This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: Triple-negative breast cancer (TNBC) is one of the most aggressive and treatment-resistant subtypes of breast cancer, accounting for 15% to 20% of all cases. Unlike other breast cancers, TNBC lacks targetable receptors, leaving patients dependent largely on chemotherapy, with limited treatment options.
Even immunotherapy—an approach that has transformed cancer treatment—benefits fewer than 20% of TNBC patients, largely because tumors contain large numbers of regulatory T cells (Tregs) that suppress the immune system and prevent it from effectively attacking cancer cells. A research team led by Professor Eijiro Miyako at the Institute of Multidisciplinary Research for Advanced Materials, Tohoku University, has developed a multifunctional nanoplatform called B-LM-DMX-αCD25 that simultaneously addresses three key barriers to effective TNBC immunotherapy. Their findings are published in the journal Advanced Science.
The platform uses gallium-based liquid metal nanoparticles, a photothermal material with a conversion efficiency exceeding 54%, coated with whole-blood components. This camouflage makes the particles appear as "self" to the body, allowing them to evade immune clearance and accumulate in tumors at five times the efficiency of conventional nanoparticles. Once at the tumor site, the platform deploys three synchronized therapeutic mechanisms.
First, anti-CD25 antibodies on the nanoparticle surface selectively eliminate intratumoral Tregs, releasing the "immunological brake" that suppresses anticancer immunity. Second, near-infrared laser irradiation heats the tumor to 58°C (136°F) within five minutes, destroying cancer cells and triggering immunogenic cell death. This process releases tumor antigens and danger signals that alert the immune system.
Third, the STING agonist DMX, released on demand by laser activation, activates innate immunity by promoting dendritic cell maturation and stimulating the production of interferon-β, which drives tumor-specific cytotoxic T cell responses. In preclinical studies using orthotopic mouse models of drug-resistant TNBC, the platform achieved 100% complete tumor regression, suppressed pulmonary metastases by more than 90%, and extended median survival beyond 70 days. Comprehensive molecular analysis confirmed robust immune activation, including a more than 13-fold increase in CD3-positive T cells and an 11-fold increase in dendritic cells within treated tumors.
The researchers' strategy addresses the immunosuppressive environment that makes TNBC difficult to treat by combining tumor destruction with targeted removal of Tregs and activation of innate immunity. By coordinating these three mechanisms, the platform converts an immunologically "cold" tumor environment into one that is more responsive to the immune system. The whole-blood camouflage strategy also provides a straightforward approach to biomimetic nanoparticle engineering.
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