ArticleClinical lymphoma, myeloma & leukemia2015
Loss of TRIM62 expression is an independent adverse prognostic factor in acute myeloid leukemia.
Article in Clinical lymphoma, myeloma & leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- An investigation of the molecular characterization of the tripartite motif (TRIM) family and primary validation of TRIM31 in gastric cancer.Human genomics · 2024Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- Advancements in Oncoproteomics Technologies: Treading toward Translation into Clinical Practice.Proteomes · 2023Review
- RETRACTED: TRIM10 Is Downregulated in Acute Myeloid Leukemia and Plays a Tumor Suppressive Role via Regulating NF-κB Pathway.Cancers · 2023Article
- TRIM family contribute to tumorigenesis, cancer development, and drug resistance.Experimental hematology & oncology · 2022Review
- Article
- TRIM44 links the UPS to SQSTM1/p62-dependent aggrephagy and removing misfolded proteins.Autophagy · 2022Article
- The TRIM proteins in cancer: from expression to emerging regulatory mechanisms.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Reverse phase protein arrays in acute leukemia: investigative and methodological challenges.Expert review of proteomics · 2021Review
- Pharmacological Modulation of Ubiquitin-Proteasome Pathways in Oncogenic Signaling.International journal of molecular sciences · 2021Review
- A Regulatory Axis of circ_0008193/miR-1180-3p/TRIM62 Suppresses Proliferation, Migration, Invasion, and Warburg Effect in Lung Adenocarcinoma Cells Under Hypoxia.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Avian leukosis virus subgroup J and reticuloendotheliosis virus coinfection induced TRIM62 regulation of the actin cytoskeleton.Journal of veterinary science · 2020Article
- TRIM31 promotes acute myeloid leukemia progression and sensitivity to daunorubicin through the Wnt/β-catenin signaling.Bioscience reports · 2020Article
- Association ofBreast cancer : basic and clinical research · 2020Article
- TRIM62 From Chicken as a Negative Regulator of Reticuloendotheliosis Virus Replication.Frontiers in veterinary science · 2020Article
- The Tripartite Nexus: Autophagy, Cancer, and Tripartite Motif-Containing Protein Family Members.Frontiers in pharmacology · 2020Review
- Review
- The Role of Tripartite Motif Family Proteins in TGF-β Signaling Pathway and Cancer.Journal of cancer prevention · 2018Review
- Shining a light on cell signaling in leukemia through proteomics: relevance for the clinic.Expert review of proteomics · 2018Review
- Conserved structural and functional aspects of the tripartite motif gene family point towards therapeutic applications in multiple diseases.Pharmacology & therapeutics · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTripartite motif (TRIM)-62 is a putative tumor suppressor gene whose role in leukemia is unknown. MATERIALS AND
methodsWe evaluated the effect of TRIM62 protein expression in patients with acute myeloid leukemia (AML). We used reverse-phase protein array methodology to determine TRIM62 levels in leukemia-enriched protein samples from 511 patients newly diagnosed with AML.
resultsTRIM62 levels in AML cells were significantly lower than in normal CD34-positive cells, suggesting that TRIM62 loss might be involved in leukemogenesis, but was not associated with specific karyotypic abnormalities or Nucleophosmin (NPM1), Fms-like Tyrosine Kinase-3 (FLT3), or rat sarcoma viral oncogene (RAS) mutational status. Low TRIM62 levels were associated with shorter complete remission duration and significantly shorter event-free and overall survival rates, particularly among patients with intermediate-risk cytogenetics. In that AML subgroup, age and TRIM62 levels were the most powerful independent prognostic factors for survival. TRIM62 protein levels further refined the risk associated with NPM1 and FLT3 mutational status. TRIM62 loss was associated with altered expression of proteins involved in leukemia stem cell homeostasis (β-catenin and Notch), cell motility, and adhesion (integrin-β3, ras-related C3 botulinum toxin substrate [RAC], and fibronectin), hypoxia (Hypoxia-inducible factor 1-alpha [HIF1α], egl-9 family hypoxia-inducible factor 1 [Egln1], and glucose-regulated protein, 78 kDa [GRP78]), and apoptosis (B-cell lymphoma-extra large (BclXL) and caspase 9).
conclusionLow TRIM62 levels, consistent with a tumor suppressor role, represent an independent adverse prognostic factor in AML.
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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.