Various collision tumors have been documented in different organs of the body. Previously documented cases of collision tumor in the gastrointestinal tract include gastric collision tumor such as an unusual combination of adenocarcinoma and immature neuroepitheliomatous teratoma¹ in the stomach, collision of Epstein-Barr virus-associated gastric carcinoma and primary gastric extranodal marginal zone lymphoma,² gastrointestinal stromal tumor and gastric adenocarcinoma collision tumors,³ gastric collision tumor of large cell neuroendocrine carcinoma and adenocarcinoma,⁴ and mixed adenocarcinoma-carcinoid in the appendix;⁵ a rare combination of an adenocarcinoma and small cell neuroendocrine tumor in the ileum;⁶ adenoma-carcinoid tumors of the colon;⁷ and collision tumor of the ampulla of Vater with carcinoid and adenocarcinoma components.^8,9

Microscopically, the main tumor showed poorly differentiated adenocarcinoma morphology (Figure 2A) that had infiltrated into subserosal adipose tissue; the other lesion in the same location located deeper from the adenocarcinoma described above showed neuroendocrine morphology, such as nests and trabeculae with variable amounts of eosinophilic cytoplasm, indicating a completely distinct and independent neuroendocrine carcinoma (Figure 3A). Histologically, the pancreas was not involved with either tumor. Three positive lymph nodes were identified out of a total of forty. One of them demonstrated coexistent metastatic adenocarcinoma and neuroendocrine carcinoma (Figure 4A). The immunohistochemical characteristics were analyzed to determine whether the origins of the 2 cancers were different or not. The adenocarcinoma neoplastic cells revealed expression of CK7, CK20 and Cd×2 but no expression of neuroendocrine markers such as CD56, chromogranin and synaptophysin (Figure 2B, C, D). The tumor cells in the independent 1 cm tumor nodule show strong neuroendocrine marker expression including CD56, chromogranin and synaptophysin, but negativity for CK7, CK20 and Cd×2 (Figure 3B,C,D). The immunostains were also done on the involved lymph node which confirmed the double metastasis (Figure 4B,C). This phenomenon is very rare and can be referred to as collision metastasis. The other two lymph nodes were positive for neuroendocrine carcinoma. As a result, it was concluded that this was a case of collision cancer of primary duodenal adenocarcinoma and neuroendocrine carcinoma with collision metastasis into one lymph node. The patient has recovered well from his operation, and is currently symptom-free.

Conventional explorations usually do not confirm the coexistence of both tumors, as these findings are frequently made incidentally during histopathologic examination of the specimen. Given their extreme rarity in this location and the nature of collision tumors, it is of certain diagnostic benefit to extensively examine and section the tumor for histologic evaluation, and distinguish collision tumor from the more commonly encountered neoplasms demonstrating heterologous differentiated elements or mixed elements.

Indeed, this case could easily have been mis-considered as an adenocarcinoma with neuroendocrine features given the rarity of collision tumors in this location, and one may even completely miss the concurrent distinct and independent neuroendocrine tumor component, especially if only a limited examination and sectioning of the tumor are performed for histologic evaluation.

Two main features that are important in the diagnosis of collision tumor rather than neoplasms demonstrating mixed elements include: i) two distinctive and spatially independent tumor components macroscopically in the same location, and ii) demarcated morphology and immuno-expression patterns among the two tumors microscopically. Morphological and immunohistochemical examinations will show that the two components have a clear-cut distinction, and they have no intervening intermediate cell population.