HER-2 overexpression

HER2-low status was associated with worse OS in breast cancer patients with certain negative prognostic factors compared with HER2-zero status. Additionally, HER2-low1+ and HER2-low2+/ISH(-) subgroups predominantly exhibited HR+ status.

This study establishes a fully automated CT-based deep learning pipeline for HER2 status prediction in unresectable GBC. Validation in larger, multi-institutional cohorts is warranted.

The molecular subtypes of breast cancer exhibited distinct multimodal ultrasonographic characteristics. Multimodal ultrasonography showed potential value for noninvasive prediction of breast cancer molecular subtypes and may provide auxiliary information for individualized therapeutic decision-making.

P2, N=63, Completed, City of Hope Medical Center | Active, not recruiting --> Completed

The patient underwent neoadjuvant chemothera- py, right-sided mastectomy, and trastuzumab therapy, achieving complete pathological regression (pCR) with no recur- rence after ten months of follow-up. Although the CASR p.Glu755Asp variant's pathogenic role is unproven, emerging evidence links CASR overexpression with hER2-positive breast cancers, promoting tumor progression via calcium- dependent signaling pathways (PI3K/AKt, MAPK). This case highlights the potential role of CASR as a low-penetrance susceptibility gene in breast cancer and supports further functional and genomic studies to clarify its clinical impact.

STARD10 promotes malignant progression of HER2+ breast cancer and lipid droplets accumulation by activating the cAMP/PKA/CREB1 pathway. These findings suggest that STARD10 and the cAMP/PKA/CREB1 signaling axis as potential therapeutic targets for the treatment and prevention of HER2+ breast cancer.

P2, N=8, Active, not recruiting, H. Lee Moffitt Cancer Center and Research Institute | Recruiting --> Active, not recruiting | N=36 --> 8

A cross-tumor perspective contrasts GC/GEJ testing and biology with the breast cancer paradigm and summarizes the importance of HER2-low expression in non-gastric malignancies. Finally, we discuss the therapeutic strategies in HER2-low GC/GEJ and highlight key safety and monitoring considerations for HER2-directed ADCs.

However, clinical implementation requires greater methodological standardization, validated predictive biomarkers, accessible diagnostic platforms, and dynamic monitoring strategies capable of capturing subtype evolution under therapeutic pressure. TNBC should therefore not be regarded as a single disease, but as a spectrum of biologically distinct and clinically evolving entities whose integrated characterization may be essential to improving outcomes in this historically poor-prognosis population.

Together, these findings establish GRN-300 as a promising therapeutic agent that enhances paclitaxel efficacy through complementary disruption of mitotic regulatory pathways, providing strong preclinical rationale for clinical development in TNBC.

HER2 DISH advantages included the ability of pathologists to directly score slides in correlation with morphology and immunohistochemistry, improved turnaround time, and greater automation for high-volume HER2 testing, as compared with FISH. In summary, we found HER2 DISH to be an accurate and practical alternative.

PLD demonstrated modest efficacy in metastatic BC lacking HER2 overexpression, with comparable outcomes in HER2-low and HER2-negative subgroups. These findings suggest that HER2-low status does not predict anthracycline benefit and support the view that HER2-low is unlikely to represent a distinct therapeutic subtype. Further research is needed to refine treatment selection in this heterogeneous population.