Common region of ALL-1 gene disrupted in epipodophyllotoxin-related secondary acute myeloid leukemia.

Abstract

Translocations at chromosomal band 11q23 characterize most de novo acute lymphoblastic leukemias (ALL) of infants, acute myeloid leukemias (AML) of infants and young children, and secondary AMLs following epipodophyllotoxin exposure. The chromosomal breakpoints at 11q23 have been cloned from isolated cases of de novo ALL and AML. Using an 859-base pair BamHI fragment of human ALL-1 complementary DNA that recognizes the genomic breakpoint region for de novo ALL and AML, we investigated two cases of secondary AML that followed etoposide-treated primary B-lineage ALL. In the first case, the translocation occurred between chromosomes 9 and 11 and the breakpoint at 11q23 localized to the same 9-kilobase region of the ALL-1 gene that is disrupted in most of the de novo leukemias. In the second case the translocation was between chromosomes 11 and 19. The breakpoint occurred outside of the ALL-1 breakpoint cluster region.

• Authors: C A Felix, N J Winick, M Negrini, W P Bowman, C M Croce, B J Lange
• Journal: Cancer research (Cancer Res) Vol. 53 Issue 13 Pg. 2954-6 (Jul 01 1993) ISSN: 0008-5472 [Print] United States
• PMID: 8319201 (Publication Type: Journal Article)

Chemical References

• DNA, Neoplasm
• Etoposide
• DNA modification methylase BamHI
• DNA-Cytosine Methylases
• Podophyllotoxin

Topics

• Child, Preschool
• Chromosomes, Human, Pair 11 (drug effects, physiology)
• DNA, Neoplasm (genetics, metabolism)
• DNA-Cytosine Methylases (metabolism)
• Etoposide (adverse effects, therapeutic use)
• Humans
• Leukemia, Monocytic, Acute (chemically induced, genetics)
• Male
• Neoplasms, Second Primary (chemically induced, genetics)
• Podophyllotoxin (adverse effects, therapeutic use)
• Precursor Cell Lymphoblastic Leukemia-Lymphoma (drug therapy, genetics)
• Translocation, Genetic (drug effects)