ABSTRACT
A 74-year-old man presented with symptoms suggestive of acute pancreatitis, and a mass lesion measuring 25 mm was detected in the pancreatic head. Cytological and histopathological examinations of EUS-FNA specimens taken from the lesion demonstrated small cell (neuroendocrine) carcinoma. Tumor cells were immunoreactive for cytokeratin, synaptophysin, chromogranin A, CD56, and TTF-1, and PET-CT of the chest revealed a small tumor in the upper lobe of the left lung. Pulmonary carcinoma, particularly small cell carcinoma, infrequently presents with a solitary metastatic lesion in the pancreas as an initial manifestation and clinically simulates a primary pancreatic neoplasm. Because primary small cell carcinoma of the pancreas is very uncommon, metastasis from the lung should always be considered when evaluating pancreatic neoplasms showing a "small cell" morphology. Immunohistochemistry for TTF-1 is useful for determining the pulmonary origin of this type of neoplasm, and its application to cytology specimens is recommended.
ABSTRACT
Activation-induced cytidine deaminase (AID) is an enzyme required for antibody diversification, and it causes DNA mutations and strand breaks. Constitutive AID expression in mice invariably caused lung lesions morphologically similar to human atypical adenomatous hyperplasia (AAH), which can be a precursor of bronchioloalveolar carcinoma. Similar to AAH, mouse AAH-like lesion (MALL) exhibited signs of alveolar differentiation, judging from the expression of alveolar type II (AT2) cell marker surfactant protein C (SP-C). However, electron microscopy indicated that MALL, which possessed certain features of a mucous cell, is distinct from an AAH or AT2 cell. Although MALL developed in all individuals within 30 weeks after birth, lung tumors occurred in only 10%; this suggests that the vast majority of MALLs fail to grow into visible tumors. MALL expressed several recently described markers of lung alveolar regeneration such as p63, keratin 5, keratin 14, leucine-rich repeat containing G protein-coupled receptor 5 (Lgr5), and Lgr6. Increased cell death was observed in the lungs of AID transgenic mice compared with wild-type mice. Based on these observations, we speculate that MALL is a regenerating tissue compensating for cellular loss caused by AID cytotoxicity. AID expression in such regenerating tissue should predispose cells to malignant transformation via its mutagenic activity.
