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Research Paper

A nine-gene signature to improve prognosis prediction of colon carcinoma

, , , , , & show all
Pages 1021-1032 | Received 13 Oct 2020, Accepted 13 Mar 2021, Published online: 14 May 2021

Figures & data

Figure 1. Screening of candidate genes for the prognostic model

(a) The volcano diagram shows the differential genes in colon carcinoma patients in GSE39582; (b) LASSO coefficient in regression analysis; C Tuning parameter (lambda) in LASSO model selected through 10-fold cross validation.
Figure 1. Screening of candidate genes for the prognostic model

Table 1. Screening of survival-related genes via univariate COX regression

Table 2. The optimal multivariate COX regression model identified based on the AIC

Figure 2. The optimal 9 survival-related genes in multivariate COX regression analysis

Figure 2. The optimal 9 survival-related genes in multivariate COX regression analysis

Figure 3. Analysis of the prognostic performance of the 9-gene model in the training dataset, testing dataset and TCGA-COAD independent dataset

A-B RFS curves of patients in the training dataset (a) and the testing dataset (b) drawn by Kaplan-Meier; C-E OS curves of patients in the high- and low-risk groups in the training dataset (c), testing dataset (d) and TCGA-COAD independent dataset (e) drawn by Kaplan-Meier; F-H ROC curves were plotted to testify the performance of the 9-gene model in predicting the prognosis of colon carcinoma patients in the training dataset (f), testing dataset (g) and TCGA-COAD independent dataset (h), respectively.
Figure 3. Analysis of the prognostic performance of the 9-gene model in the training dataset, testing dataset and TCGA-COAD independent dataset

Figure 4. The expression of the 9 model genes, the riskscore distribution and survival status of patients in the training dataset and testing dataset

A, B show the heatmap of the 9 model genes in patients in the training dataset (a) and the testing dataset (b); C, D present the riskscore distribution of patients in the training dataset (c) and the testing dataset (d); E, F display the survival status of patients in the training dataset (e) and the testing dataset (f); G, H, I suggest significant differences in ECM RECEPTOR INTERACTION (g), DNA REPLICATION (h), CELL CYCLE (i) pathways between high-risk group and low-risk group.
Figure 4. The expression of the 9 model genes, the riskscore distribution and survival status of patients in the training dataset and testing dataset

Table 3. Statistics of the basic clinical date of patients in the train dataset

Table 4. Statistics of the basic clinical data of patients in the test dataset

Figure 5. The prognostic performance of the 9-gene model in patients with different clinical subtypes in the training dataset and testing dataset

A-J The differences of OS in the high- and low-risk group in the training dataset and testing dataset (age>65 (a), age <65 (b), tumor stage I/II (c), tumor stage III/IV (d), T1&T2 (e), T3&T4 (f), N0&N1 (g), N2&N3 (h), M0 (i), M1 (j)) shown by Kaplan-Meier; K Nomogram quantitatively predicts the OS of patients.
Figure 5. The prognostic performance of the 9-gene model in patients with different clinical subtypes in the training dataset and testing dataset

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