Panc 02.13 Xenograft Model Overview

The Panc 02.13 xenograft model is derived from a human pancreatic cancer cell line, Panc 02.13, established from a patient with pancreatic ductal adenocarcinoma (PDAC). PDAC is one of the deadliest cancers due to its aggressive nature, late-stage diagnosis, and resistance to most conventional therapies. The Panc 02.13 model is highly valuable for preclinical research in pancreatic cancer, offering a robust system to study tumor biology, metastasis, drug resistance, and therapeutic efficacy. Given its molecular characteristics and response to chemotherapy, the Panc 02.13 xenograft model is extensively used for evaluating novel drugs, including targeted therapies and combination treatments, that aim to overcome chemotherapy resistance and improve clinical outcomes for pancreatic cancer patients.

Request a Custom Quote for Panc 02.13 Xenograft Model

Biological and Molecular Characteristics

Panc 02.13 cells are characterized by their epithelial origin, similar to other PDAC cell lines, and express markers such as cytokeratins, epithelial membrane antigen (EMA), and CA19-9, a glycoprotein often elevated in pancreatic cancer patients. This model exhibits key molecular features associated with pancreatic cancer, including mutations in the KRAS oncogene, which is a hallmark of PDAC and contributes to tumor initiation, progression, and resistance to treatment. Additionally, Panc 02.13 cells show dysregulated signaling in the PI3K/AKT and MAPK pathways, both of which promote cell survival, proliferation, and tumor invasion. The model is also known for its ability to develop resistance to chemotherapy agents like gemcitabine, which makes it particularly useful for investigating the molecular mechanisms of resistance and testing novel agents that can sensitize tumors to chemotherapy.

Marker	Expression Level	Function
Cytokeratin	High	Epithelial cell marker
EMA	High	Epithelial membrane antigen
CA19-9	Elevated	Pancreatic cancer biomarker
KRAS	Mutated	Oncogene involved in tumor initiation and progression
PI3K/AKT pathway	Dysregulated	Promotes cell survival and proliferation

In Vivo Model Development and Tumorigenicity

The Panc 02.13 xenograft model is typically established by subcutaneously implanting Panc 02.13 cells into immunocompromised mice, such as NOD/SCID or NSG mice. Upon implantation, the cells form tumors that closely resemble human pancreatic ductal adenocarcinoma in terms of histology, growth patterns, and response to treatment. Panc 02.13 tumors are highly vascularized, reflecting the angiogenic properties of pancreatic tumors, and exhibit significant necrosis due to the rapid proliferation of tumor cells. The model is particularly useful for evaluating chemotherapy agents, such as gemcitabine and cisplatin, which are commonly used to treat PDAC, but also for testing new agents aimed at overcoming chemotherapy resistance.

In addition to subcutaneous implantation, orthotopic implantation of Panc 02.13 cells into the pancreas of immunocompromised mice can be performed to replicate the natural site of tumor growth. This orthotopic model provides a more clinically relevant setting for studying tumor progression, metastasis, and peritoneal dissemination. Panc 02.13 xenografts are capable of metastasizing to distant organs such as the liver, lungs, and peritoneum, which is a key feature of pancreatic cancer and further enhances the model’s relevance for evaluating new therapeutic strategies.

Request a Custom Quote for Panc 02.13 Xenograft Model

Histopathology and Immunohistochemical Profile

Histopathological analysis of Panc 02.13 xenografts reveals tumors with a characteristic morphology of pancreatic ductal adenocarcinoma, including glandular structures and areas of necrosis. The tumors are composed of pleomorphic cells with irregular nuclear morphology, high mitotic activity, and abundant cytoplasm. Immunohistochemical staining of Panc 02.13 xenografts shows strong expression of epithelial markers, such as cytokeratin and EMA, confirming the epithelial origin of the tumor. The tumors also show elevated levels of CA19-9, a marker commonly associated with pancreatic cancer, and KRAS mutations, reflecting the molecular features of PDAC. Additionally, Panc 02.13 xenografts exhibit high levels of phosphorylated AKT, indicating activation of the PI3K/AKT signaling pathway, which plays a critical role in tumor growth and survival. The tumors are also highly vascularized, as indicated by CD31 staining, and show evidence of immune evasion, which is characteristic of pancreatic cancer.

Preclinical Applications and Drug Response

The Panc 02.13 xenograft model is widely used to evaluate the efficacy of chemotherapy agents, particularly gemcitabine and cisplatin, which are standard treatments for pancreatic cancer. The model is particularly valuable for investigating the development of drug resistance and for testing combination therapies designed to overcome chemotherapy resistance. In addition to chemotherapy, the Panc 02.13 xenograft model is used to evaluate novel targeted therapies that inhibit the dysregulated signaling pathways commonly involved in PDAC, such as the KRAS, PI3K/AKT, and MAPK pathways. Furthermore, the model is increasingly used to assess the potential of immunotherapies, including immune checkpoint inhibitors and CAR-T cell therapies, which have shown promise in clinical trials for various cancers, including pancreatic cancer.

The model’s ability to replicate key features of pancreatic cancer, including its high metastatic potential and resistance to therapy, makes it an essential preclinical platform for evaluating new drug candidates, combination therapies, and immunotherapies aimed at improving the treatment and prognosis of pancreatic cancer patients.

Request This Model

To request the Panc 02.13 xenograft model for your preclinical studies, please use the form below. A customized quote and additional model specifications will be provided upon inquiry.

Request a Custom Quote for Panc 02.13 Xenograft Model