PMID- 35117360
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220501
IS  - 2219-6803 (Electronic)
IS  - 2218-676X (Print)
IS  - 2218-676X (Linking)
VI  - 9
IP  - 12
DP  - 2020 Dec
TI  - A comprehensive assessment of the prognostic role of cell adhesion molecules in 
      acute myeloid leukemia.
PG  - 7605-7618
LID - 10.21037/tcr-20-3315 [doi]
AB  - BACKGROUND: The outcomes for patients with acute myeloid leukemia (AML) have been 
      shown to vastly differ, predominantly due to genetic heterogeneity. Cell adhesion 
      molecules (CAMs) concluding numerous genes play an important role in AML. We 
      aimed to systematically assess the expression characteristics of adhesion 
      molecules and their correlation to the outcomes of AML. METHOD: A total of 173 
      patients with AML were enrolled in this study. The genetic expressional 
      information and clinical data sourced in previous studies were collected from the 
      Cancer Genome Atlas (TCGA) database. The expression profiles of 141 CAMs were 
      assessed, and the AML subgroups with specific patterns of expression were 
      identified. The outcomes and clinical features of each AML subgroup were compared 
      to detect the factors associated with prognosis. The differentially expressed 
      genes (DEGs) between each subgroup were identified and the prognostic roles of 
      those molecules were evaluated. RESULTS: According to subgroup clustering, both 
      the primary cluster_1 and subcluster_1 showed a favorable prognosis compared to 
      that of the other patients (26.3 vs. 17.0 months of overall survival (OS) and 
      46.5 vs. 15.8 months of OS, respectively). Both of the two subgroups were 
      characterized by depressed human leukocyte antigen (HLA) genes. Assessment of the 
      expression of prognosis-associated CAMs revealed that the expressions of SELE, 
      NRCAM, ITGA4, and SDC1 were positively correlated with AML prognosis, while the 
      expression of L1CAM, PDCD1, CD276, SELPLG, and CLDN14 were negatively correlated 
      with AML. Among the abovementioned genes, we detected that the individual gene 
      expressions of NRCAM and VCAM1 were capable of independently predicting OS, and 
      the OS was correlated with CAMs closely enough to enable the construction of 
      models for prognosis prediction [area under the curve (AUC) =0.78 and AUC=0.77, 
      respectively]. CONCLUSIONS: This study showed a landscape of the expression of 
      CAMs in AML and identified a distinct subgroup with a significantly favorable 
      prognosis. We detected that CAMs can assist in distinguishing the cohort with 
      long term survival and constructed two models to predict the prognosis. Those 
      CAMs have the potential to be developed as therapy targets in the treatment of 
      AML.
CI  - 2020 Translational Cancer Research. All rights reserved.
FAU - Cheng, Jing
AU  - Cheng J
AD  - Department of Blood Transfusion, The First Affiliated Hospital of Soochow 
      University, Suzhou, China.
FAU - Han, Juan
AU  - Han J
AD  - Department of Laboratory, 904th Hospital of Joint Logistic Support Force of PLA, 
      Suzhou, China.
FAU - Lin, Chunyan
AU  - Lin C
AD  - Department of Blood Transfusion, The First Affiliated Hospital of Soochow 
      University, Suzhou, China.
LA  - eng
PT  - Journal Article
PL  - China
TA  - Transl Cancer Res
JT  - Translational cancer research
JID - 101585958
PMC - PMC8798378
OTO - NOTNLM
OT  - Acute myeloid leukemia (AML)
OT  - cell adhesion molecules (CAMs)
OT  - prognosis
OT  - subgroup
COIS- Conflicts of Interest: All authors have completed the ICMJE uniform disclosure 
      form (available at http://dx.doi.org/10.21037/tcr-20-3315). The authors have no 
      conflicts of interest to declare.
EDAT- 2020/12/01 00:00
MHDA- 2020/12/01 00:01
PMCR- 2020/12/01
CRDT- 2022/02/04 05:51
PHST- 2020/11/03 00:00 [received]
PHST- 2020/12/15 00:00 [accepted]
PHST- 2022/02/04 05:51 [entrez]
PHST- 2020/12/01 00:00 [pubmed]
PHST- 2020/12/01 00:01 [medline]
PHST- 2020/12/01 00:00 [pmc-release]
AID - tcr-09-12-7605 [pii]
AID - 10.21037/tcr-20-3315 [doi]
PST - ppublish
SO  - Transl Cancer Res. 2020 Dec;9(12):7605-7618. doi: 10.21037/tcr-20-3315.