Collision tumor is a well-documented but uncommon phenomenon characterized by the coexistence of two completely distinct and independent tumors at the same organ. The two malignant neoplasms may originate from the same primary site or metastasize from other sites. Collision tumors display a sharp and distinct transition between the two tumor types, unlike mixed tumors, in which there is an intermediate transition zone with cells displaying features of both tumors. Collision tumors are not easy to diagnose on clinical presentation and radiology and require pathological identification.
While lung is the most common site for metastatic disease, collision tumors are more likely to present in the gastrointestinal tract.1 Reports of pulmonary collision tumors are limited, and cytologic descriptions of collision tumors are very rare. Most case reports describe collisions involving a primary lung carcinoma and another tumor such as chronic lymphocytic leukemia,2 lymphoma,3 choriocarcinoma,4 malignant melanoma,5 epithelioid hemangioendothelioma,6 malignant fibrous histiocytoma,7 metastatic adenoid cystic carcinoma,8 colon,9-10 breast,11 or large cell neuroendocrine carcinoma.12 We found only four pulmonary collision case reports involving carcinoid; the associated malignancies included marginal zone lymphoma,13 high-grade spindle cell sarcoma, 14 mesothelioma15 and lung adenocarcinoma.16 No cytologic descriptions or images were available for these four cases, although two cases briefly stated that a prior FNA was performed and had identified lymphoma and mesothelioma respectively. We believe that this may be the first cytologic report of a pulmonary collision tumor consisting of carcinoid and metastatic colonic adenocarcinoma.
This case depicts a 50 year-old woman with a single pulmonary nodule and a sigmoid colon mass. In the FNA smears from the lung lesion, two distinct cell populations were seen - one was consistent with colon adenocarcinoma ("cigar shaped" long columnar hyperchromatic nuclei and necrosis, with nuclear CDX-2 staining) and the other was suspicious for neuroendocrine tumor (single and loosely clustered cells, "salt and pepper" chromatin, and indistinguishable nucleoli).
The patient underwent sigmoid colectomy (Figure 6) three months after the lung FNA. Her 4.2 cm low grade colon adenocarcinoma showed invasion through most of the muscularis propria without lymph node involvement. The morphology was similar to the atypical columnar cells in the lung core biopsy, but no neuroendocrine component or differentiation was identified. The tumor was K-ras mutated; mutations in MLH1, MSH2, MSH6, and PMS2 were not observed. No other metastatic sites were identified on PET-CT.
After 3 months of chemotherapy, she underwent a right-sided lower lobe wedge resection. The lung mass (Figure 7) revealed nests of small cells that highlighted with TTF-1, synaptophysin and chromogranin. The cells did not express CK7, CK20 or CDX2. The Ki67 index was less than 2%. The histology and immunohistochemistry profile was consistent with a primary pulmonary well-differentiated neuroendocrine tumor (carcinoid), with morphology similar to the smaller background cells in the previous FNA. The entire lung lesion was embedded, but no residual colonic adenocarcinoma was identified. Imaging studies revealed no other metastatic lesions. The patient continued to be stable on physical exams and imaging, without recurrent disease. It is presumed that the metastatic colon adenocarcinoma in the lung resolved after chemotherapy, while the neuroendocrine tumor persisted until resection.
Although collision tumors are rare, accurate cytologic diagnosis is possible and requires careful attention.