In this single-center analysis, MMR-proficient/MS-stable cancers were a frequent cause of death among individuals with LS. MMR-D/MSI-H cancers resistant to immunotherapy and treatment-associated deaths were other significant contributors to mortality. Larger, multicenter studies are warranted to validate these findings.

We apply a NIR-IV photodynamic therapy, mediated by LaB6-PEG-folate nanoparticles using 2240 nm NIR light excitation, to generate reactive oxygen species, kill cancer cells, in situ produce whole cancer vaccines for priming of CD8+ T cells, and induce immunogenic responses in the presence of immunomodulator anti-OX40. A multifunctional anti-OX40 agonist could co-stimulate naive T cells to proliferate with tumor-recognizing properties, as well as suppress the activities of immunosuppressive Treg, and M2-phenotype macrophages, resulting in the complete disappearance of the primary melanoma tumor (that exposes to NIR light irradiation) as well as the effective suppression of remote/metastatic tumors' growths in the lung (that did not receive photo-irradiation).

Encouragingly, SB525334, a TGF-β inhibitor in OMV@PCB NPs, could significantly polarize NEs into anti-tumor N1 phenotype, which could not only promote neutrophil elastase (ELANE) release to selectively eliminate cancer cells, but also elevate anticancer immunity by reversing the immunosuppressive tumor microenvironment, thereby achieving effective immuno-photodynamic therapy against tumor growth. This study offers a prospective avenue for enhancing cancer therapy.

The IS + PIV dual-parameter model, by integrating local immune activity and systemic inflammatory status, accurately identifies NACI beneficiaries (high IS + low PIV) and high-risk patients (low IS + high PIV), providing an efficient prognostic tool for personalized treatment strategies.

Baseline MTV is preliminarily associated with PFS in sOM-NSCLC patients treated with immunotherapy, but results are exploratory and need prospective validation in larger cohorts.

The coordinated PANoptosis and cGAS-STING-mediated immune activation could reverse tumor immunosuppression, effectively suppressing primary tumor progression and metastatic dissemination. This combined bacteria-nanomaterial approach for inducing PANoptosis and stimulating innate immunity offers a promising new direction for precision cancer immunotherapy.

This dual metabolic system disrupts tumor self-protection against ROS by glycine depletion and enriches photosensitizers by functionalized-UCNPs, enabling self-reinforcing PDT. Additionally, it promotes ROS-mediated immunogenic cell death, dendritic cell activation, and M1 macrophage polarization, exhibiting robust antitumor growth and metastasis.

Using mZ-PD-L1, we achieve high-sensitivity and precise imaging of PD-L1 in microtumors (≤1 mm) and lymph node micrometastases, with imaging signal-to-background ratios as high as 27 and 37, respectively. This study provides a strategy to precisely and comprehensively evaluate PD-L1 in microtumors or micrometastases, significantly broadening the ICBT applications and offering a new method for personalized and precise ICBT.

Herein, we developed a mito-specific "Trojan Horse" nanoplatform (2-pN@LNPs) coloaded with Niclosamide (Nic) and 2-deoxy-d-glucose (2-DG) to attack key metabolism pathways and synergistically ignite pyroptosis for restoring antitumor immunity. Moreover, the synergistic treatment regimen can promote cytotoxic and helper T cells (CD8+/CD4+ T cells) recruitment and M1-type macrophage polarization, facilitating the establishment of a boost in immunological memory to prevent recurrence and metastasis. Overall, this work provides a robust strategy targeting metabolism through mitochondrial uncoupling and glycolysis inhibition, which can effectively improve the antitumor effect, inhibit lung metastasis, and help modulate antitumor immunity.

Compared to PTX or Lipusu® (PTX-Lipo), APS-PTX NPs increased cellular uptake by binding to high expressed glucose transporter of 4T1 cells, and synergistically enhanced cytotoxicity of PTX...In the TNBC model, APS-PTX NPs synergistically activates a potent systemic anti-tumor immunity, effectively inhibiting tumor growth and lung metastasis, and alleviating the reduction of white blood cell induced by PTX. Overall, the multifunctional nanoplatforms based on APS could overcome the harsh tumor biological barriers, and boost chemo-immunotherapy for TNBC treatment.

Taken together, these results support that longitudinal analysis of TME to generate multiomics data that can lead to rich insight into disease process and to provide clinical value in evaluating treatment responses. Trial registration number NCT04521179.

Our findings reveal cross-talk between the HBP, steroid hormone pathway, and tumor immune evasion, and suggest potential strategies for sensitizing UCEC to immunotherapy.