Cloning of ELL, a gene that fuses to MLL in a t(11; 19)(q23; p13. 1) in acute myeloid leukemia
Abstract
To characterize the functions of MLL fusion transcripts, we cloned the gene that fuses to MLL in the translocation t(11;19)(q23;p13.1). This translocation is distinct from another type of 11;19 translocation with a 19p13.3 breakpoint that results in the fusion of MLL to the ENL gene. By PCR screening of a cDNA library prepared from a patient's leukemia cells with this translocation, we obtained a fusion transcript containing exon 7 of MLL and sequence of an unknown gene. The sequence of this gene was amplified and used as a probe to screen a fetal brain cDNA library. On Northern blot analysis, this cDNA detected a 4.4-kb transcript that was abundant in peripheral blood leukocytes, skeletal muscle, placenta, and testis and expressed at lower levels in spleen, thymus, heart, brain, lung, kidney, liver, and ovary. In addition, a 2.8-kb transcript was present in peripheral blood, testis, and placenta. On [open quotes]zoo blots,[close quotes] this gene was shown to be evolutionarily conserved in 10 mammalian species as well as in chicken, frog, and fish. We have named this gene ELL (for eleven-nineteen lysine-rich leukemia gene). A highly basic, lysine-rich motif of the predicted ELL protein is homologous to similar regions of several proteins,more »
- Authors:
-
- Univ. of Chicago Medical Center, IL (United States)
- Publication Date:
- OSTI Identifier:
- 6609250
- Resource Type:
- Journal Article
- Journal Name:
- Proceedings of the National Academy of Sciences of the United States of America; (United States)
- Additional Journal Information:
- Journal Volume: 91:25; Journal ID: ISSN 0027-8424
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 59 BASIC BIOLOGICAL SCIENCES; MYELOID LEUKEMIA; GENETIC CONTROL; LEUKEMOGENESIS; CARCINOGENESIS; CONTROL; DISEASES; IMMUNE SYSTEM DISEASES; LEUKEMIA; NEOPLASMS; PATHOGENESIS; PEST CONTROL; 550900* - Pathology; 550400 - Genetics
Citation Formats
Thirman, M J, Levitan, D A, Kobayashi, H, Simon, M C, and Rowley, J D. Cloning of ELL, a gene that fuses to MLL in a t(11; 19)(q23; p13. 1) in acute myeloid leukemia. United States: N. p., 1994.
Web. doi:10.1073/pnas.91.25.12110.
Thirman, M J, Levitan, D A, Kobayashi, H, Simon, M C, & Rowley, J D. Cloning of ELL, a gene that fuses to MLL in a t(11; 19)(q23; p13. 1) in acute myeloid leukemia. United States. https://doi.org/10.1073/pnas.91.25.12110
Thirman, M J, Levitan, D A, Kobayashi, H, Simon, M C, and Rowley, J D. 1994.
"Cloning of ELL, a gene that fuses to MLL in a t(11; 19)(q23; p13. 1) in acute myeloid leukemia". United States. https://doi.org/10.1073/pnas.91.25.12110.
@article{osti_6609250,
title = {Cloning of ELL, a gene that fuses to MLL in a t(11; 19)(q23; p13. 1) in acute myeloid leukemia},
author = {Thirman, M J and Levitan, D A and Kobayashi, H and Simon, M C and Rowley, J D},
abstractNote = {To characterize the functions of MLL fusion transcripts, we cloned the gene that fuses to MLL in the translocation t(11;19)(q23;p13.1). This translocation is distinct from another type of 11;19 translocation with a 19p13.3 breakpoint that results in the fusion of MLL to the ENL gene. By PCR screening of a cDNA library prepared from a patient's leukemia cells with this translocation, we obtained a fusion transcript containing exon 7 of MLL and sequence of an unknown gene. The sequence of this gene was amplified and used as a probe to screen a fetal brain cDNA library. On Northern blot analysis, this cDNA detected a 4.4-kb transcript that was abundant in peripheral blood leukocytes, skeletal muscle, placenta, and testis and expressed at lower levels in spleen, thymus, heart, brain, lung, kidney, liver, and ovary. In addition, a 2.8-kb transcript was present in peripheral blood, testis, and placenta. On [open quotes]zoo blots,[close quotes] this gene was shown to be evolutionarily conserved in 10 mammalian species as well as in chicken, frog, and fish. We have named this gene ELL (for eleven-nineteen lysine-rich leukemia gene). A highly basic, lysine-rich motif of the predicted ELL protein is homologous to similar regions of several proteins, including the DNA-binding domain of poly(ADP-ribose) polymerase. The characterization of the normal functions of ELL as well as its altered function when fused to MLL will be critical to further our understanding of the mechanisms of leukemogenesis. 30 refs., 7 figs.},
doi = {10.1073/pnas.91.25.12110},
url = {https://www.osti.gov/biblio/6609250},
journal = {Proceedings of the National Academy of Sciences of the United States of America; (United States)},
issn = {0027-8424},
number = ,
volume = 91:25,
place = {United States},
year = {Tue Dec 06 00:00:00 EST 1994},
month = {Tue Dec 06 00:00:00 EST 1994}
}