Prof. Jakub Golab Profile

Prof. Jakub Golab

at Medical Univ of Warsaw

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Publications (2)

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Proceedings Article | 14 August 2019 Presentation

Photochemical internalization (PCI) of bleomycin induces T-cell activation of importance for curative effect and systemic anti-tumor immunity (Conference Presentation)

Kristian Berg, Ane Sofie Fremstedal, Anette Weyergang, Jakub Golab, Ole-Jacob Norum

Proceedings Volume 11070, 110702P (2019) https://doi.org/10.1117/12.2526088

KEYWORDS: Tumors, Colon, Semiconductor lasers, Spleen

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Photochemical internalization (PCI) is a technology to enhance intracellular drug delivery by light-induced translocation of endocytosed therapeutics into the cytosol. The aim of this study was to explore the efficacy of PCI-based delivery of bleomycin and the impact on systemic anti-tumor immunity. Mouse colon carcinoma cells (CT26.CL25), stably expressing the bacterial β-galactosidase, were inoculated into the legs of athymic or immuno-competent BALB/c mice strains. The mice were injected with the photosensitizer AlPcS2a and bleomycin (BLM) prior to tumor light exposure from a 670 nm diode laser. Photochemical activation of BLM was found to induce synergistic inhibition of tumor growth as compared to the sum of the individual treatments. However, a curative effect was not observed in the athymic mice exposed to 30 J/cm2 of light while more than 90% of the thymic mice were cured after exposure to only 15 J/cm2 light. Cured thymic mice, re-challenged with CT26.CL25 tumor cells on the contralateral leg, rejected 57-100% of the tumor cells inoculated immediately and up to 2 months after the photochemical treatment. T-cells from the spleen of PCI-treated mice were found to inhibit the growth of CT26.CL25 cells in naïve thymic mice with a 60% rejection rate. The results show that treatment of CT26.CL25 tumors in thymic mice by PCI of BLM induces a systemic anti-tumor immunity.

Proceedings Article | 13 July 2009 Paper

Improvement of anti-tumor activity of photodynamic therapy through inhibition of cytoprotective mechanism in tumor cells

Dominika Nowis, Angelika Szokalska, Marcin Makowski, Magdalena Winiarska, Jakub Golab

Proceedings Volume 7380, 73804F (2009) https://doi.org/10.1117/12.822929

KEYWORDS: Proteins, Photodynamic therapy, Tumors, Cancer, Oxygen, Cell death, Oncology, Tissues, Macromolecules, In vivo imaging

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Photodynamic therapy (PDT) leads to oxidative damage of cellular macromolecules, including numerous proteins that undergo multiple modifications such as fragmentation, cross-linking and carbonylation that result in protein unfolding and aggregation. Several mechanisms are involved in the protective responses to PDT that include activation of transcription factors, heat shock proteins, antioxidant enzymes and antiapoptotic pathways. Identification of these cytoprotective mechanisms might result in the design of more effective combination strategies to improve the antitumor efficacy of PDT. By using various molecular biology approaches, including microarray-based technologies we have identified genes that are up-regulated following PDT. Subsequent experiments revealed that some of these gene products can become targets for the combined therapeutic regimens encompassing PDT and selective small-molecule inhibitors. These include superoxide dismutase (SOD-2), cyclooxygenase 2 (COX-2), heme oxygenase 1 (HO-1), and proteins engaged in signaling endoplasmatic reticulum (ER) stress and unfolded protein response (UPR). Since a major mechanism for elimination of carbonylated proteins is their degradation by proteasomes, we hypothesized that a combination of PDT with proteasome inhibitors might lead to accumulation of carbonylated proteins in ER, aggravated ER stress and potentiated cytotoxicity towards tumor cells. Indeed, we observed that incubation of tumor cells with three different proteasome inhibitors, including bortezomib, MG132 and PSI gave increased accumulation of carbonylated and ubiquitinated proteins in PDT-treated cells. Proteasome inhibitors effectively sensitized tumor cells to PDT-mediated cytotoxicity and augmented antitumor effects of PDT in vivo.

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