NUP98/NSD1 and FLT3/ITD coexpression is more prevalent in younger AML patients and leads to induction failure: a COG and SWOG report

Author:

Ostronoff Fabiana12,Othus Megan34,Gerbing Robert B.5,Loken Michael R.6,Raimondi Susana C.7,Hirsch Betsy A.8,Lange Beverly J.9,Petersdorf Stephen10,Radich Jerald12,Appelbaum Frederick R.12,Gamis Alan S.511,Alonzo Todd A.512,Meshinchi Soheil15

Affiliation:

1. Fred Hutchinson Cancer Research Center, Clinical Research Division, Seattle, WA;

2. University of Washington, Seattle, WA;

3. Fred Hutchinson Cancer Research Center, Public Health Sciences Division, Seattle, WA;

4. SWOG Statistical Center, Seattle, WA;

5. Children's Oncology Group, Arcadia, CA;

6. Hematologics, Inc., Seattle, WA;

7. St. Jude Children's Research Hospital, Pathology Division, Memphis, TN;

8. University of Minnesota Medical Center-Fairview, Minneapolis, MN;

9. Children's Hospital of Philadelphia, Department of Pediatrics, Division of Oncology, Philadelphia, PA;

10. Seattle Genetics, Inc., Seattle, WA;

11. Children's Mercy Hospitals and Clinics, Kansas City, MO; and

12. University of Southern California, Los Angeles, CA

Abstract

Key Points Coexpression of NUP98/NSD1 and FLT3/ITD in AML is associated with very low complete remission rates and poor survival. It is the interaction between NUP98/NSD1 and FLT3/ITD that determines poor outcome in NUP98/NSD1-associated AML.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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