7 research outputs found
Additional file 1: of Genomics of NSCLC patients both affirm PD-L1 expression and predict their clinical responses to anti-PD-1 immunotherapy
Table S1. Molecules with immunosuppressive functions used in simulation models to predict PD-1 drug responder status. (DOCX 55Â kb
Additional file 8: of Genomics of NSCLC patients both affirm PD-L1 expression and predict their clinical responses to anti-PD-1 immunotherapy
Table S6. Comparisons of clinical and predicated responses and match scores. We used a cross-validation approach to assess the match scores in Table 1 of the PD-1 predicted responses against the PD-1 clinical responses in the Rizvi et al. 2015 Discovery dataset vs. the Validation dataset. We then pooled and re-partitioned the dataset into two new Training and Test datasets. We then used a similar cross-validation approach to assess the match scores of the PD-1 predicted responses vs. the PD-1 clinical responses. (DOCX 17Â kb
Additional file 6: of Genomics of NSCLC patients both affirm PD-L1 expression and predict their clinical responses to anti-PD-1 immunotherapy
Table S5. Analysis of the Discovery and Validation datasets was performed using Weka 3. The first number in each column represented the number of patient treatment responses correctly classified by the model. The second number represented the number of incorrectly classified patient treatment responses. The GOAL row at the bottom of each column described the number of correctly and incorrectly classified patients in the simulation models. The Test Set columns described the output from applying the model trained on the Discovery set to the Validation set. The âTest and Trainâ columns described test set accuracy (test set column) plus the training error (results obtained by applying the model to the training set, i.e. training error). (DOCX 19Â kb
Additional file 7: of Genomics of NSCLC patients both affirm PD-L1 expression and predict their clinical responses to anti-PD-1 immunotherapy
Figure S2. An example of the relationship between PD-L1 expression and predicted TGFB1 expression using Weka 3 algorithms for all patients in the dataset. Similar trends were seen when comparing the PD-L1 expression level to the other 13 predicted molecules. For this, the number of gene mutations identified for each patient ranged from 2 to 36 with a total of 264 unique genes between all patients. This categorical data was preprocessed and expanded into a gene vector of length 264 to represent each of the unique genes. For each gene in the vector, the data was represented in binary; a 1 was assigned if the patient had a mutation in this gene, a 0 otherwise. Two datasets, one including gene mutations (Molecules and Gene Mutations) and one without (Molecules), were both used to learn prediction models. The Discovery and Validation datasets were determined based on the split provided to allow for comparable results. The performance of a subset of these models on the testing and training sets for both Molecules and Molecules and Gene Mutations datasets are shown. The SMO support vector machine with a normalized polynomial kernel had the best performance when applied to the molecule dataset. This model correctly identified 24 out of 29 patients whereas the simulation models correctly identified 25 of 29. This was only a difference of one match between the two prediction methods. Still, several other methods, while not performing as well overall, were able to identify 9 patients in the test dataset accurately. This was near the computational simulation model prediction capability in which 10 patients were successfully identified in the test dataset. In general, adding the gene mutation data to the molecule data either maintained or decreased the performance of a model. (DOCX 4114Â kb
Additional file 2: of Genomics of NSCLC patients both affirm PD-L1 expression and predict their clinical responses to anti-PD-1 immunotherapy
Table S2. Individual mutational profiles of patient drug responders (n = 11) and nonresponders (n = 18). (DOCX 19 kb
Additional file 4: of Genomics of NSCLC patients both affirm PD-L1 expression and predict their clinical responses to anti-PD-1 immunotherapy
Supplementary Materials and Methods (DOCX 109Â kb
Additional file 5: of Genomics of NSCLC patients both affirm PD-L1 expression and predict their clinical responses to anti-PD-1 immunotherapy
Table S4. Creation of the dendritic cell infiltration index for the patient SA97V5-specific simulation model. Chemokines CCL11, CCL20, CCL2, CCL3, CCL4, CCL5, CCL7, CX3CL1, and CXCL14, capable of trafficking of dendritic cells into the tumor microenvironment, were used to create the index. Individual chemokine percent expression (with respect to non-tumorigenic baseline controls) was predicted and given weightage so as to normalize the total to 1. The index was then calculated to be the sum of each prediction % change * weightage. (DOCX 16Â kb