The aim of this study was whether quercetin induces cell death by caspase and MAPK signaling pathway in EGFR mutant lung cancer cells

PC-9 cells, EGFR mutant lung cancer cells, were treated various times and concentrations of quercetin and harvested and measured using MTT assay, DNA fragmentation, Western blotting, and FACS analysis.

Treatment with quercetin in PC-9 cells resulted in inhibition of cell growth through apoptosis. Quercetin-induced apoptosis was associated with caspase-dependent manner. Quercetin also significantly increased levels of phosphor-p38 and decreased levels of phosphor-ERK, indicating that quercetin induces p38 MAPK signaling pathway in PC-9 cells. Quecetin treatment also generated the release of cytochrome c in PC-9 cells; however, pretreatment with rotenone or z-LEHD-fmk, significantly attenuated quercetin-induced apoptosis.

Our data indicate that quercetin exhibits EGFR mutant lung cancer effects through apoptosis by caspase dependent and mitochondrial pathway.

Pulmonary carcinoid tumors consisting of typical carcinoid tumors (TC) and atypical carcinoid tumors (AC) are rare, accounting for 2–5% of all lung tumors. TC is considered a low-grade tumor with a rate of distant metastasis up to 12%. In contrast, ACs are more aggressive tumors, displaying a metastatic rate up to 70%. Surgery is the treatment of choice; however, the current treatment outcomes of metastatic lung carcinoids are discouraging. This study aimed to investigate the EGFR mutation using the PNA-mediated clamping method and to provide basic data for using EGFR-TK1 and its clinical implications.

A total of 14 cases that underwent surgery were diagnosed as carcinoid tumors and pathologically classified as TC and AC. The paraffin-embedded tissues were analyzed for EGFR mutations using the PNA-mediated PCR clamping technique. The mutant type was noted in the cases with a^△Ct greater than 2.0.

Of 14 cases, eight were AC and six cases were TC. No known EGFR mutation was detected with a^△Ct less than 2.0.

The EGFR genotype determined using the PNA-mediated PCR clamping method was wild-type in all pulmonary carcinoid tumors. Therefore, the application of EGFR-TK1 is limited in pulmonary carcinoid tumors.

The aim of this study was to explore the changes of bronchoscopic features according to epidemiologic change of lung cancer.

We performed a retrospective review of the clinical characteristics of 1,139 lung cancer patient who underwent bronchoscopy at Kosin University Hospital from January 2000 to December 2010.

The age of patients increased significantly during the last decade (P < 0.001). The most common histological type was adenocarcinoma (38.1%), followed by squamous carcinoma (35.7%) and small cell carcinoma (15.3%). There was an increasing incidence of adenocarcinoma over the time (P < 0.001). Bronchoscopic feature were divided into two classes; central type, peripheral type. The peripheral type was predominant (62.3%). The proportion of peripheral type has been increased in process of time (49.7% vs. 63.7% vs. 73.7%; P < 0.01). Among the major histopathologic type of lung cancer, adenocarcinoma (81.3%) and unclassifiable non-small-cell lung cancer (73.4%), small cell carcinoma (56.9%) were associated with preferential occurrence of peripheral type. Squamous cell carcinoma of the lung more often arised in central type (59%). However, the proportion of peripheral squamous cell carcinoma has been increased. On the subgroup analysis, the median survival time of peripheral type with adenocarcinoma and small cell carcinoma were longer than central type (P < 0.05).

The age of the lung cancer patients at diagnosis was getting older. The most frequent histopathologic type was adenocarcinoma. The proportion of peripheral type lung cancer gradually increased over the time. The survival time of peripheral type lung cancer was longer than central type.