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We report an unusual case of a subpleural bronchiolar/glandular proliferation in a 76-year-old Hispanic woman with microscopic features reminiscent of those of the so-called ciliated muconodular papillary tumor (CMPT). The lesion presented radiologically as a solitary subpleural nodule measuring 2.7 × 1.2 cm with low standard uptake value (SUV) of 1.4. Microscopically, it was circumscribed but unencaspulated and consisted of mucous-filled spaces lined by cytologically bland cuboidal to low columnar cells, including goblet cells and ciliated epithelium, with underlying nodular collections of basaloid cells. The lining cells stained diffusely for CK7 but only focally for TTF-1 and CEA, whereas the basal cells expressed CK5/6. Ki-67 showed a proliferative index of less than 1%. Target gene mutation analysis with a 50-cancer-related-gene panel using next-generation sequencing showed the bronchiolar proliferation to harbor an EGFRin frame exon 20 insertion mutation with 30% allele frequency, which supports a neoplastic diagnosis. Accordingly, given the mutually exclusive nature of driver mutations, a BRAF V600Emutation was absent by both immunohistochemical and next-generation sequencing analysis. Microscopic evidence of metastatic spread was not seen in 8 regional lymph nodes examined. Given the histomorphology and immunohistochemical findings, the mutational profile and the reported heterogeneous microscopic patterns of CMPTs, including glandular component, we suggest the tumor herein described be a glandular variant of CMPT. We therefore suggest that the term ciliated muconodular tumormay be more appropriate for this group of lesions.

Control of apoptosis is fundamental for dendritic cell (DC) homeostasis. Numerous factors maintain DC viability throughout their lifespan, including inhibitor of apoptosis proteins. Among them, survivin is overexpressed in many human malignancies, but its physiological function in normal cells has not been fully delineated. Prostaglandin E2(PGE2), also overproduced in several malignancies, has shown to induce proapoptotic and antiapoptotic effects in different cell types, including immune cells. In DC, PGE2predominantly affects maturation and modulates immune functions. Here, we show that exposure of monocyte‐derived DC to PGE2(10−5M) for 72 h significantly increased DC survivin mRNA and protein expression. In contrast, DC, matured with lipopolysaccharide or tumor necrosis factor α, did not reveal survivin induction in response to PGE2. Following exposure to apoptotic stimuli, DC treated with PGE2exhibited an overall increased viability compared with control DC, and this effect was correlated inversely with caspase‐3 activation. Moreover, PGE2‐treated, survivin‐deficient DC demonstrated reduced viability in response to apoptotic stimuli. Further analysis indicated that PGE2induced DC survivin expression in an E prostanoid (EP)2/EP4receptor and phosphatidylinositol‐3 kinase‐dependent manner. These findings suggest that PGE2‐dependent regulation of survivin is important in modulating apoptosis resistance in human DC.

The balance between proteases and antiproteases plays an essential role in the pathogenesis of emphysema. This study was designed to evaluate the impact of all-transretinoic acid (ATRA) on the balance of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in patients with emphysema.