For research use only
| Cat No. | ABC-TC0915 |
| Product Type | Human Pancreas Cancer Cell Lines |
| Cell Type | Epithelial |
| Species | Human |
| Growth Conditions | 37 ℃, 5% CO2 |
| Source Organ | Pancreas |
| Disease | Adenocarinoma |
| Product Code | PSN-1 |
PSN-1 pancreatic tumor cells show epithelial morphology, harbor c-myc and Ki-ras mutations, p53 loss; established via nude mouse xenograft for cancer.
PSN-1 is a human pancreatic adenocarcinoma cell line isolated from the pancreas of a patient with adenocarcinoma. PSN-1 exhibits typical epithelial morphology and adherent culture properties. It was established via xenografting of patient tumor tissue into nude mice, followed by in vitro derivation. PSN‑1 is distinguished by concurrent c-myc amplification (~50-fold) and activated c-Ki-ras amplification (3–6 fold), harboring a point mutation at codon 12 (GGT → CGT), reflecting retention of the original tumor genotype. It also shows loss of one p53 allele and a missense mutation in the remaining allele (codon 132 AAG → CAG), indicating disruption of tumor suppressor function. Increased c-myc and c-Ki-ras transcripts are also presented. PSN‑1 retains transcriptional upregulation of both c-myc and mutant Ki-ras, making it a genetically defined model for oncogenic signaling in pancreatic tumor biology.
| Product Code | PSN-1 |
| Species | Human |
| Cat.No | ABC-TC0915 |
| Product Category | Tumor Cell Lines |
| Size/Quantity | 1 vial |
| Cell Type | Epithelial |
| Growth Mode | Adherent |
| Shipping Info | Dry Ice |
| Growth Conditions | 37 ℃, 5% CO2 |
| Source Organ | Pancreas |
| Disease | Adenocarinoma |
| Biosafety Level | 1 |
| Storage | Liquid Nitrogen |
| Product Type | Human Pancreas Cancer Cell Lines |
PSN‑1 serves as an excellent in vitro model for investigating oncogenic signaling and therapeutic response in pancreatic adenocarcinoma, especially in contexts involving c-Myc and mutant KRAS pathways. It is routinely used in cytotoxicity assays, drug screening (e. g. irinotecan, topotecan), chemoradiation sensitivity studies, and evaluation of targeted inhibitors against Ras‑driven tumor progression. The defined genetic alterations of PSN-1 support mechanistic research into c-Myc and KRAS co-dependency and p53 pathway deficiency. The line enables robust assay reproducibility for high-throughput drug discovery, signalling pathway dissection, and validation of anti‑oncogene therapeutics in pancreatic cancer models.
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