Triple Negative Breast Cancer

P=N/A, N=100, Recruiting, University of California, San Francisco | Not yet recruiting --> Recruiting

This noncanonical function of EZH2, which operates independently of its methyltransferase activity, is linked to enhanced tumor cell proliferation and inhibition of apoptosis. Our findings reveal that EZH2 functions in a chromatin context-dependent manner by cooperating with E2F1 in TNBC, highlighting that the EZH2-E2F1 interaction, independent of PRC2, plays a key role in remodeling chromatin structure and facilitating TNBC proliferation.

Our work establishes ALDH3A2 as a pivotal regulator of lipid metabolic reprogramming in TNBC metastasis, providing mechanistic insights into AA-mediated tumor progression. These findings position ALDH3A2 as a promising therapeutic target and prognostic biomarker for TNBC management.

The effect in Orai expression mediated by activation of Notch1 signaling pathway was mimicked by the expression of HEY1 or the non-phosphorylatable HEY1-S68A mutant; by contrast, expression of the phosphomimetic HEY1-S68D mutant was without effect on Orai expression. Understanding the Notch1-HEY1-Orai axis might provide insights into the development of subtype-specific therapeutic strategies targeting breast cancer.

Mechanistically, MBRT downregulated HIF-1α/VEGFR signaling, alleviating hypoxia and angiogenesis, and enhanced vascular normalization via increased pericyte coverage. These findings suggest MBRT reprograms the TNBC microenvironment, supporting its potential as a radiosensitizing strategy for clinical translation.

DEX treatment of an orthotopic mouse model of TNBC attenuated paclitaxel-mediated tumor growth inhibition, increased M2-like TAMs in primary tumors, and enhanced lung metastasis. Transcriptomic analysis of DEX-treated M1 macrophages revealed not only transcriptomic overlap with M2 macrophages, but also with human breast cancer TAM transcriptomic data, and further to a specific TAM signature associated with aggressive estrogen receptor-negative breast cancer. Our study illustrates a remarkable macrophage repolarization plasticity upon DEX exposure that can promote tumorigenesis, warranting care in prescribing high doses of GCs to breast cancer patients, especially to those considered for chemotherapy.

P=N/A, N=120, Recruiting, Fudan University

Finally, we further validated the biosafety profile and efficacy of platelet-CAR-T in a postsurgical patient-derived xenograft TNBC-bearing humanized mouse model. The results suggested that the CAR-T cell strengthened by platelet engineering is a promising adjuvant therapy against postsurgical tumor recurrence.

This study evidences a substantial shift towards SLNB as the primary axillary surgery following NAT during the study period. This trend emphasizes a preference for less invasive procedures, likely due to the efficacy of neoadjuvant therapy in reducing axillary lymph node involvement.

Rescue experiments showed that N-cadherin knockdown attenuated the effects of circ_0105487 overexpression on TNBC metastasis. In conclusion, circ_0105487 is an oncologic factor that promotes TNBC growth and metastasis and presents a novel therapeutic target for TNBC.

Parathyroid metastases from breast carcinoma are rare, although more frequent than primary malignancies of the parathyroid gland. This case highlights the need to consider metastatic involvement in cases of parathyroid adenoma, particularly in patients with a history of malignancy. Further research is warranted to elucidate the mechanisms underlying tumor-to-tumor metastases and to assess its impact on clinical management and prognosis.

P3, N=228, Recruiting, Sun Yat-sen University | Trial completion date: Dec 2025 --> Jul 2026 | Trial primary completion date: Jul 2025 --> Jun 2026