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Targeting the Core Binding Factor tumor suppressor in MLL-fusion AML

Award Information
Agency: Department of Health and Human Services
Branch: National Institutes of Health
Contract: 1R43CA176907-01A1
Agency Tracking Number: R43CA176907
Amount: $224,629.00
Phase: Phase I
Program: SBIR
Solicitation Topic Code: NCI
Solicitation Number: PA13-088
Solicitation Year: 2014
Award Year: 2014
Award Start Date (Proposal Award Date): N/A
Award End Date (Contract End Date): N/A
Small Business Information
10101 Alliance Rd
CINCINNATI, OH 45242-4739
United States
DUNS: 182472162
HUBZone Owned: No
Woman Owned: No
Socially and Economically Disadvantaged: No
Principal Investigator
 (513) 636-1338
Business Contact
Phone: (513) 475-6618
Research Institution

DESCRIPTION (provided by applicant): RUNX1 is considered a beneficial tumor suppressor in myeloid neoplasms. Inhibition of RUNX1 function has been implicated as an important mechanistic event in the development of core-binding factor-(CBF)-leukemia and MLL-fusion leukemia. Inactivating RUNX1 mutations are frequently found in patients with acute myeloid leukemia (AML). However, RUNX1 mutation is usually heterozygous, complete loss of RUNX1 in AML is rare and no somatic RUNX1 mutation have been found in AMLswith common fusion proteins, such as CBF- and MLL-fusion leukemias. These data raise the possibility that a certain (low) level of RUNX1 activity is required for survival and growth of AML. We have developed human models for AML by transducing leukemogenicfusion proteins into human cord blood CD34+ cells. MLL-AF9-expressing cord blood cells cause human leukemia when transplanted into immunodeficient mice. We recently found that these AML cells critically depend on RUNX1 activity for sustained growth a

* Information listed above is at the time of submission. *

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