Triple Negative Breast Cancer

Furthermore, spiegelmers can inhibit oncogenic microRNAs such as miR-155, offering new avenues for treating aggressive subtypes like triple-negative breast cancer. Despite challenges in synthesis and target range, spiegelmers represent a promising next-generation platform for theranostic applications that integrate precise diagnosis with personalized treatment, potentially revolutionizing breast cancer management.

Immunotherapy showed substantial benefits in improving pCR rates in both TNBC and HR+HER2- patients when combined with neoadjuvant chemotherapy, especially in lymph node-positive breast cancer patients.

Our findings demonstrate that clitocine exerts potent anti-TNBC effects by upregulating CCRL2 expression, thereby activating the clitocine/CCRL2/chemerin axis. This axis disrupts critical oncogenic signaling pathways and reprograms the immunosuppressive tumor microenvironment.

This study is the first to reveal that PA induces ferroptosis in TNBC cells by regulating the PTGS2/NOS2/ABCB1 signaling axis, providing new potential targets for TNBC treatment. However, this study has limitations, as validation has been conducted only at the cellular level and not yet confirmed in animal models or clinical samples. Future research should validate this mechanism in more TNBC models and across different molecular subtypes of breast cancer to promote the clinical application of PA.

These findings support the existence of greater variability in surrogate and intrinsic molecular subtypes within secretory carcinomas, providing potential personalized therapeutic strategies for the treatment of these patients.

Because pathway-causality was not tested using NF-κB rescue or pharmacological inhibition controls, the mechanistic conclusions are presented as supportive associations rather than definitive proof. Future studies should focus on bioassay-guided compound purification, synergistic combination assessment, and in vivo validation for translational advancement.

This study demonstrates, for the first time, the potential of FTIR imaging combined with AI to distinguish between HER2+ and TNBC subtypes directly from tissue sections. These findings highlight the relevance of spectral histopathology for rapid, nondestructive, and accurate breast cancer diagnosis, paving the way for integration into clinical workflows.

Furthermore, STC2 knockdown reduced anoikis-related apoptotic rates in an MDA-MB-231-based anoikis-mimic model in vitro. This study established an anoikis-related gene signature that may improve prognostic stratification and reflect immunotherapy-related features in TNBC.

Given the small sample size and the inclusion of immune checkpoint inhibitors in a subset of patients, all of whom achieved pCR, these observations should be considered strictly hypothesis-generating. Larger and more homogeneous cohorts will be required to validate these findings and to determine their potential clinical relevance.

We review the current epidemiologic, mechanistic, and clinical evidence on how the gut microbiome influences TNBC biology, with particular attention to the tumor immune microenvironment and response to therapy. We highlight protective and pro-tumorigenic microbial signatures, the impact of antibiotics and obesity, and emerging strategies, such as dietary modulation and microbiome-targeted interventions, that may ultimately be used to optimize TNBC management and improve patient outcomes.

Collectively, 2C6 couples photoinduced DNA damage to cytosolic dsDNA sensing, type I interferon signaling, and adaptive immune activation through a defined cascade encompassing DNA damage, dsDNA accumulation, cGAS-STING engagement, inflammatory signaling, and immune-cell infiltration. Together, these findings demonstrate that rationally engineered DNA-targeted photosensitizers can convert localized photodynamic tumor ablation into a systemic photoimmunotherapeutic response, providing a strategy to transform immunologically "cold" tumors into immune-responsive states.

To address this, a multifunctional nanoparticle, TPI@RPB, was constructed with RGD-PEG-BSA as the carrier for tumor-targeted delivery, while co-loading the self-synthesized endoplasmic reticulum (ER) target photosensitizer TSE-Ppa and Indoleamine 2,3-dioxygenase 1 (IDO-1) inhibitor 1-MT...In vivo, TPI@RPB not only demonstrates active tumor targeting but also significant antitumor efficacy with a favorable safety profile; specifically, tumor weight reduced to 13.70%, intratumoral CD8+ T-cell infiltration increased 1.92-fold, Treg cells decreased to 51.7%, and splenic effector-memory T cells increased 4.70-fold of control, with no observable systemic toxicity. These results suggest that ER-targeted PDT combined with IDO-1 blockade effectively remodels the tumor microenvironment and elicits durable antitumor immunity in TNBC.