Publications by authors named "G Tigyi"
The autotaxin-lysophosphatidic acid receptor (ATX-LPAR) signaling axis is pivotal in various clinical conditions, including cancer and autoimmune disorders. This axis promotes tumorigenicity by interacting with the tumor microenvironment, facilitating metastasis, and conceding antitumor immunity, thereby fostering resistance to conventional cancer therapies. Recent studies highlight the promise of ATX/LPAR inhibitors in combination with conventional chemotherapeutic drugs to overcome some forms of this resistance, representing a novel therapeutic strategy.
View Article and Find Full Text PDFDeoxyhypusine synthase (DHPS) is an enzyme encoded by the DHPS gene, with high expression in various cancers, including ovarian cancer (OC). DHPS regulates the translation initiation factor EIF5A, and EIF5A2 knockout inhibits OC tumor growth and metastasis by blocking the epithelial-to-mesenchymal transition (EMT) and the TGFβ pathway. In this study, we show that DHPS is amplified in OC patients, and its elevated expression correlates with poor survival.
View Article and Find Full Text PDFArticle Synopsis
- Autotaxin (ATX) is an enzyme that produces lysophosphatidic acid (LPA), which influences cancer spread, treatment resistance, and immune responses in tumors.
- Researchers discovered that myeloid cells in melanoma biopsies highly express ATX and studied its effect on tumor immunity in two melanoma models (spontaneous and experimental).
- Knockout of ATX in specific myeloid cells reduced melanoma metastasis by over 50%, revealing important immune differences in the tumor environment that change depending on the type of model used.
The development of drug resistance in cancer cells poses a significant challenge for treatment, with nearly 90% of cancer-related deaths attributed to it. Over 50% of ovarian cancer patients and 30-40% of breast cancer patients exhibit resistance to therapies such as Taxol. Previous literature has shown that cytotoxic cancer therapies and ionizing radiation damage tumors, prompting cancer cells to exploit the autotaxin (ATX)-lysophosphatidic acid (LPA)-lysophosphatidic acid receptor (LPAR) signaling axis to enhance survival pathways, thus reducing treatment efficacy.
View Article and Find Full Text PDFArticle Synopsis
- Immune checkpoint inhibitors (ICIs) are effective for treating metastatic melanoma, but about 50% of patients show poor responses, often linked to low HLA-DR levels in tumors.
- The study highlights how lysophosphatidic acid (LPA), abundant in melanoma, increases IL-10 release and negatively impacts HLA-DR expression through the LPAR1-DR6 pathway.
- A significant correlation was found between the expression of LPAR1, DR6, and IL-10 in melanoma tissues, suggesting this pathway may contribute to tumor cells' ability to evade immune detection and compromise ICI therapy effectiveness.