High expression of COMMD7 is an adverse prognostic factor in acute myeloid leukemia
Acute myeloid leukemia (AML) is a frequent malignancy in adults worldwide; identifying preferable biomarkers has become one of the current challenges. Given that has been reported associated with tumor progression in various human solid cancers but rarely reported in AML, herein, RNA sequencing data...
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Veröffentlicht in: | Aging (Albany, NY.) NY.), 2021-04, Vol.13 (8), p.11988-12006 |
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Sprache: | eng |
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Zusammenfassung: | Acute myeloid leukemia (AML) is a frequent malignancy in adults worldwide; identifying preferable biomarkers has become one of the current challenges. Given that
has been reported associated with tumor progression in various human solid cancers but rarely reported in AML, herein, RNA sequencing data from TCGA and GTEx were obtained for analysis of
expression and differentially expressed gene (DEG). Furthermore, functional enrichment analysis of
-related DEGs was performed by GO/KEGG, GSEA, immune cell infiltration analysis, and protein-protein interaction (PPI) network. In addition, the clinical significance of
in AML was figured out by Kaplan-Meier Cox regression and prognostic nomogram model. R package was used to analyze incorporated studies. As a result,
was highly expressed in various malignancies, including AML, compared with normal samples. Moreover, high expression of
was associated with poor prognosis in 151 AML samples, as well as subgroups with age >60,
mutation-positive,
mutation-negative, and DNMT3A mutation-negative, et al. (
< 0.05). High
was an independent prognostic factor in Cox regression analysis; Age and cytogenetics risk were included in the nomogram prognostic model. Furthermore, a total of 529 DEGs were identified between the high- and the low- expression group, of which 92 genes were up-regulated and 437 genes were down-regulated. Collectively, high expression of
is a potential biomarker for adverse outcomes in AML. The DEGs and pathways recognized in the study provide a preliminary grasp of the underlying molecular mechanisms of AML carcinogenesis and progression. |
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ISSN: | 1945-4589 1945-4589 |
DOI: | 10.18632/aging.202901 |