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Additional file 2: Table S1-S4., Figure S1-S7. Table S1. List of genes in the 3DMed 150-gene panel. Table S2. HER2 mutations identified at baseline. Table S3. Clinical response to pyrotinib according to different HER2 mutation types. Table S4. The detected molecular alterations at baseline and progression. Fig. S1. HER2 mutational map at baseline. Green: receptor L domain; red: furin-like cysteine rich region; blue: growth factor receptor domain IV; yellow: protein tyrosine kinase. Fig. S2. Survival curves of pyrotinib treated HER2-mutated NSCLC patients according to baseline characteristics. (A, B) progression-free survival (PFS) and overall survival (OS) according to the ECOG performance status. PS represents ECOG performance score. (C, D) PFS and OS of pyrotinib treated patients with or without brain metastasis. mPFS, median progression-free survival; mOS, median overall survival; HR, hazard ratio; 95%CI, 95% confidence interval. Fig. S3 Objective response rate in pre-specific subgroups. Fig. S4 Survival curves of NSCLC patients treated with pyrotinib according to previous treatment. (A, B) progression-free survival (PFS) and overall survival (OS) according to the treatment lines of pyrotinib. (C, D) PFS and OS of patients according to the prior exposures to afatinib. mPFS, median progression-free survival; mOS, median overall survival; HR, hazard ratio; 95%CI, 95% confidence interval. Fig. S5 Survival curves of pyrotinib treated NSCLC patients with different HER2 mutation. mPFS, median progression-free survival; mOS, median overall survival; HR, hazard ratio; 95%CI, 95% confidence interval. Fig. S6 Survival curves of pyrotinib treated HER2-mutated NSCLC patients according to molecular characteristics. (A, B) progression-free survival and overall survival according to HER2 amplification. (C, D) PFS and OS of pyrotinib treated patients according to the occurrence of co-mutations in other driver genes. mPFS, median progression-free survival; mOS, median overall survival; HR, hazard ratio; 95%CI, 95% confidence interval. Fig. S7 Pyrotinib resistance in a patient with HER2 and EGFR amplification. CT scans were performed at baseline (2 weeks before starting pyrotinib), best response (2 months after starting pyrotinib) and disease progression (7 months after starting pyrotinib), respectively. Mm, millimeter.

Additional file 3.

Additional file 1: Supplementary Figure 1. CARMN is a valuable biomarker in distinguishing tumor from normal tissue. Supplementary Figure 2. CARMN regulates cell proliferation and cisplatin sensitivity of TNBC. Supplementary Figure 3. RNA-seq indicates CARMN participating in essential cancer related pathways. Supplementary Figure 4. CARMN participates in DNA replication and downregulates DNA replication related genes. Supplementary Figure 5. CARMN suppression causes suppressed DNA replication and altered cell cycle distribution in TNBC. Supplementary Figure 6. MiR143-3p inhibits proliferation and cisplatin sensitivity in TNBC. Supplementary Figure 7. Confirmation of CARMN/miR143-3p/MCM5 axis in normal breast epithelium cell line MCF10A. Supplementary Figure 8. CARMN exon5 inhibits TNBC cell proliferation and promotes cisplatin sensitivity. Supplementary Figure 9. MCM5 promotes TNBC cell proliferation and decreases cisplatin sensitivity. Supplementary Figure 10. MiR143-3p and MCM5 are both prognostic factors of breast cancer and TNBC.

Additional file 2: Supplementary Table 1. Primers of qRT-PCR. Supplementary Table 2. Sequence of siRNAs, miR143-3p inhibitor and miR-143-3p mimics. Supplementary Table 3. miRNAs predicted to bind with MCM5.

The anti-fouling poly (vinyl alcohol) TFC membranes were dynamically prepared when an aqueous solution containing poly (vinyl alcohol), cross-linking agents and additives passed through porous substrate membranes under definite pressure followed by heat treatment resulting in cross-linking reaction and drying. By means of dead-end filtration the poly (vinyl alcohol) solution deposited on the surface and entered the pores of porous substrate and thus an even poly (vinyl alcohol) gel layer was formed on both the external and internal surface. The effects of poly (vinyl alcohol) concentration, dynamic coating time, additive concentration, cross-linking agent concentration, curing time and support membrane on pure water flux and protein rejection of the resultant membranes were studied. Membrane morphology was characterized by SEM studies. The modified membranes were investigated in ultrafiltration experiments with pepsin to assess their resistance to fouling. The experimental results prove that modified membranes with an even poly (vinyl alcohol) hydrogel layer show dramatically high anti-fouling characteristics compared to inadequately modified and unmodified membranes. Moreover, it is possible that a series of dynamic membranes within broader molecular weight cut-off can be readily obtained by suitable control and combination of various preparative conditions.