Inactivation of SHIP1 in T-cell acute lymphoblastic leukemia due to mutation and extensive alternative splicing
Open accessAbstract
To understand the mechanism behind aberrant Akt activation in T-ALL, PIK3CA, PTEN and SHIP1 expression and genotype were assessed. No cell lines or primary ALLs harbored PIK3CA mutations. PTEN was expressed in just one-third of the cell lines, but in two-thirds of the primary ALLs, though in the inactivated (phosphorylated) form. SHIP1 was undetectable in most primary ALL and in the T-ALL cell line Jurkat, which harbored a bi-allelic null mutation and a frame-shift deletion; primary ALL harbored the frame-shift as well as other translationally-inactivating deletions and insertions. The inactivation of SHIP1 could play a central role in the deregulation of Akt pathway and tumorigenesis, perhaps in conjunction with PTEN inactivation.
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Loss-of-function mutations in INPP5D are linked to myeloproliferative cancers such as acute myeloid leukemia.
“Loss-of-function mutations in INPP5D have been linked to myeloproliferative cancers such as acute myeloid leukemia [50–52].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [50]
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Terzioglu, G., & Young-Pearse, T. L. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00674-9 · Cited by 95 · see citing works
- Authors
- Lo, T. C. T., Barnhill, L. M., Kim, Y., Nakae, E. A., Yu, A. L., & Diccianni, M. B.
- Affiliations
- University of California San Diego (US)
- Genomics Research Center, Academia Sinica (TW)
- Corresponding author
- Diccianni, Mitchell B.
- Venue
- Leukemia Research
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 33
- Issue
- 11
- Pages
- 1562-1566
- ISSN
- 0145-2126 (ISSN-L)
- PMC
- PMC2735879
- OpenAlex
- W2071481623
- Cited by
- 59
- References
- 0
- Citations by year
- 2025: 4 · 2024: 2 · 2023: 4 · 2022: 2 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 2 · 2016: 4 · 2015: 2 · 2014: 6 · 2013: 3 · 2012: 10
- FWCI
- 7.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Leukemia Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of California, San Diego
- National Cancer Institute (P30CA023100)
- National Center for Research Resources
- NIH Clinical Center
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Acute Lymphoblastic Leukemia research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- SHIP1, T-cell acute lymphoblastic leukemia, alternative splicing, PTEN, PIK3CA, frameshift deletion, tumor suppressor inactivation, Jurkat cells
- MeSH terms
- Inositol Polyphosphate 5-Phosphatases, Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases, Base Sequence, Child, Humans, Mutation, Phosphoric Monoester Hydrolases, Polymerase Chain Reaction, Alternative Splicing, DNA Primers, Gene Silencing, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
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