Triple Negative Breast Cancer

Here, we reported a doxorubicin (DOX)-Fe complex and RSL3 co-loaded liposomes (DOX-Fe/RSL3@LIPs) for ferroptosis-enhanced chemotherapy on TNBC tumors. The tumor cell ferroptosis was observably enhanced via supplements of the ferrous ions and H2O2, and RSL3-derived GPX4 inhibition to severely destroy the oxidation balance in cells. In this paper, the DOX-Fe/RSL3@LIPs have exerted a synergistic anticancer effect on TNBC by combining ferroptosis and conventional chemotherapy, and made a meaningful exploration of new strategies for TNBC therapy.

P=N/A, N=450, Not yet recruiting, Institut Curie | Trial completion date: Dec 2028 --> Aug 2031 | Trial primary completion date: Dec 2026 --> Aug 2031

Early clinical data demonstrated activity of BLU-222, a potent and selective CDK2 inhibitor, both as monotherapy (CCNE1 amplified) and in combination with ribociclib and fulvestrant in patients with HR+/HER2- breast cancer. These findings provide evidence that CDK2i combined with CDK4/6i can address multiple known mechanisms of resistance to CDK4/6i, enhancing antitumor responses in preclinical breast cancer models.

Critically, targeted knockdown of STEAP3 remarkably inhibited TNBC cells proliferation, migration and xenograft tumor growth. These findings unveil a critical pro-tumorigenic copper-driven pathway-distinct from cuproptosis-operating through STEAP3/copper/CDK16/JAK1 axis, and highlight STEAP3 as a promising therapeutic target for TNBC.

Here, we developed and characterized a phage-derived single-chain fragment variable (scFv) against a highly specific ROR1 region and generated scFv-derived chimeric monoclonal antibodies and anti-ROR1-CAR NK cells, which show anti-cancer efficacy against TNBC cells. Additionally, we found TGF-β inhibition using either small-molecule inhibitors or CRISPR-Cas9-edited NK cells could further enhance ROR1-targeting therapy persistence and efficacy in controlling TNBC tumor growth.

This study demonstrates the feasibility of localized tumor-normal sequencing in Nigerian BC patients, revealing actionable variants with clinical relevance. These findings highlight the need to integrate genomic profiling into routine cancer care and establish molecular tumor boards to advance precision oncology in Nigeria.

P1, N=180, Recruiting, Novartis Pharmaceuticals

P1, N=16, Completed, Providence Health & Services | Active, not recruiting --> Completed

While challenges remain in distinguishing Luminal B2, the use of BT imaging and AI demonstrates promise for refining molecular subtype assessment and improving clinical decision-making.Clinical Relevance-This study demonstrates that AI-driven analysis of digital breast tomosynthesis can capture tumor and microenvironment characteristics, providing valuable insights into disease staging and progression. By leveraging comprehensive imaging data rather than limited biopsy samples, this approach has the potential to improve non-invasive molecular subtyping, aiding personalized treatment decisions while reducing reliance on invasive procedures.

Overall, the features extracted from baseline data and follow-up data or after the first course of NAC, combined with information of breast cancer subtype, offer strong predictive value for pCR in follow-up patients.Clinical Relevance-By providing a more accurate assessment of treatment response after the first course of NAC, this approach empowers clinicians to make artificial intelligence-driven decisions, customize therapy plans for individual patients, and avoid ineffective treatments. Consequently, this strategy could improve patient outcomes and optimize therapeutic efficacy.

Silencing circEIF6 suppressed glycolysis, angiogenesis, and proliferation (P<0.05) by sponging miR-296-3p to downregulate MT2A. We conclude that circEIF6 promotes aerobic glycolysis and angiogenesis in TNBC via the miR-296-3p to target MT2A.

Understanding the mechanisms underlying BRCA1-mediated lineage plasticity offers novel therapeutic avenues to target early-stage tumor initiation and progression in BRCA1-mutated breast cancer. This review perspective sheds light on the role of BRCA1 in lineage plasticity and highlights probable mechanisms by which BRCA1 could promote this lineage plasticity.