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High expression of CPNE3 predicts adverse prognosis in acute myeloid leukemia.
- Source :
- Cancer Science; Sep2017, Vol. 108 Issue 9, p1850-1857, 8p
- Publication Year :
- 2017
-
Abstract
- CPNE3, a member of a Ca<superscript>2+</superscript>-dependent phospholipid-binding protein family, was identified as a ligand of ERBB2 and has a more general role in carcinogenesis. Here, we identified the prognostic significance of CPNE3 expression in acute myeloid leukemia ( AML) patients based on two datasets. In the first microarray dataset ( n = 272), compared to low CPNE3 expression ( CPNE3<superscript>low</superscript>), high CPNE3 expression ( CPNE3<superscript>high</superscript>) was associated with adverse overall survival ( OS, P < 0.001) and event-free survival ( EFS, P < 0.001). In the second independent group of AML patients ( TCGA dataset, n = 179), CPNE3<superscript>high</superscript> was also associated with adverse OS and EFS ( OS, P = 0.01; EFS, P = 0.036). Notably, among CPNE3<superscript>high</superscript> patients, those received allogenic hematopoietic cell transplantation ( HCT) had longer OS and EFS than those with chemotherapy alone (allogeneic HCT, n = 40 vs chemotherapy, n = 46), but treatment modules played an insignificant role in the survival of CPNE3<superscript>low</superscript> patients (allogeneic HCT, n = 32 vs chemotherapy, n = 54). These results indicated that CPNE3<superscript> high</superscript> is an independent, adverse prognostic factor in AML and might guide treatment decisions towards allogeneic HCT. To understand its inherent mechanisms, we investigated genome-wide gene/micro RNA expression signatures and cell signaling pathways associated with CPNE3 expression. In conclusion, CPNE3<superscript>high</superscript> is an adverse prognostic biomarker for AML. Its effect may be attributed to the distinctive genome-wide gene/micro RNA expression and related cell signaling pathways. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 13479032
- Volume :
- 108
- Issue :
- 9
- Database :
- Complementary Index
- Journal :
- Cancer Science
- Publication Type :
- Academic Journal
- Accession number :
- 124969377
- Full Text :
- https://doi.org/10.1111/cas.13311