- Title
- High Expression of ENO1 and Low Levels of Circulating Anti-ENO1 Autoantibodies in Patients with Myelodysplastic Neoplasms and Acute Myeloid Leukaemia
- Creator
- Lincz, Lisa F.; Theron, Danielle Z.; Barry, Daniel L.; Scorgie, Fiona E.; Sillar, Jonathan; Sefhore, Opelo; Enjeti, Anoop K.; Skelding, Kathryn A.
- Relation
- Cancers Vol. 16, Issue 5, no. 884
- Publisher Link
- http://dx.doi.org/10.3390/cancers16050884
- Publisher
- MDPI AG
- Resource Type
- journal article
- Date
- 2024
- Description
- In solid tumours, high expression of the glycolytic enzyme, α-enolase (ENO1), predicts for poor patient overall survival (OS), and circulating autoantibodies to ENO1 correlate positively with diagnosis and negatively with advanced disease. Although ENO1 is one of the most highly expressed genes in acute myeloid leukaemia (AML), its potential role as a biomarker in AML or its precursor, myelodysplastic neoplasms (MDS), has not been investigated. A meta-analysis of nine AML online datasets (n = 1419 patients) revealed that high ENO1 expression predicts for poor OS (HR = 1.22, 95% CI: 1.10-1.34, p < 0.001). Additionally, when compared to AML in remission (n = 5), ENO1 protein detected by immunohistochemistry was significantly higher at diagnosis in bone marrow from both AML (n = 5, p < 0.01) and MDS patients (n = 12, p < 0.05), and did not correlate with percentage of blasts (r = 0.28, p = 0.21). AML patients (n = 34) had lower circulating levels of ENO1 autoantibodies detected by ELISA compared to 26 MDS and 18 controls (p = 0.003). However, there was no difference in OS between AML patients with high vs. low levels of anti-ENO1 autoantibodies (p = 0.77). BM immunostaining for ENO1 and patient monitoring of anti-ENO1 autoantibody levels may be useful biomarkers for MDS and AML.
- Subject
- alpha-enolase; α-enolase (ENO1); autoantibodies; acute myeloid leukaemia; myelodysplastic neoplasms; bone marrow; SDG 3; Sustainable Development Goals
- Identifier
- http://hdl.handle.net/1959.13/1501187
- Identifier
- uon:55100
- Identifier
- ISSN:2072-6694
- Rights
- © 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
- Language
- eng
- Full Text
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