Renal Cell Carcinoma Metastasis to the Pancreas: A Comprehensive Review.
Pancreatic metastases are rare, accounting for approximately 2-5% of all pancreatic malignancies. Renal cell carcinoma (RCC) is the most common primary cancer that metastasizes to the pancreas and accounts for approximately 30-40% of all pancreatic metastatic lesions. Most reported cases involve clear cell RCC, while data regarding pancreatic metastases from non-clear cell RCC subtypes remain limited. Unlike metastases from other primary tumors, pancreatic metastases from RCC (PM-RCC) often follow a more indolent clinical course and are associated with a relatively favorable prognosis, suggesting distinct underlying biological behavior.
A comprehensive literature review was conducted using the MEDLINE/PubMed, Google Scholar, Cochrane Library, and Web of Science databases (January 1993-May 2025). Eligible studies included full-text articles, case reports, and original research describing renal cell carcinoma metastasis to the pancreas with an emphasis on mechanism, diagnosis, treatment, and outcomes.
The disproportionate tendency of kidney cancer to metastasize to the pancreas is best explained by the "seed and soil" hypothesis, reflecting a selective affinity between RCC cells and the pancreatic microenvironment. PM-RCC are usually metachronous, often occurring many years after nephrectomy, and are frequently asymptomatic and discovered incidentally on surveillance imaging. Characteristic imaging findings include hypervascular lesions on contrast-enhanced CT or MRI. Histopathological confirmation is critical, as PM-RCC has a markedly better prognosis than primary pancreatic neoplasms. Surgical resection remains the mainstay of treatment for isolated disease, with a 5-year survival exceeding 50%. In the era of targeted immunotherapy, systemic treatments further improve outcomes with the median overall survival surpassing that of patients with extra-pancreatic metastases.
PM-RCC is a unique clinical and biological entity characterized by indolent progression, favorable survival, and a strong response to surgical and targeted therapies. Understanding the molecular and microenvironmental mechanisms underlying this selective organotropism may refine therapeutic strategies and provide insights into the broader principles of metastatic disease.
A comprehensive literature review was conducted using the MEDLINE/PubMed, Google Scholar, Cochrane Library, and Web of Science databases (January 1993-May 2025). Eligible studies included full-text articles, case reports, and original research describing renal cell carcinoma metastasis to the pancreas with an emphasis on mechanism, diagnosis, treatment, and outcomes.
The disproportionate tendency of kidney cancer to metastasize to the pancreas is best explained by the "seed and soil" hypothesis, reflecting a selective affinity between RCC cells and the pancreatic microenvironment. PM-RCC are usually metachronous, often occurring many years after nephrectomy, and are frequently asymptomatic and discovered incidentally on surveillance imaging. Characteristic imaging findings include hypervascular lesions on contrast-enhanced CT or MRI. Histopathological confirmation is critical, as PM-RCC has a markedly better prognosis than primary pancreatic neoplasms. Surgical resection remains the mainstay of treatment for isolated disease, with a 5-year survival exceeding 50%. In the era of targeted immunotherapy, systemic treatments further improve outcomes with the median overall survival surpassing that of patients with extra-pancreatic metastases.
PM-RCC is a unique clinical and biological entity characterized by indolent progression, favorable survival, and a strong response to surgical and targeted therapies. Understanding the molecular and microenvironmental mechanisms underlying this selective organotropism may refine therapeutic strategies and provide insights into the broader principles of metastatic disease.
Authors
Aziz Aziz, Kotla Kotla, Abbey Abbey, Toliver Toliver, Gosse Gosse, Yasmine Yasmine, Aswani Aswani, Pawlik Pawlik
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