Furthermore, lung adenocarcinomas with low EZH2 levels and high expression of the lineage-specific transcription factor, TTF-1, exhibited significantly improved RFS (P = 0.009; HR = 0.51) and OS (P = 0.0011; HR = 0.45), which was confirmed in the independent set of 91 adenocarcinomas.
Here, we reveal that S100A7 overexpression facilitates the transdifferentiation from adenocarcinoma (ADC) to squamous carcinoma (SCC) in several lung cancer cells, which is confirmed by an increase in DNp63 expression and a decrease in thyroid transcription factor 1 (TTF1) and aspartic proteinase napsin (napsin A) expression.
However, the mesonephric-like adenocarcinoma component exhibited a mixture of estrogen receptor- and thyroid transcription factor 1-positive cells within the same glands.
In contrast, cytoplasmic staining of TTF-1 was observed in five of six adenocarcinoma cell lines, in six of seven small cell lung cancer cell lines, and in all three squamous cell lung cancer cell lines.
In contrast, cytoplasmic staining of TTF-1 was observed in five of six adenocarcinoma cell lines, in six of seven small cell lung cancer cell lines, and in all three squamous cell lung cancer cell lines.
In contrast, patients with adenocarcinomas with TTF-1 expression had a worse outcome if TTF-1 was amplified (median overall survival time 39.5 versus 87.5 months).
In subclasses, the expression rate of TTF-1 mRNA was obviously higher in PEs of patients with PPA (93.0%) than with metastatic pulmonary adenocarcinoma (0%) and with primary pulmonary squamous cell carcinoma (12.5%).
In summary, mixed non-mucinous bronchioloalveolar carcinoma (BAC) or papillary components and papillary predominant adenocarcinoma showed a higher frequency of EGFR mutations than mucinous BAC components; Also, EGFR mutations were significantly more common in tumors with TITF-1 or SP-A expressions than in those without (p=0.002, p=0.026), especially the sensitivity of TITF-1 (96.9%) and the negative predictive value of TITF-1 (88.2%).
In the present study we have used gel-mobility-shift experiments to show that in a pulmonary adenocarcinoma cell line (NCI-H441) that expresses TTF-1, the same single protein binds to both of these sites.
In this study, we investigated 14 intestinal type OMNs (borderline and adenocarcinoma) and 12 endocervical-like OMNs (borderline and adenocarcinoma) for their expression of PDX-1, CDX-2, CA-125, CK7, CK20, WT-1, D2-40, and TTF-1.
It has been hypothesized that EGFR mutations are restricted to terminal respiratory unit -type adenocarcinoma expressing thyroid transcription factor-1 (official symbol NKX2-1) as determined by immunohistochemistry.
Moreover, immunohistochemical staining of the tissue specimen for thyroid transcription factor 1, cytokeratin 7 (CK7), and CK20 and CT-guided gun biopsy of the lung mass confirmed the presence of an adenocarcinoma that originated from the lung.
Moreover, the regulation of TTF-1 gene expression described in this report is accompanied by the same regulation in its promoter activity, as demonstrated in transfection experiments performed in H-441 human lung-derived adenocarcinoma cells.
Motivated by its specific expression pattern, pathologists adopted the NKX2-1 immunoreactivity to distinguish pulmonary from nonpulmonary nonthyroid adenocarcinomas.
Napsin A-positive adenocarcinomas were significantly more prevalent among tumors characterized as relatively small (p = 0.023), non-solid predominant (p < 0.001), non-mucinous/enteric (p < 0.001), positive for TTF-1 expression (p < 0.001), and positive for EGFR mutation (p = 0.001).
Ninety-two pulmonary adenocarcinomas (53 women and 39 men) confirmed by clinical presentation and positive immunohistochemistry for thyroid transcription factor-1 (TTF-1) were included in this study.
Nuclear extracts from H441 adenocarcinoma cells bound to the TTF-1 binding sites, were supershifted by anti-TTF-1 antibody, and were competed by other TTF-1 DNA binding motifs.