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Center for Computational Systems Medicine
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Gene summary

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Literatures describing the association of the gene and immune escape mechanisms

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Comparison of the expression level between tumor and normal groups

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Comparison of the methylation level between tumor and normal groups

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Summary of the copy number in TCGA tumor samples

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The differentially expressed genes (DEGs) and enrichment analysis between mutated and wild type groups

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Expression and mutation differences between non-responders and responders after immunotherapy

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Correlation between the gene expression, copy number, methylation and tumor infiltrating lymphocytes

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The association between gene expression and immune subtypes/status

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Drug-gene interaction and disease-gene association

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Survival analysis based on gene expression

Gene summary for CDCA8

icon Gene summary
Gene Symbol

CDCA8

Gene ID

55143

Gene namecell division cycle associated 8
SynonymsDASRAB;BOR;MESRGP;FLJ12042
Type of geneprotein_coding
UniProtAcc

Q53HL2


icon Gene ontology (Biological Process only)
GO IDGO term
GO:0007049cell cycle
GO:0051301cell division
GO:0007080mitotic metaphase plate congression
GO:0051276chromosome organization
GO:0000281mitotic cytokinesis
GO:0000278mitotic cell cycle
GO:0051256mitotic spindle midzone assembly
GO:0090267positive regulation of mitotic cell cycle spindle assembly checkpoint
GO:0090307mitotic spindle assembly
GO:1901970positive regulation of mitotic sister chromatid separation
GO:1902425positive regulation of attachment of mitotic spindle microtubules to kinetochore
GO:1903490positive regulation of mitotic cytokinesis
GO:0000070mitotic sister chromatid segregation

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Literatures describing the association of CDCA8 and immune escape mechanisms

icon The table presents literature evidences demonstrating the involvement of CDCA8 in cancer immune escape mechanisms.

IconPMIDCancer TypeMechanismEvidence Sentences
Inhibiting_recruitment_of_dendritic_cells36855818Hepatocellular carcinomaInhibiting recruitment of dendritic cellsWe observed a direct link between CDCA8 levels and Th2 and T helper cells, and a negative link between CDCA8 levels and dendritic cells (DC), neutrophils, cytotoxic cells, and CD8 T cells.

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Comparison of the CDCA8 expression level between tumor and normal groups

icon Gene expression level in TCGA (Tumor vs Normal). The threshold for adjusted p-value is shown as : ***, padj < 0.001; **: 0.001 < padj < 0.01; 0.01 < padj < 0.05; NS: padj > 0.05. (Click on the image to enlarge it in a new window.)


icon The table shows the significant results for TCGA cancers with (adjusted P value < 0.05) and (|logFC| > 1).

Cancer typeLog2FoldChangeP valueAdjusted P value
LUSC3.82e+004.88e-2445.14e-241
BRCA3.03e+001.48e-1675.73e-165
UCEC3.57e+008.31e-1063.22e-102
LUAD3.03e+003.13e-911.26e-88
LIHC3.17e+004.97e-713.37e-68
HNSC1.44e+004.60e-374.66e-35
KIRC1.47e+006.72e-328.11e-31
COAD1.05e+005.54e-261.12e-24
BLCA2.31e+001.74e-256.97e-23
GBM4.09e+003.46e-235.72e-21
PRAD1.23e+001.71e-226.16e-21
CHOL3.52e+005.47e-213.14e-19
KIRP1.71e+004.47e-191.03e-17
STAD1.36e+001.56e-187.03e-17
ESCA1.86e+002.15e-164.54e-14
KICH1.36e+005.75e-082.49e-07

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Comparison of the CDCA8 methylation level between tumor and normal groups

icon The boxplot shows the mean beta value in normal and tumor group, and the dotplot shows the correlation between methylation level and expression level. Methylation level of the promoter region using TCGA data. The promoter regions were defined as the genomic regions spanning 2000 base pairs upstream and 500 base pairs downstream of the transcription start sites of genes. The average methylation value across all CpG sites within its promoter region was calculated to obtain the gene-level methylation value.


icon The table shows the significant results for TCGA cancers with (adjusted P value < 0.05) and (|diff_beta| > 0.1).

No significant differences were found in CDCA8 methylation in promoter region.


icon Methylation level of the genebody region using TCGA data. The genebody regions were defined from 500 base pairs downstream of the transcription start site to the transcription end site.


icon The table shows the significant results for TCGA cancers with (adjusted P value < 0.05) and (|diff_beta| > 0.1).

No significant differences were found in CDCA8 methylation in genebody region.


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Summary of the copy number in TCGA tumor samples

icon The gene level copy number is annotated as: 0: homozygous deletion; 1: deletion leading to LOH; 2: wild type, including copy-neutral LOH; 3/4: minor gain; 5-8: moderate gain; >=9: high-level amplification, as referenced in [1].

all structure

icon The violin plot shows the correlation between copy number and expression level.


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DEGs and the enrichment analysis between the mutated and wild type groups

icon For each cancer type in TCGA, if samples in the mutated group are no less than 5, we performed the differential gene expression analysis. The table shows DEGs with (adjusted p-value < 0.05) and (|logFC| > 1). Then we performed the KEGG, GOBP and Hallmark enrichment analysis for up-regulated and down-regulated DEGs separately (logFC > 1 means the gene is upregulated in the mutated group).


Gene IDSymbolLog2 Fold ChangeP-valueAdjusted P-value
ENSG00000284309NA-3.84e+001.25e-033.28e-02
ENSG00000272763RP11-357H14.17-2.64e+001.25e-033.28e-02
ENSG00000130383FUT5-3.91e+001.25e-033.28e-02
ENSG00000265962GACAT2-4.59e+001.25e-033.29e-02
ENSG00000162994CLHC1-1.02e+001.26e-033.29e-02
ENSG00000143850PLEKHA6-1.31e+001.26e-033.29e-02
ENSG00000117595IRF6-1.01e+001.27e-033.30e-02
ENSG00000128536CDHR3-2.46e+001.26e-033.30e-02
ENSG00000166104RP11-299H22.3-2.91e+001.26e-033.30e-02
ENSG00000234327AC012146.71.11e+001.27e-033.30e-02
ENSG00000256870SLC5A8-4.19e+001.27e-033.31e-02
ENSG00000173376NDNF-2.07e+001.27e-033.31e-02
ENSG00000114547ROPN1B-2.54e+001.28e-033.32e-02
ENSG00000255545RP11-627G23.1-2.92e+001.28e-033.32e-02
ENSG00000287415NA-3.41e+001.29e-033.33e-02
ENSG00000131910NR0B2-3.76e+001.29e-033.33e-02
ENSG00000225439BOLA3-AS1-1.42e+001.29e-033.33e-02
ENSG00000253141CTB-164N12.1-3.24e+001.29e-033.34e-02
ENSG00000215478CES5AP1-3.41e+001.29e-033.34e-02
ENSG00000224153RP11-433C9.22.44e+001.30e-033.35e-02
Page: 1 2 ... 49 50 51 52 53 ... 70 71

Up-regulated KEGG pathways

KEGG pathways

Up-regulated GOBP pathways

GOBP pathways

Up-regulated Hallmark pathways

Hallmark pathways

Down-regulated KEGG pathways

KEGG pathways

Down-regulated GOBP pathways

GOBP pathways

Down-regulated Hallmark pathways

Hallmark pathways

Gene expression and mutation differences between non-responders and responders after immunotherapy

icon In ImmunEscpMap, we integrated 10 pre-calculated transcriptomic datasets, and 6 genomic datasets to study the response after immunotherapy [2, 3]. The figure shows the logFC and the -log10(p value) between non-responders and responders in different datasets. The significant results (p value < 0.05 and |logFC| > 1), including the detailed information of datasets are presented in the table.

ExpressionMutation
Gene expression differences between non-responders and responders after immunotherapyMutation differences between non-responders and responders after immunotherapy

icon Expression

No significant differences were found in CDCA8 expression.


icon Mutation

No significant differences were found in CDCA8 mutation.


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Correlation between the composition of TIL and gene expression, methylation and CNV

icon The clustered correlation matrix shows the association between the abundance of TIL subpopulations [4] and gene expression, methylation and copy number level. Users can check if the pattern is similar across cancer types or TIL subtypes. The value of each cell represents the spearman correlation of gene expression and an immune cell subtype within one TCGA cancer type. Only cells with p-values < 0.05 were colored, while non-significant correlations were set to NA and displayed as white cells.

ExpressionCopy number variation
Correlation between the abundance of tumor-infiltrating lymphocytes and gene expressionCorrelation between the abundance of tumor-infiltrating lymphocytes and copy number variation
Promoter methylationGenebody methylation
Correlation between the abundance of tumor-infiltrating lymphocytes and methylation in promoter regionCorrelation between the abundance of tumor-infiltrating lymphocytes and methylation in genebody region

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The association between CDCA8 expression and immune subtypes/status

icon Thorsson et al identified six immune subtypes: Wound Healing, IFN-gamma Dominant, Inflammatory, Lymphocyte Depleted, Immunologically Quiet, and TGF-b Dominant [5]. Zapata et al classified tumors as immune edited when antigenic mutations were removed by negative selection and immune escaped when antigenicity was covered up by aberrant immune modulation. In addition, they used immune dN/dS, the ratio of nonsynonymous to synonymous mutations in the immunopeptidome, to measure immune selection [6]. Cortes-Ciriano et al investigated the microsatellite instability (MSI) status, which is related to the antitumour immune responses [7]. The expression level was compared among immune subtype/status.


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Drugs targeting CDCA8 and diseases related to CDCA8.

icon The drug-gene interactions are extracted from the Drug-Gene Interaction Database (DGIdb, https://dgidb.org) 5.0 [8], while the disease-gene associations are obtained from Diseases 2.0 (https://diseases.jensenlab.org/Search), which collects disease-gene associations from curated databases, genome-wide association studies (GWAS) and automatic text mining of the biomedical literature [9].

Drug-gene interactionDisease-gene association

No drugs targeting CDCA8.

Disease-gene association

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Survival analysis based on CDCA8 expression

icon The Kaplan-Meir curves reflects the association of gene expression with overall survival across different cancers. The significance (p value) is assessed by log-rank test.


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Reference
[1] Steele CD, Abbasi A, Islam SMA, et al. Signatures of copy number alterations in human cancer. Nature. 2022 Jun;606(7916):984-991. doi: 10.1038/s41586-022-04738-6. Epub 2022 Jun 15. PMID: 35705804; PMCID: PMC9242861.
[2] Beibei Ru, Ching Ngar Wong, Yin Tong, et al. TISIDB: an integrated repository portal for tumor–immune system interactions, Bioinformatics, Volume 35, Issue 20, October 2019, Pages 4200–4202, https://doi.org/10.1093/bioinformatics/btz210.
[3] Zhongyang Liu, Jiale Liu, Xinyue Liu, et al. CTR–DB, an omnibus for patient-derived gene expression signatures correlated with cancer drug response, Nucleic Acids Research, Volume 50, Issue D1, 7 January 2022, Pages D1184–D1199, https://doi.org/10.1093/nar/gkab860.
[4] Charoentong P, Finotello F, Angelova M, et al. Pan-cancer Immunogenomic Analyses Reveal Genotype-Immunophenotype Relationships and Predictors of Response to Checkpoint Blockade. Cell Rep. 2017 Jan 3;18(1):248–262. doi: 10.1016/j.celrep.2016.12.019. PMID: 28052254.
[5] Thorsson V, Gibbs DL, Brown SD, et al. The Immune Landscape of Cancer. Immunity. 2018 Apr 17;48(4):812-830.e14. doi: 10.1016/j.immuni.2018.03.023. Epub 2018 Apr 5. Erratum in: Immunity. 2019 Aug 20;51(2):411-412. doi: 10.1016/j.immuni.2019.08.004. PMID: 29628290; PMCID: PMC5982584.
[6] Zapata L, Caravagna G, Williams MJ, et al. Immune selection determines tumor antigenicity and influences response to checkpoint inhibitors. Nat Genet. 2023 Mar;55(3):451-460. doi: 10.1038/s41588-023-01313-1. Epub 2023 Mar 9. PMID: 36894710; PMCID: PMC10011129.
[7] Cortes-Ciriano I, Lee S, Park WY, et al. A molecular portrait of microsatellite instability across multiple cancers. Nat Commun. 2017 Jun 6;8:15180. doi: 10.1038/ncomms15180. PMID: 28585546; PMCID: PMC5467167.
[8] Cannon M, Stevenson J, Stahl K, et al. DGIdb 5.0: rebuilding the drug-gene interaction database for precision medicine and drug discovery platforms. Nucleic Acids Res. 2024 Jan 5;52(D1):D1227-D1235. doi: 10.1093/nar/gkad1040. PMID: 37953380; PMCID: PMC10767982.
[9] Grissa D, Junge A, Oprea TI, Jensen LJ. Diseases 2.0: a weekly updated database of disease-gene associations from text mining and data integration. Database (Oxford). 2022 Mar 28;2022:baac019. doi: 10.1093/database/baac019. PMID: 35348648; PMCID: PMC9216524.