MLL translocations specify a distinct gene expression profile, distinguishing a unique leukemia

Abstract

The present invention relates to the diagnosis of mixed lineage leukemia (MLL), acute lymphoblastic leukemia (ALL), and acute myelogenous leukemia (AML) according to the gene expression profile of a sample from an individual, as well as to methods of therapy and screening that utilize the genes identified herein as targets.

Description

RELATED APPLICATIONS [0001] This application is a continuation of U.S. application Ser. No. 10 / 198,064, filed Jul. 17, 2002, which claims the benefit of U.S. Provisional Application No. 60 / 306,103 filed on Jul. 17, 2001. The entire teachings of the above applications are incorporated herein by reference.GOVERNMENT SUPPORT [0002] The invention was supported, in whole or in part, by a grant P01CA68484 from the National Institutes of Health. The Government has certain rights in the invention.BACKGROUND OF THE INVENTION [0003] A subset of human acute leukemias with a decidedly unfavorable prognosis possess a chromosomal translocation involving the Mixed Lineage Leukemia (MLL, HRX, AU-1) gene on chromosome segment 11q23. The leukemic cells, which typically have a lymphoblastic morphology, have been classified as Acute Lymphoblastic Leukemia (ALL). However, unlike the majority of childhood ALL, the presence of the MLL translocations often results in an early relapse after chemotherapy. As...

AI Technical Summary

Benefits of technology

[0026] It is well known that proper diagnosis of disease is essential for successful treatment of individuals. The present invention will significantly improve the diagnosis of MLL, ALL, and ALL, and thereby improve the treatment of leukemic individuals.

Problems solved by technology

However, unlike the majority of childhood ALL, the presence of the MLL translocations often results in an early relapse after chemotherapy.

As MLL translocations are typically found in leukemias of infants and chemotherapy-induced leukemia, it has remained uncertain whether host related factors or tumor-intrinsic biological differences are responsible for the poor survival in patients with the translocations.

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