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Abstract
Pulmonary carcinoids combined with a non-neuroendocrine component have rarely been described, and this histological subtype is not included as a specific entity in the current World Health Organization classification of pulmonary neoplasms. Here, we described the molecular and histological features of two rare cases of mixed lung neoplasms, composed of atypical carcinoid and adenocarcinoma. The targeted next-generation sequencing analysis covering single nucleotide variations, copy number variations, and transcript fusions in a total of 161 cancer genes of the two different tumor components shows a similar molecular profile of shared and private gene mutations. These findings suggest their monoclonal origin from a transformed stem/progenitor tumor cell, which acquires a divergent differentiation during its development and progression and accumulates novel, specific mutations.
Highlights
Combined or collision pulmonary tumors are primary lung neoplasms with two or more histologically distinct phenotypes (Olofson and Tafe, 2018)
Immunoreactivity for chromogranin A, synaptophysin, TTF1, and pan-cytokeratins AE1–3 was documented in carcinoid component, while adenocarcinomatous component was positive only for TTF-1 and cytokeratins (Figure 1)
Due to their exceptional rarity, very few molecular data supporting this hypothesis are available for mixed lung neoplasms with epithelial carcinomatous component combined with a well-differentiated neuroendocrine component (La Rosa et al, 2018; Olofson and Tafe, 2018)
Summary
Combined or collision pulmonary tumors are primary lung neoplasms with two or more histologically distinct phenotypes (Olofson and Tafe, 2018). Rare cases of typical and atypical carcinoids associated with squamous cell carcinoma or adenocarcinoma have been reported and extensively profiled at the molecular level (La Rosa et al, 2018). These combinations are not included as a specific entity in the WHO classification (WHO, 2021), and the pathogenesis of mixed histology is not well elucidated due to the rarity of presentation. The second and more supported hypothesis indicates a monoclonal origin with a divergent differentiation of the two phenotypes starting from the same precursor clone (combined tumors) (La Rosa et al, 2018; Olofson and Tafe, 2018)
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