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3. System to Correct Toxic Expression with BERT and to Determine the Effect of the Attention Value

12. Melting Transition of Vortex Lattice in Point Vortex Systems

14. Neutral selection and clonal expansion during the development of colon cancer metastasis.

19. Modeling Relations Between Profiles and Texts

20. Emoticon-Based Emotion Analysis for Weibo Articles in Sentence Level

21. Cancer stem-like properties and gefitinib resistance are dependent on purine synthetic metabolism mediated by the mitochondrial enzyme MTHFD2

22. Distributed Representations for Words on Tables

23. Transient IGF-1R inhibition combined with osimertinib eradicates AXL-low expressing EGFR mutated lung cancer

24. Judgment of Slang Based on Character Feature and Feature Expression Based on Slang’s Context Feature

25. Refinement by Filtering Translation Candidates and Similarity Based Approach to Expand Emotion Tagged Corpus

26. Table Topic Models for Hidden Unit Estimation

29. Supplementary Figure Legend from Combined Therapy with Mutant-Selective EGFR Inhibitor and Met Kinase Inhibitor for Overcoming Erlotinib Resistance in EGFR-Mutant Lung Cancer

30. Supplementary Table 1 from Combined Therapy with Mutant-Selective EGFR Inhibitor and Met Kinase Inhibitor for Overcoming Erlotinib Resistance in EGFR-Mutant Lung Cancer

31. Supplementary Figure 5 from Combined Therapy with Mutant-Selective EGFR Inhibitor and Met Kinase Inhibitor for Overcoming Erlotinib Resistance in EGFR-Mutant Lung Cancer

32. Supplementary Figure 6 from Combined Therapy with Mutant-Selective EGFR Inhibitor and Met Kinase Inhibitor for Overcoming Erlotinib Resistance in EGFR-Mutant Lung Cancer

33. Supplementary Figure 1 from Combined Therapy with Mutant-Selective EGFR Inhibitor and Met Kinase Inhibitor for Overcoming Erlotinib Resistance in EGFR-Mutant Lung Cancer

34. Data from Combined Therapy with Mutant-Selective EGFR Inhibitor and Met Kinase Inhibitor for Overcoming Erlotinib Resistance in EGFR-Mutant Lung Cancer

35. Supplementary Figure 2 from Combined Therapy with Mutant-Selective EGFR Inhibitor and Met Kinase Inhibitor for Overcoming Erlotinib Resistance in EGFR-Mutant Lung Cancer

36. Supplementary Figure 3 from Combined Therapy with Mutant-Selective EGFR Inhibitor and Met Kinase Inhibitor for Overcoming Erlotinib Resistance in EGFR-Mutant Lung Cancer

37. Supplementary Figure 4 from Combined Therapy with Mutant-Selective EGFR Inhibitor and Met Kinase Inhibitor for Overcoming Erlotinib Resistance in EGFR-Mutant Lung Cancer

39. Extracting Corpus-Specific Strings by Using Suffix Arrays Enhanced with Longest Common Prefix

40. Unsupervised Analysis of Web Page Semantic Structures by Hierarchical Bayesian Modeling

42. A Joint Prediction Model for Multiple Emotions Analysis in Sentences

43. Relationship Between Personality Patterns and Harmfulness

44. Sup. Figure 4: Foretinib and nintedanib inhibited p TRK-A in KM12SM-ER cells more efficiently than that in KM12SM cells. from Foretinib Overcomes Entrectinib Resistance Associated with the NTRK1 G667C Mutation in NTRK1 Fusion–Positive Tumor Cells in a Brain Metastasis Model

45. Sup. Figure 3: Foretinib and nintedanib inhibited the TRK-A in the kinase inhibition profile assay. from Foretinib Overcomes Entrectinib Resistance Associated with the NTRK1 G667C Mutation in NTRK1 Fusion–Positive Tumor Cells in a Brain Metastasis Model

46. Sup. Figure 1: EGFP-Eluc gene transfection did not affect the sensitivity of KM12SM cells to entrectinib. from Foretinib Overcomes Entrectinib Resistance Associated with the NTRK1 G667C Mutation in NTRK1 Fusion–Positive Tumor Cells in a Brain Metastasis Model

47. Sup. Figure 7: Knockdown of NTRK1 but not of VEGFR-2 or MET inhibited the viability of KM12SM-ER cells in vitro. from Foretinib Overcomes Entrectinib Resistance Associated with the NTRK1 G667C Mutation in NTRK1 Fusion–Positive Tumor Cells in a Brain Metastasis Model

48. Sup. Figure 2: KM12SM-ER cells were resistant to treatment with 15mg/kg and 30mg/kg entrectinib in the brain metastasis-mimicking model. from Foretinib Overcomes Entrectinib Resistance Associated with the NTRK1 G667C Mutation in NTRK1 Fusion–Positive Tumor Cells in a Brain Metastasis Model

49. Sup. Figure 8: Foretinib treatment was feasible in the liver metastasis and brain metastasis-mimicking models obtained using KM12SM-ER cells. from Foretinib Overcomes Entrectinib Resistance Associated with the NTRK1 G667C Mutation in NTRK1 Fusion–Positive Tumor Cells in a Brain Metastasis Model

50. Sup. Figure 9: Foretinib treatment had no remarkable anti-angiogenic effect in the liver metastasis model or brain metastasis-mimicking model. from Foretinib Overcomes Entrectinib Resistance Associated with the NTRK1 G667C Mutation in NTRK1 Fusion–Positive Tumor Cells in a Brain Metastasis Model

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