Abstract

Metastatic carcinomas involving the lung are a common specimen encountered in surgical pathology. These metastases may have different morphologic, and architectural patterns and may mimic primary pulmonary adenocarcinoma, especially the intra-alveolar (lepidic) pattern of spread which may simulate a primary pulmonary bronchioloalveolar carcinoma (adenocarcinoma in situ). We present the case of a metastatic pancreatic adenocarcinoma that morphologically mimicked bronchioloalveolar carcinoma of the lung in that the tumor had an exclusive intra-alveolar pattern of spread and had an immunophenotype that was noninformative as to the site of origin (cytokeratin 7+, cytokeratin 20−, TTF-1−). In this case, we used KRAS gene mutation analysis to support that the lung carcinoma represented a metastatic pancreatic carcinoma as they both possessed identical codon 12 KRAS mutations. We show that this method may be a useful way to prove site of origin of metastatic carcinoma—particularly if standard morphologic or immunohistochemical analysis is not definitive.

Highlights

  • The lungs are a frequent site of both metastatic and primary carcinoma

  • Metastatic carcinoma was present in regional lymph nodes

  • K-Ras is a protein encoded by the Kirsten rat sarcoma viral oncogene homolog (KRAS) gene with GTPase activity that is involved in signal transduction of the cells and acts downstream of epidermal growth factor receptor (EGFR)

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Summary

Introduction

Many different patterns of metastases to the lungs have been described: nodules/masses, lymphangitic carcinomatosis, tumor emboli, endobronchial growth, and intra-alveolar (lepidic) spread. In intra-alveolar spread, the tumor cells replace the lining of alveoli, mimicking bronchioloalveolar carcinoma (adenocarcinoma in situ). Metastases from gastrointestinal tract carcinomas, including the pancreas, are known to have an intra-alveolar pattern of spread [1, 2]. In many instances immunohistochemistry may not be as useful, when one encounters an adenocarcinoma with mucinous differentiation that is TTF-1 negative. In this setting, morphology and immunohistochemistry may not be definitive and clinical correlation is often relied on to make the distinction

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