Objective: This study investigates the efficacy of indocyanine green-mediated photodynamic therapy (PDT) in targeting MCF-7 breast cancer cells, a representative model of luminal A subtype, compared to healthy breast epithelial cells. Methods: MCF-7 cells and healthy breast cells were cultured in a three-dimensional (3D) hollow fiber bioreactor to mimic the tumor microenvironment in vivo. Cells were treated with ICG at concentrations ranging from 1 to 1000 μM and then photoactivated using a diode laser. Cell viability was assessed by trypan blue staining, and the production of reactive oxygen species (ROS), including singlet oxygen (¹O₂) was measured. Results: Cell viability, assessed via trypan blue exclusion, decreased dose-dependently with ICG concentrations (1–1000 μM), with MCF-7 viability dropping from 94.5% ± 0.8% at 0.1 μM to 15.83% ± 0.66% at 1000 μM, compared to healthy cells retaining >50% viability up to 500 μM (55.2% ± 2.0% at 1000 μM). Student’s t-tests confirmed significant differences (p < 0.05) between MCF-7 and control (0 μM) at all concentrations, and between MCF-7 and healthy cells, indicating selective cytotoxicity (IC₅₀: ~75 μM for MCF-7). Flow cytometry revealed MCF-7 cell concentrations were significantly lower than healthy cells’ across all ICG doses and seeding densities (p < 0.05). Spectroscopic analyses showed ICG absorption peaks at 800–900 nm, fluorescence at 800–820 nm, and singlet oxygen phosphorescence at 1270 nm, confirming effective ROS generation. Conclusions: Cell concentrations confirmed selective MCF-7 cytotoxicity (p < 0.05). Spectroscopic data validated ROS generation, supporting ICG-PDT’s potential as a selective therapy for early-stage breast cancer within a 50–500 μM therapeutic window.

Background/Aim: Photodynamic therapy uses a photosensitizer and light to generate reactive oxygen species that kill tumor cells and can shift inflammatory signaling. Hypericin is a potent photosensitizer, but its immunomodulatory impact in breast cancer needs clarification. We evaluated the phototoxic and cytokine-modulating effects of hypericin-mediated photodynamic therapy in MCF-7 human breast adenocarcinoma cells. This study examines how HYP-PDT affects MCF-7 breast cancer cells by assessing viability and cytokine secretion to guide the development of targeted, immune-enhancing PDT protocols. Methods: MCF-7 cells were incubated with hypericin at 0, 0.125, 0.25, 0.5, or 1 μM, then exposed to light doses of 0, 1, 2, or 5 J/cm². Viability was measured 24 h later by MTT; selected conditions were also assessed by Trypan Blue. Cell supernatants collected after sublethal treatment were analyzed for IL-6, IL-8, IL-10, and TNF-α using a multiplex immunoassay. Experiments were repeated four times. Statistical analyses followed the study’s plan for group comparisons. Results: At 1 J/cm², MTT values did not differ from matched dark controls across hypericin concentrations. At 2 and 5 J/cm², some conditions showed increased MTT signal relative to controls, indicating higher metabolic activity; Trypan Blue performed at 0 J/cm² showed a concentration-dependent reduction in viability with hypericin. Hypericin-PDT decreased IL-6 and IL-8 concentrations and increased TNF-α in MCF-7 supernatants. No statistically significant changes were detected for IL-10. Conclusions: Hypericin-PDT altered inflammatory readouts in MCF-7 cells, with reductions in IL-6 and IL-8 and an increase in TNF-α, consistent with a pro-inflammatory shift. Viability results suggest condition-dependent changes in metabolic activity or survival effects that warrant confirmation with matched cell counts across all light doses. These findings support further standardized dosimetry and multi-line validation of hypericin-PDT in breast cancer models.

Gliomas account for 24% of all the primary brain and Central Nervous System (CNS) tumors. These tumors are diverse in cellular origin, genetic profile, and morphology but collectively have one of the most dismal prognoses of all cancers. Work is constantly underway to discover a new effective form of glioma therapy. Photodynamic therapy (PDT) may be one of them. It involves the local or systemic application of a photosensitive compound—a photosensitizer (PS)—which accumulates in the affected tissues. Photosensitizer molecules absorb light of the appropriate wavelength, initiating the activation processes leading to the formation of reactive oxygen species and the selective destruction of inappropriate cells. Research focusing on the effective use of PDT in glioma therapy is already underway with promising results. In our work, we provide detailed insights into the molecular changes in glioma after photodynamic therapy. We describe a number of molecules that may contribute to the resistance of glioma cells to PDT, such as the adenosine triphosphate (ATP)-binding cassette efflux transporter G2, glutathione, ferrochelatase, heme oxygenase, and hypoxia-inducible factor 1. We identify molecular targets that can be used to improve the photosensitizer delivery to glioma cells, such as the epithelial growth factor receptor, neuropilin-1, low-density lipoprotein receptor, and neuropeptide Y receptors. We note that PDT can increase the expression of some molecules that reduce the effectiveness of therapy, such as Vascular endothelial growth factor (VEGF), glutamate, and nitric oxide. However, the scientific literature lacks clear data on the effects of PDT on many of the molecules described, and the available reports are often contradictory. In our work, we highlight the gaps in this knowledge and point to directions for further research that may enhance the efficacy of PDT in the treatment of glioma.

Bakuchiol (BAK), a natural meroterpenoid with antioxidant, anti-inflammatory and anticancer properties, has recently gained attention as a potential adjunct in breast cancer therapy. This review contextualizes breast cancer as a major global health challenge and highlights BAK as a bioactive compound capable of modulating pathways relevant to tumor development and progression. A structured literature search identified studies examining its molecular activity, pharmacological profile, and effects on breast cancer cells and stem cells. Results show that BAK influences oxidative stress regulation, mitochondrial function, apoptosis and estrogen receptor signaling while also affecting PI3K/AKT, MAPK, NF-κB, and EMT-related pathways. In breast cancer models, BAK acts as a selective phytoestrogen, induces S-phase arrest, activates the ATM/ATR–Chk1/Chk2 axis, and triggers mitochondrial apoptosis, particularly in ERα-positive cells. It also suppresses breast cancer stem-cell renewal, promotes BNIP3- and DAPK2-mediated apoptosis, reduces metabolic and transcriptional drivers of metastasis, and shows enhanced anticancer activity in derivative forms. These findings suggest that BAK may provide therapeutic benefit across several mechanisms central to breast cancer biology. In this review, the inclusion criteria encompassed publications describing the action of bakuchiol, its chemical and pharmacological properties, as well as its role in the treatment of various conditions, including cancers. Exclusion criteria included works not related to BAK or its therapeutic use in breast cancer, as well as publications that did not meet basic scientific standards, such as lacking methodological rigor or presenting a low level of scientific evidence. However, current evidence is predominantly in vitro, and limitations such as poor bioavailability and lack of clinical validation underscore the need for further in vivo and translational studies before therapeutic application can be established.

Breast cancer is one of the major health threats to women worldwide; thus, a need has arisen to reduce the number of instances and deaths through new methods of diagnostic monitoring and treatment. The present review is the synthesis of the recent clinical studies and technological advances in the application of magnetic resonance imaging (MRI) to monitor the pharmacological treatment of breast cancer. The specific focus is on high-risk groups (carriers of BRCA mutations and recipients of neoadjuvant chemotherapy) and the use of novel MRI methods (dynamic contrast-enhanced (DCE) MRI, diffusion-weighted imaging (DWI), and radiomics tools). All the reviewed studies show that MRI is more sensitive (up to 95%) and specific than conventional imaging in detecting malignancy particularly in dense breast tissue. Moreover, MRI can be used to assess the response and residual disease in a tumor early and accurately for personalized treatment, de-escalate unneeded interventions, and maximize positive outcomes. AI-based radiomics combined with deep-learning models also expand the ability to predict the therapeutic response and molecular subtypes, and can mitigate the risk of overfitting models when using complex methods of modeling. Other developments are hybrid PET/MRI, image guidance during surgery, margin assessment intraoperatively, three-dimensional surgical templates, and the utilization of MRI in surgery planning and reducing reoperation. Although economic factors will always play a role, the diagnostic and prognostic accuracy and capability to aid in targeted treatment makes MRI a key tool for modern breast cancer. The growing complement of MRI and novel curative approaches indicate that breast cancer patients may experience better survival and recuperation, fewer recurrences, and a better quality of life.