HER-2 expression

Our findings highlight triple negative HER2-low BC as a distinct subtype identifiable via standard immunohistochemistry, beyond just biomarker status. The study underscores the prognostic diversity among BC subtypes and emphasizes the importance of personalized treatment strategies.

AS601245, AP.24534 and roscovitine were the top three chemotherapeutic agents showing the highest sensitivity differences between the risk groups. The RT-qPCR results indicated that the expression of electron transfer flavoprotein subunit α, rap guanine nucleotide exchange factor-like 1, keratin 7, cluster of differentiation 24, proline rich 15-like, arachidonate 15-lipoxygenase type B, ELOVL fatty acid elongase 2 and C-X-C motif chemokine ligand 9 was consistent with the results of bioinformatic analysis. In conclusion, the HER2-related risk model and nomogram developed in the present study demonstrated high accuracy in predicting patient survival.

T-DXd is potentially a safe and effective treatment option for older patients with HER2-low breast cancer and for those with impaired ADL. Further accumulation of cases and investigations of long-term outcomes are warranted.

These findings validate the broader utility of the previously identified HER2/neu-specific TCR repertoire and elucidate the molecular mechanisms driving its therapeutic efficacy, demonstrating the potential of TCR-T cells for treating solid tumors through robust cytotoxic activity and the emergence of a favorable CD4+CD8+ T cell population. This study offers critical mechanistic insights, establishing a foundation for advancing TCR-engineered therapies toward clinical use in HER2/neu-positive cancers.

The strong co-expression of ALKBH7 and NLRP3 suggests a functional association between these molecules that may be critical in shaping the tumor microenvironment. This co-expression set, particularly in aggressive subtypes (HER2+ and TNBC), warrants further mechanistic validation as a potential prognostic marker and a novel therapeutic vulnerability.

P3, N=254, Active, not recruiting, Sichuan Kelun-Biotech Biopharmaceutical Co., Ltd. | Trial completion date: Mar 2025 --> Jun 2027

AI-assisted interpretation improved observer agreement (Kappa: 0.703 vs. 0.610 in non-amplified cases) and reduced ambiguous immunohistochemistry (IHC) 2+/0 assignments. These findings delineate distinct clinicopathological characteristics of HER2-ultralow/null tumors, highlight HER2 IHC reproducibility challenges, and validate AI as an effective tool for standardizing scoring to optimize patient selection for T-DXd therapy.

Both HER2 and ESR1 are determinant of KN026 efficacy in advanced HER2-positive breast cancer, implying the potential of KN026 combined with endocrine therapy in HER2- and ER-positive breast cancer.

This case underscores the importance of integrating histomorphological features, immunohistochemical profiles, and molecular biomarkers to distinguish TCCRP from other triple-negative breast carcinomas. Recognition of this indolent entity is critical for avoiding overtreatment and ensuring appropriate clinical management, given its favorable prognosis compared to conventional triple-negative breast cancers.

Similarly, in the external validation set, T2 values showed moderate diagnostic efficacy, with AUCs of 0.837, 0.808 and 0.835 for the respective comparisons. T2 quantification derived from SyMRI shows promise as a noninvasive biomarker for identifying HER2-low-expressing breast cancer, supporting its potential role in guiding individualized treatment strategies.

By integrating clinical data and advanced MRI features, this model provides accurate predictions, improving personalized treatment strategies. Further validation in larger, multicenter studies is necessary to confirm its generalizability and clinical applicability.

HER2 heterogeneity is present in both primary breast cancer and liver metastases. Ongoing monitoring of molecular markers, particularly HER2 expression, remains essential for breast cancer patients, as it may provide opportunities for therapeutic intervention.