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Disease Models

Disease Model

Location: Home CDX Pancreatic Cancer CFPAC-1
CFPAC-1
Application

Pancreatic Cancer

Modeling Method

Verifacition

Model Introduction


CFPAC-1 is a well-characterized human pancreatic ductal adenocarcinoma (PDAC) cell line originally established from a liver metastatic lesion of a 27-year-old male patient with cystic fibrosis who subsequently developed pancreatic adenocarcinoma. This unique cell line carries the homozygous CFTR ΔF508 mutation, retaining both the malignant ductal epithelial phenotype and the cystic fibrosis transmembrane conductance regulator (CFTR) genetic background. CFPAC-1 cells express pancreatic ductal markers including CK19 and CA19-9, and exhibit moderately differentiated glandular morphology. The subcutaneous xenograft mouse model established with CFPAC-1 cells is a valuable preclinical in vivo model for pancreatic cancer research, particularly valuable for studies investigating the intersection of cystic fibrosis genetics and pancreatic oncogenesis, as well as routine anti-tumor drug screening, targeted therapy evaluation and nanoparticle delivery system validation.


Experimental Principle


Immunodeficient BALB/c nude mice lack mature functional T lymphocytes and cannot mount effective cellular immune rejection against human-derived tumor xenografts. After harvesting CFPAC-1 cells in logarithmic growth phase and preparing a single-cell suspension, the suspension is subcutaneously inoculated into the dorsal flank of recipient mice. Tumor cells progressively proliferate in subcutaneous tissue and recruit host stromal vasculature, forming solid tumor masses with ductal adenocarcinoma morphology. By regularly measuring tumor volume, body weight and histopathological tumor burden, researchers can quantitatively assess in vivo tumor growth kinetics and evaluate the anti-tumor efficacy of test compounds, biological agents or combination regimens.


Model Identification & Detection Indicators


  1. Tumor volume measurement: Starting from the day of visible tumor formation, the longest tumor diameter (L) and shortest diameter (W) are measured every 2–3 days using a vernier caliper. Tumor volume is calculated by the formula: TV (mm³) = 0.5 × L × W².
  2. Body weight monitoring: Body weight of each mouse is recorded synchronously with tumor volume measurement, serving as an indicator of systemic toxicity induced by tumor burden or drug treatment.
  3. Model success criteria: The expected tumor formation rate of the CFPAC-1 subcutaneous xenograft model is ≥85%. When tumor volume reaches 100–150 mm³ at approximately day 18–25 post inoculation, the model is considered successfully established and eligible for randomized grouping and therapeutic intervention.
  4. Histopathological verification: At the experimental endpoint, tumor tissues are excised, fixed in 4% paraformaldehyde and embedded in paraffin. H&E staining confirms ductal adenocarcinoma morphology with glandular differentiation. Immunohistochemistry detects biomarkers including CK19, CA19-9, Ki-67 and CFTR to verify tumor origin, ductal differentiation, proliferative activity and CFTR expression status.


Model Advantages


  1. CFPAC-1 is uniquely derived from a cystic fibrosis patient with pancreatic adenocarcinoma, carrying the CFTR ΔF508 mutation, providing an irreplaceable model for studying the relationship between CFTR dysfunction and pancreatic oncogenesis.
  2. The cell line exhibits moderately differentiated ductal morphology with stable CK19 and CA19-9 expression, providing a biologically relevant model for glandular PDAC.
  3. Subcutaneous inoculation is technically straightforward, with low perioperative mortality and convenient longitudinal tumor size monitoring for group-wise efficacy comparison.
  4. The model is suitable for studying CFTR-related signaling pathways, mucin secretion abnormalities and their impact on pancreatic cancer progression.


Application Scenarios


  1. In vivo anti-tumor activity evaluation of small-molecule compounds, chemotherapeutic agents and targeted drugs against pancreatic cancer.
  2. Mechanistic research on CFTR dysfunction, mucin secretion abnormalities and their role in pancreatic cancer progression and therapeutic response.
  3. Preclinical pharmacodynamic assessment of combination therapy, nanoparticle delivery system and gene therapy approaches for PDAC.
  4. Preliminary in vivo efficacy screening prior to orthotopic pancreatic cancer model or patient-derived xenograft (PDX) model studies.

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