Publications by authors named "Judith Jing Wen Wong"

The vitamin A metabolite all-trans retinoic acid (ATRA; tretinoin) has anticancer potential. However, lack of clinical success has prevented its approval for solid tumours. Herein, we propose combining short-term low-dose ATRA with fimaporfin-based photodynamic therapy (ATRA+PDT) for the improved treatment of solid cancers.

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The programmed death ligand-1 (PD-L1), also known as CD274 or B7-H1, is mainly expressed on cancer cells and/or immunosuppressive cells in the tumor microenvironment (TME) and plays an essential role in tumor progression and immune escape. Immune checkpoint inhibitors (ICIs) of the PD-1/PD-L1 axis have shown impressive clinical success, however, the majority of the patients do not respond to immune checkpoint therapy (ICT). Thus, to overcome ICT resistance there is a high need for potent and novel strategies that simultaneously target both tumor cells and immunosuppressive cells in the TME.

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Aldehyde dehydrogenases (ALDH) are detoxifying enzymes that are upregulated in cancer stem cells (CSCs) and may cause chemo- and ionizing radiation (IR) therapy resistance. By using the ALDEFLUOR assay, CD133 + human colon cancer cells HT-29, were FACSorted into three populations: ALDH, ALDH and unsorted (bulk) and treated with chemo-, radio- or photodynamic therapy (PDT) using the clinical relevant photosensitizer disulfonated tetraphenyl chlorin (TPCS/fimaporfin). Here we show that there is no difference in cytotoxic responses to TPCS-PDT in ALHD, ALDH or bulk cancer cells.

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Article Synopsis
  • This study explores how photochemical internalization (PCI) can potentially activate sunitinib, a cancer drug that accumulates in lysosomes, which is associated with drug resistance in colon cancer cells.
  • Using advanced microscopy, researchers found that sunitinib and a photosensitizer accumulated together in lysosomal membranes, and PCI enhanced the drug's effects in certain colon cancer cell lines.
  • However, while PCI reduced sunitinib accumulation in resistant cells, it did not overcome their resistance, nor did it significantly improve tumor growth outcomes in mouse models, indicating complex interactions at play in treatment efficacy.
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Background: Development of resistance to 5-fluorouracil (5-FU) is a major problem in treatment of various cancers including pancreatic cancer. In this study, we reveal important resistance mechanisms and photochemical strategies to overcome 5-FU resistance in pancreatic adenocarcinoma.

Methods: 5-FU resistant (5-FUR), epithelial-to-mesenchymal-like sub-clones of the wild type pancreatic cancer cell line Panc03.

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