ArticleThe American journal of pathology2000
Lack of phosphotyrosine phosphatase SHP-1 expression in malignant T-cell lymphoma cells results from methylation of the SHP-1 promoter.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 128 citations in OpenAlex.
- Trial
- Chimeric kinase ALK induces expression of NAMPT and selectively depends on this metabolic enzyme to sustain its own oncogenic function.Leukemia · 2023Article
- Repair of Limb Ischemia Is Dependent on Hematopoietic Stem Cell Specific-SHP-1 Regulation of TGF-β1.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Article
- SHP-1 dephosphorylates histone H2B to facilitate its ubiquitination during transcription.The EMBO journal · 2022Article
- Interfering B cell receptor signaling via SHP-1/p-Lyn axis shows therapeutic potential in diffuse large B-cell lymphoma.Molecular medicine (Cambridge, Mass.) · 2022Article
- Article
- Epigenetics in psoriasis: perspective of DNA methylation.Molecular genetics and genomics : MGG · 2021Review
- Epigenetics of cutaneous T-cell lymphoma: biomarkers and therapeutic potentials.Cancer biology & medicine · 2021Review
- Exploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy.Frontiers in immunology · 2021Review
- Epigenetic alterations and advancement of treatment in peripheral T-cell lymphoma.Clinical epigenetics · 2020Review
- Cellular Interactions and Inflammation in the Pathogenesis of Cutaneous T-Cell Lymphoma.Frontiers in cell and developmental biology · 2020Review
- STAT3 Dysregulation in Mature T and NK Cell Lymphomas.Cancers · 2019Review
- Re-Expression of Bone Marrow Proteoglycan-2 by 5-Azacytidine is associated with STAT3 Inactivation and Sensitivity Response to Imatinib in Resistant CML CellsAsian Pacific journal of cancer prevention : APJCP · 2018Article
- Malignant inflammation in cutaneous T-cell lymphoma-a hostile takeover.Seminars in immunopathology · 2017Review
- Article
- Jak3, STAT3, and STAT5 inhibit expression of miR-22, a novel tumor suppressor microRNA, in cutaneous T-Cell lymphoma.Oncotarget · 2015Article
- Promoter-Specific Hypomethylation Is Associated with Overexpression of PLS3, GATA6, and TWIST1 in the Sezary Syndrome.The Journal of investigative dermatology · 2015Article
- Article
- Tumor Suppressor Inactivation in the Pathogenesis of Adult T-Cell Leukemia.Journal of oncology · 2015Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
SHP-1 is an important negative regulator of signaling by several receptors including receptors for interleukin-2 (IL-2R) and other cytokines. SHP-1 acts by dephosphorylating the receptors and receptor-associated kinases such as IL-2R-associated Jak3 kinase. We found that SHP-1 protein was not detectable or greatly diminished in most (six of seven) T cell lines derived from various types of T cell lymphomas and all (eight of eight) cutaneous T-cell lymphoma tissues with a transformed, large-cell morphology. All T-cell lymphoma lines tested (eight of eight) expressed diminished amounts or no detectable SHP-1 mRNA. These T cell lines did not, however, carry any mutations in the SHP-1 gene-coding, splice-junction, and promoter regions. Importantly, SHP-1 DNA promoter region in the T cell lines was resistant to digestion with three different methylation-sensitive restriction enzymes. This resistance was reversed by treatment of the cells with a demethylating agent, 5-deoxyazacytidine. The treatment resulted also in the expression of SHP-1 mRNA and, less frequently, SHP-1 protein. The expression of SHP-1 protein was associated with dephosphorylation of the Jak3 kinase. These results show that lack of SHP-1 expression is frequent in malignant T cells and results from methylation of the SHP-1 gene promoter. Furthermore, they indicate that SHP-1 loss may play a role in the pathogenesis of T cell lymphomas by permitting persistence of signals generated by IL-2R and, possibly, other receptor complexes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.