This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ Preprints) and either DOI or URL of the article must be cited.
Intermediate-risk AML is a group of heterogeneous disease, complete and accurate understanding of their molecular pattern are urgent. We downloaded gene expression profile from TCGA, and performed the differential gene expression analysis of 98 intermediate-risk AML patients according to the different clinical outcome. By studying the overlap of differential genes based on OS and EFS classification, we identified 6 distinct genes (SPANXC, ADAMTS15, C8B, FAM183A, FLJ42875 and PXDN). Only FLJ42875 and PXDN were relatively widely expressed in intermediate-risk AML. Moreover, Q1 (0-25%) of PXDN was associated significantly shortened OS and EFS (P=0.0001, P=0.0032, respectively), while OS and EFS of Q2 (25-50%) of FLJ42875 expression group were significantly longer than that of low FLJ42875 expression patients (P=0.0157, P=0.0074, respectively). In the multivariable model of OS, PXDN Q1 group had a shorter OS and EFS (P < 0.001, P =0.009; respectively). While FLJ42875 Q2 group had a tendency of prolonged OS and EFS (P=0.050, P=0.023; respectively). Our results suggest that FLJ42875 and PXDN may play a role in the leukemogenesis of intermediate-risk AML.
Intermediate-risk AML is a group of heterogeneous disease, complete and accurate understanding of their molecular pattern are urgent. In this article, we evaluated to understand the molecular pattern of intermediate-risk AML. We found that FLJ42875 and PXDN may play a role in the leukemogenesis of intermediate-risk AML by analyzing the data downloaded from TCGA. This is a preprint submission to PeerJ Preprints.