Alternative splicing generates HER2 isoform diversity underlying antibody–drug conjugate resistance in breast cancer

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Figure 3.
Figure 3.

Expression profiles of HER2 gene and splicing isoforms in breast cancer samples classified by immunohistochemistry status of HER2 and hormone receptor. (A,B) HER2 gene expression levels in HR+ (A) and HR− (B) breast cancer samples, stratified by HER2-high (red), HER2-low (green), and HER2-zero (blue) status. Mann–Whitney U test statistical significance: (*) P-value < 0.05, (***) P-value < 0.001, (****) P-value < 0.0001. (C,D) Expression profiles of the top 10 most-expressed HER2 isoforms in HR+ (C) and HR− (D) breast cancer samples, stratified by HER2 status. The canonical HER2 isoform is highlighted in bold. Expression levels are shown in log2(TPM + 1). (E,F) Dot plots showing the percentage of HR+ (E) and HR− (F) TCGA breast cancer samples expressing each HER2 isoform group (ISO 1–13), stratified by HER2 status: zero (blue), low (green), and high (red).

This Article

  1. Published in Advance July 15, 2025, doi: 10.1101/gr.280304.124 Genome Res. 35: 1942-1958

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