 1999; M. Osata et al., Blood, 93: 1817–1824, 1999) have led to the widely held view that RUNX1 loss-of-function is a key event. However, we now report that the gene is a target for insertional mutagenesis in T-cell lymphomas of mice carrying a MYC oncogene, where promoter insertion results in overexpression without affecting the integrity of the coding sequence. Moreover, Runx1 haploinsufficiency does not accelerate lymphoma development in MYC/Runx2 transgenic or murine leukemia virus-infected mice. These findings reveal that the Runx1 gene can also act as a dominant oncogene and suggest that the involvement of the Runx gene family in human leukemia may be more widespread and complex than previously realized.

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