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- W4312935967 abstract "Introduction: Pancreatic ductal adenocarcinoma (PDAC) is poised to become amongst the top three cause of deaths in cancer patients by 2030. Due to the biology of PC, current drug treatments usually lead to poor tumour response rates and early relapse. Hence, the discovery of potential new therapeutic targets by understanding underlying molecular pathways is essential. Investigating the gene expression patterns of signaling pathways utilizing samples obtained from South African PDAC patients, in order to better understand the cross-talk between these pathways and identify potential targets. Method: Tissue samples were obtained from 15 PDAC patients (Ethics number- M150778). From each patient, one tumour and one corresponding normal tissue was obtained. Real-time PCR was performed using both the RT2Profiler Human Growth factor and Signal Transduction pathway PCR arrays. Subsequently, the verification of Identified targets were verified by real-time PCR. Results: From the Growth factor array panel, we observed 48 upregulated and 10 downregulated genes in tumours. Similarly, the signaling pathway panel showed 56 upregulated and 10 downregulated genes in tumours. From these dysregulated genes, SPP-1 was verified to be significantly (p=0.00021) upregulated in tumour samples. Conclusion: SPP-1 has been reported to enhance cancer cell survival, angiogenesis and metastasis. The expression of SPP1 in PDAC tumours may hint at its possible involvement in tumourigenesis. Targeting SPP-1 gene may inhibit tumour progression providing a potential target for PDAC. Ongoing work aims to verify the expression and function of SPP-1 including its possible mechanism of action in PDAC progression." @default.
- W4312935967 created "2023-01-05" @default.
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- W4312935967 date "2022-01-01" @default.
- W4312935967 modified "2023-09-26" @default.
- W4312935967 title "SPP-1 is Overexpressed in Resected Pancreatic Ductal Adenocarcinoma (PDAC) Tumours" @default.
- W4312935967 doi "https://doi.org/10.1016/j.hpb.2022.05.547" @default.
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