243 Combined Lung Cancer with Adenocarcinoma and Atypical Carcinoid: A rare Case in an Elderly Smoker

Introduction/Objective Composite lung cancers, which contain more than one histologic subtype within a single tumor, are rare and often difficult to classify. This case features a tumor made up of both adenocarcinoma and atypical carcinoid components, with diagnosis supported by both histology and molecular profiling. Methods/Case Report An 82-year-old woman with a 42-pack-year smoking history (2 packs per day from age 21, quit in 1999) underwent PET/CT, which showed a 1.6 cm nodule in the left lower lobe. No lymphadenopathy was present. Surgical resection revealed a 1.5 cm tumor invading the visceral pleura; with negative margins. The tumor was staged as pT2a pN0. Histology showed two distinct components. Poorly differentiated adenocarcinoma comprised 60% of the tumor (1.1 cm), positive for AE1/AE3 and TTF-1, focally positive for napsin, and negative for neuroendocrine markers. The remaining 40% (0.8 cm) was consistent with atypical carcinoid, showing focal necrosis, mitotic activity up to 8 per mm², and a Ki-67 index of 15%. These cells were positive for TTF-1, synaptophysin, chromogranin, and weakly CD56, but negative for p40 and p63. The neuroendocrine component was noted to invade the pleural elastic layer (PL1). All surgical margins and lymph nodes were negative (0/16). Molecular testing showed KRAS G12C and TP53 mutations. Additional findings included PD-L1 expression at 50%, ERBB2 amplification, tumor mutational burden of 10.1 mutations/Mb, and microsatellite stability. Results N/A Conclusion This case involves a rare composite lung tumor made up of poorly differentiated adenocarcinoma and atypical carcinoid in an elderly smoker. Histologically, the two components were clearly distinct, with the adenocarcinoma showing typical glandular features and the neuroendocrine component demonstrating findings consistent with atypical carcinoid, including focal necrosis and an elevated mitotic rate. The tumor invaded the visceral pleura but had negative margins and no lymph node involvement, staged as pT2a pN0. Molecular profiling of the adenocarcinoma revealed clinically relevant alterations, including KRAS G12C and TP53 mutations, ERBB2 amplification, and high PD-L1 expression. These findings are increasingly important in the management of lung cancer, especially when considering immunotherapy and targeted treatment options. The identification of a composite tumor reinforces the need for pathologists and oncologists to recognize mixed histology and consider their impact on prognosis and therapy. As precision medicine continues to evolve, understanding the molecular landscape of each case can help refine treatment planning even in uncommon presentations like our current case.