Additional file 1 of Distinct clinical and somatic mutational features of breast tumors with high-, low-, or non-expressing human epidermal growth factor receptor 2 status
Creators: name: Zhang, Guochun
name: Ren, Chongyang
name: Li, Cheukfai
name: Wang, Yulei
name: Chen, Bo
name: Wen, Lingzhu
name: Jia, Minghan
name: Li, Kai
name: Mok, Hsiaopei
name: Cao, Li
name: Chen, Xiaoqing
name: Lin, Jiali
name: Wei, Guangnan
name: Li, Yingzhi
name: Zhang, Yuchen
name: Balch, Charles M.
name: Liao, Ning
Publisher: name: figshare
Year: 2022
Subjects: subject: Space Science
subject: Medicine
subject: Cell Biology
subject: Genetics
subject: FOS: Biological sciences
subject: Biotechnology
subject: Biological Sciences not elsewhere classified
subject: Cancer

description: Additional file 1: Table S1. Mutations in other members of the HER family detected from our cohort. Figure S1. Somatic mutation landscape of the cohort. Figure S2. Comparison of mutational profile of the HER2 subgroups. Figure S3. Distribution of TP53 mutations among the HER2 subgroups. Figure S4. Distribution of PIK3CA mutations among the HER2 subgroups. Figure S5. Genes frequently mutated across HER2 subgroups according to hormone receptor (HR) status. Figure S6. Comparison of TP53 (A) and PIK3CA (B) mutation rates across HER2 subgroups according to hormone receptor (HR) status. Figure S7. Genes frequently mutated across immunohistochemistry-based molecular subgrouping between HER2-low and HER2-zero subgroups. TNBC, triple negative breast cancer. Figure S8. Comparison of TP53 (A) and PIK3CA (B) mutation rates between HER2-zero and HER2-low subgroups according to immunohistochemistry-based molecular subgrouping. Figure S9. Comparison of genes (top 11) and signaling pathways (top 5) differentially mutated between HER2-low and HER2-zero subgroups according to immunohistochemistry-based molecular subgrouping: A. triple negative breast cancer (TNBC), B. luminal A, and C. luminal B. Figure S10. Tumor mutational burden (TMB) were comparable across HER2 subgroups. TMB were not statistically different among patients with HER2-zero (IHC 0), HER2-low (IHC1+ or IHC 2+/FISH-negative), and HER2-positive (IHC 3+ or IHC 2+/FISH-positive) breast tumors. Figure S11. Distribution of ERBB/HER family mutations according to HER2 status. Figure S12. Molecular clustering across hormone receptor (HR) status (A) and immunohistochemistry-based molecular subgrouping (B). Figure S13. Pathological complete response (pCR) rate is comparable between HER2-low and HER2-zero subgroups across hormone receptor (HR) status (A-B) and immunohistochemistry-based molecular subgrouping (C-E). Figure S14. Disease-free survival (DFS) was comparable between women with HER2-low and HER2-zero tumors as shown by Kaplan-Meier survival plot of the whole cohort (A) and when considering only the relapsed patients per group (B). Figure S15. Disease-free survival (DFS) was comparable between HER2-zero and HER2-low subgroups regardless of pathological complete response (pCR) status. Figure S16. Disease-free survival (DFS) was comparable between HER2-zero and HER2-low subgroups regardless of hormone receptor (HR) status. Figure S17. Disease-free survival (DFS) was comparable between HER2-zero and HER2-low subgroups across immunohistochemistry-based molecular subgrouping.