The persistent failure of standard chemotherapy underscores the urgent need for innovative and targeted approaches in cancer treatment. Photodynamic therapy (PDT) has emerged as a promising photochemistry-based approach to address chemoresistance in cancer regimens. PDT not only induces cell death but also primes surviving cells, enhancing their susceptibility to subsequent therapies. This review explores the principles of PDT and discusses the concept of photodynamic priming (PDP), which augments the effectiveness of treatments like chemotherapy. Furthermore, the integration of nanotechnology for precise drug delivery at the right time and location and PDT optimization are examined. Ultimately, this study highlights the potential and limitations of PDT and PDP in cancer treatment paradigms, offering insights into future clinical applications.

This review describes nanoparticle and dye diffusion in bacterial biofilms in the context of antimicrobial photodynamic inactivation (aPDI). aPDI requires the diffusion of a photosensitizer (Sens) into the biofilm and subsequent photoactivation of oxygen for the generation of reactive oxygen species (ROS) that inactivate microbes. Molecular diffusion in biofilms has been long investigated, whereas this review is intended to draw a logical link between diffusion in biofilms and ROS, a combination that leads to the current state of aPDI and superhydrophobic aPDI (SH‐aPDI). This review should be of interest to photochemists, photobiologists and researchers in material and antimicrobial sciences as is ties together conventional aPDI with the emerging subject of SH‐aPDI.

Water conductivity sensing relies universally on electrical measurements, which are subject to corrosion of the electrodes and subsequent signal drift in prolonged in situ uses. Furthermore, they cannot provide contactless sensing or remote readout. To this end, a novel device for water conductivity monitoring has been developed by employing a microenvironment-sensitive ruthenium complex, [Ru(2,2′-bipyridine-4,4′-disulfonato)₃]⁴⁻, embedded into a quaternary ammonium functionalized cross-linked polymer support. The degree of swelling of the latter, which leads to a change in the emission lifetime, depends on the water conductivity. The sensor displays a reversible response (2 min ≤ t₉₀ ≤ 3 min) and has been shown to be stable for >65 h of continuous monitoring of 0.8–12.8 mS cm⁻¹ KCl solutions. Changes to the cation do not affect the sensor response, while changes to the anion type induce small effects. Variations in the dissolved O₂ or temperature require corrections of the response. The sensor can be interrogated alongside dissolved O₂ and pH luminescent sensors based on the same family of indicator dyes to exploit the definite advantages of luminescence lifetime-based detection.

The lack of robust and tunable redox reporters continues to hinder the development of high-performance electrochemical biosensors. In this work, we present a combined computational and experimental investigation of a family of water-compatible Os(II) complexes as pH-insensitive alternatives to the gold-standard methylene blue (MB). We systematically engineered, synthesized, and characterized, both computationally and electrochemically, four Os(II) polypyridyl complexes. We achieved a broad formal potential (E0′) range from 0.0 to +0.34 V vs Ag/AgCl, while maintaining fast, quasi-reversible one-electron behavior. These trends were reproduced by theoretical calculations and linked to systematic changes in the highest occupied molecular orbital (HOMO) energy/metal–ligand charge distribution. Covalent immobilization of the complexes onto carboxylated self-assembled monolayers on gold via amide coupling underscored their suitability as redox reporters in electrochemical biosensors. The redox potential remained pH-invariant from acidic to basic conditions, in contrast to the pronounced shifts observed for MB-derived probes. Stability under rapid and continuous electrochemical pulses by square-wave voltammetry was also assessed, with complexes 1, 2, and 4 displaying high stability after 200 scans in buffer compared to complex 3 and MB-based probes. Collectively, these results provide design rules and establish Os(II) complexes as modular redox reporters with on-demand features for advanced electrochemical sensors, including ratiometric and multiplexed sensing.

Pancreatic ductal adenocarcinoma (PDAC) exhibits early metastatic dissemination, dense desmoplastic stroma, and significant resistance to therapy. Our previous studies have shown that Photodynamic therapy (PDT) combined with chemotherapy reduces the incidence of distant metastases in immunodeficient mouse models of PDAC. Given the absence of functional T cells in these models, we wondered why a local treatment reduced distant metastases. We hypothesized that the innate immune mechanisms, particularly macrophages, mediate the antimetastatic effects of PDT-chemotherapy combinations. To test this hypothesis, orthotopic xenograft tumors derived from metastatic human AsPC-1 PDAC cells were established in nude Swiss mice, and PDT with nanoliposomal irinotecan (nal-IRI) was evaluated in both pre-metastatic and advanced metastatic stages. In the pre-metastatic setting, combination therapy resulted in significant tumor regression, decreased stromal collagen, and reprogramming of TAMs from immunosuppressive to a pro-inflammatory phenotype. It increased natural killer (NK) cell recruitment and granzyme B-mediated cytotoxicity. In the advanced metastatic model, in which treatment was initiated after metastasis was established, a similar dominance of pro-inflammatory macrophage polarization was observed compared to pretreatment. However, these effects were less pronounced than observed with early intervention. Given the lack of pronounced polarization effects with either monotherapy alone, these findings suggest that PDT, when combined with nal-IRI, induces antitumor and antimetastatic responses by remodeling innate immunity, even in the absence of adaptive T-cell activity. It also supports macrophage polarization as a key mechanism underlying PDT-irinotecan combination therapeutic increase both in local and distant tumor burden.