The DOI matches its Crossref record; 124 of the 124 references it cites were found in a registry or an index.
NUP98 gene fusions and hematopoietic malignancies: common themes and new biologic insights
Open accessAbstract
Structural chromosomal rearrangements of the Nucleoporin 98 gene (NUP98), primarily balanced translocations and inversions, are associated with a wide array of hematopoietic malignancies. NUP98 is known to be fused to at least 28 different partner genes in patients with hematopoietic malignancies, including acute myeloid leukemia, chronic myeloid leukemia in blast crisis, myelodysplastic syndrome, acute lymphoblastic leukemia, and bilineage/biphenotypic leukemia. NUP98 gene fusions typically encode a fusion protein that retains the amino terminus of NUP98; in this context, it is important to note that several recent studies have demonstrated that the amino-terminal portion of NUP98 exhibits transcription activation potential. Approximately half of the NUP98 fusion partners encode homeodomain proteins, and at least 5 NUP98 fusions involve known histone-modifying genes. Several of the NUP98 fusions, including NUP98-homeobox (HOX)A9, NUP98-HOXD13, and NUP98-JARID1A, have been used to generate animal models of both lymphoid and myeloid malignancy; these models typically up-regulate HOXA cluster genes, including HOXA5, HOXA7, HOXA9, and HOXA10. In addition, several of the NUP98 fusion proteins have been shown to inhibit differentiation of hematopoietic precursors and to increase self-renewal of hematopoietic stem or progenitor cells, providing a potential mechanism for malignant transformation.
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Metadata
- Authors
- Gough, S. M., Slape, C. I., & Aplan, P. D.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2011-12-08
- Volume
- 118
- Issue
- 24
- Pages
- 6247-6257
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2049625449
- Cited by
- 342
- References
- 124
- FWCI
- 11.32
- Type
- journal article
- Language
- en
- Open access
- green
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