Gastrin Mimicry in Pancreatic Cancer

January 12, 2024by Dr. S. F. Czar0

Case Study:

Patient: Mrs. A, a 52-year-old woman presenting with persistent abdominal pain, weight loss, and jaundice.

Initial Diagnosis: Pancreatic adenocarcinoma.

Medical History: No prior significant medical history, no smoking history, occasional alcohol consumption.

Diagnostic Workup:

  • Blood tests: Elevated its levels, suggesting possible Zollinger-Ellison syndrome (gastrinoma).
  • Imaging: CT scan and endoscopic ultrasound reveal a mass in the head of the pancreas.
  • Biopsy: Confirms pancreatic adenocarcinoma.

Further Investigation:

  • Genetic analysis: No mutations typically associated with hereditary pancreatic cancer identified.
  • Immunohistochemistry: Tumor cells show strong expression of bombesin receptors and moderate its expression.
  • Functional assays: Tumor cells demonstrate increased cell proliferation and migration upon its stimulation.

Clinical Reasoning:

Mrs. A’s case deviates from the typical profile of pancreatic cancer. The elevated its levels and bombesin receptor expression in the tumor suggest a potential role for gastrin beyond acid secretion.

Hypothesis: Its mimicry plays a role in Mrs. A’s pancreatic cancer development and progression.

Supporting Evidence:

  • Elevated levels despite no evidence of gastrinoma suggest autonomous gastrin production by the tumor.
  • Tumor cells express both gastrin and bombesin receptors, indicating potential for self-stimulation and hijacking of growth-promoting pathways.
  • Functional assays demonstrate gastrin-induced cell proliferation and migration, mimicking bombesin’s effects.

Treatment Implications:

  • Traditional chemotherapy may not be sufficient, targeting additional pathways involved in gastrin-mediated tumor growth is crucial.
  • Potential treatment options include:
    • Its receptor antagonists: Block gastrin from binding to its receptors, hindering its tumor-promoting effects.
    • Tyrosine kinase inhibitors: Target downstream signaling pathways activated by gastrin mimicry.
    • Personalized therapies: Develop targeted strategies based on the specific gastrin-mediated pathways active in Mrs. A’s tumor.


While its mimicry adds complexity to Mrs. A’s case, understanding its role offers opportunities for tailored and potentially more effective treatment strategies.


This case study highlights the intricate and potentially deceptive nature of gastrin mimicry in cancer development. By unraveling the masquerade, we gain valuable insights into novel therapeutic targets and personalize cancer treatment, offering hope for improved patient outcomes in cases like Mrs. A’s.

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