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The probe plays a pivotal role in the early diagnosis of tumor, especially tumor microenvironment (TME)-responsive probe, which could exploit differences between tumor and normal tissue to achieve better signal-to-noise ratio. In view of overexpressed glutathione (GSH) in microenvironment considered as one of the important characteristics of tumor distinct from normal tissue, we constructed a GSH activated near-infrared fluorescent (NIRF) and photoacoustic (PA) dual-modal probe (Probe-GSH) based on the hybrid of xanthene-based hemicyanines and dicyanoisophorone. The activated Probe-GSH could exhibit 8-fold PA signal/10-fold NIRF intensity enhancement. Besides, compared with the existing xanthene-based hemicyanines (XBH), Probe-GSH possessed longer absorbance/emission wavelength and larger Stokes shift. More importantly, Probe-GSH has been successfully applied to the image of 4T1-bearing tumor mice under NIRF and PA dual modality. [Display omitted] • Compared with the reported xanthene-based hemicyanines, Probe-GSH possess longer the absorbance/ emission wavelength. • Compared with the reported xanthene-based hemicyanines, Probe-GSH has larger Stokes shift. • Probe-GSH was capable for imaging of tumor mouse under NIRF and PA dual modality image. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor, characterized by high heterogeneity, strong invasiveness, poor prognosis, and a low survival rate. A broad range of nanoparticles have been recently developed as drug delivery systems for GBM therapy owing to their inherent size effect and ability to cross the blood–brain barrier (BBB). Lipid-based nanoparticles (LBNPs), such as liposomes, solid lipid NPs (SLNs), and nano-structured lipid carriers (NLCs), have emerged as the most promising drug delivery system for the treatment of GBM because of their unique size, surface modification possibilities, and proven bio-safety. In this review, the main challenges of the current clinical treatment of GBM and the strategies on how novel LBNPs overcome them were explored. The application and progress of LBNP-based drug delivery systems in GBM chemotherapy, immunotherapy, and gene therapy in recent years were systematically reviewed, and the prospect of LBNPs for GBM treatment was discussed. [Display omitted] [ABSTRACT FROM AUTHOR]

M1 polarization of tumor-associated macrophages (TAMs) is a promising approach to breaking through therapeutic barriers imposed by the immunosuppressive tumor microenvironment (TME). As a clinically-used immunopotentiator for cancer patients after chemotherapies; however, the immunomodulatory mechanism and potential of polyporus polysaccharide (PPS) remains unclear. Here, we present mannose-decorated PPS-loaded superparamagnetic iron-based nanocomposites (Man/PPS-SPIONs) for synergistic M1 polarization of TAMs and consequent combinational anti-breast cancer therapy. Once internalized by M2-like TAMs, PPS released from Man/PPS-SPIONs induces the M1 polarization via IFN-γ secretion and downstream NF-κB pathway activating. The SPIONs within the nanocomposites mediate a Fenton reaction, producing OH· and activating the subsequent NF-κB/MAPK pathway, further facilitating the M1 polarization. The Man/PPS-SPIONs thereby establish a positive feedback loop of M1 polarization driven by the "IFN-γ-Fenton-NF-κB/MAPK" multi-pathway, leading to a series of anti-tumoral immunologic responses in the TME and holding promising potential in combinational anticancer therapies. Our study offers a new strategy to amplify TME engineering by combinational natural carbohydrate polymers and iron-based materials. [Display omitted] • Man/PPS-SPIONs exhibit tumor accumulation facilitated by an external magnetic field. • PPS and iron-based nanocarriers synergistically induce M1 polarization of TAMs. • The "IFN-γ-Fenton-NF-κB/MAPK" multi-pathway works for M1 polarization of TAMs. • Man/PPS-SPIONs created a favorable condition for celastrol-based therapy. • Man/PPS-SPIONs overcomes the limitations of celastrol in anti-tumor therapy. [ABSTRACT FROM AUTHOR]