Virtual Library
Start Your Search
K. Furukawa
Author of
-
+
P2.02 - Poster Session with Presenters Present (ID 462)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Locally Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 12/06/2016, 14:30 - 15:45, Hall B (Poster Area)
-
+
P2.02-017 - A Clinical Outcome of Resected Small-Sized Non-Small Cell Lung Cancer 1 cm or Less in Diameter with N2 Lymph Node Metastasis (ID 5573)
14:30 - 14:30 | Author(s): K. Furukawa
- Abstract
Background:
The detection of small-sized (≤ 1cm) non-small cell lung cancer (NSCLC) has increased with the development of high-resolution computed tomography. The reported 5-year survival rate of T1a (≤ 2cm) N0M0 patients is more than 80%, and that of p-T1a (≤ 2cm) N2M0 patients has also steadily improved.
Methods:
Between 1991 and 2011, a total of 917 patients with small-sized (≤ 2cm) NSCLC underwent curative pulmonary resection with systematic lymph node dissection at Tokyo Medical University Hospital and Tokyo Medical University Ibaraki Medical Center. We retrospectively evaluated their postoperative clinical outcomes and survival rates. Survival was analyzed using the Kaplan-Meier method and log-rank test.
Results:
There were 46 (5.0%) patients with mediastinal lymph node metastasis in pT1a (≤ 2cm). And there were 6 (0.6%) patients with pT1a (≤ 1cm) N2M0. The histological types were 3 cases of adenocarcinoma, 2 case of squamous cell carcinoma, and one large cell carcinoma. The respectively status of lymph node metastasis was single station in 2 cases and multiple station in 4 cases. Skip lymph node metastasis was observed in 2 cases. There were 26 cases (56.5%) that were upstaged from clinical diagnosis in pT1a (≤ 2 cm) N2M0 patients. There was one upstaging case from cT1a (≤ 1 cm) N0M0 to pT1a (≤ 2 cm) N2M0. The median overall survival period and 5-year survival of patients in pT1 (≤ 2 cm) N2M0 was 52.1 months and 45%. And patients with pT1a (≤ 1 cm) N2M0 has 29.8 months and 0% (3 year overall survival rate was 33.3%). The recurrence rate was 71.7% (5/6) and disease free survival was 13.2 months.
Conclusion:
This study showed that 5.0% of small-sized (≤ 2 cm) NSCLC had N2 disease and 0.6% of T1a (≤ 1 cm) NSCLC has pN2. Moreover, 56.5% of small-sized (≤ 2 cm) NSCLC was upstaged from clinical diagnosis to pathological diagnosis. The patients with pT1a (≤ 1 cm) N2M0 had worse survival data than the patients with pT1a (≤ 2 cm) N2M0. We recommend systematic lymph node dissection for local treatment as well as accurate diagnosis. As multiple mediastinal node metastases showed an unfavorable prognosis, surgery combined with systematic treatment is recommended.
-
+
P3.01 - Poster Session with Presenters Present (ID 469)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)
-
+
P3.01-035 - Nicotine Enhances Hepatocyte Growth Factor-Mediated Lung Cancer Cell Migration (ID 3860)
14:30 - 14:30 | Author(s): K. Furukawa
- Abstract
Background:
Cigarette smoking not only promotes lung carcinogenesis, but it has also been demonstrated to promote the progression of lung cancer. Despite nicotine being a major component of cigarette smoke, it is not carcinogenic when acting alone. Instead, it is believed to function as a tumor promoter that stimulates the processes of invasion and metastasis. In the present study we aimed to determine the effect of nicotine on the migratory activity of lung cancer cells.
Methods:
The effect of nicotine on the migration of lung cancer A549 cells was evaluated by a wound healing assay. Hepatocyte growth factor (HGF) was used as a pro‑migratory stimulus. During several of the experiments, specific inhibitors of α7‑nicotine acetylcholine receptor (α7‑nAchR), phosphoinositide kinase‑3 (PI3K) and extracellular signal‑related kinase (ERK)1/2 were included. The phosphorylation levels of Akt and ERK1/2 were examined using a cell‑based protein phosphorylation assay.
Results:
Nicotine did not induce cell migration by itself, but it instead promoted HGF‑induced cell migration (Figure). The effects of nicotine were inhibited by the pretreatment of the cells with the α7‑nAchR inhibitor, methyllycaconitine, and the PI3K inhibitor, LY294002. The mitogen‑activated protein kinase/ERK kinase kinase inhibitor exerted modest, but non‑significant inhibitory activity on the effect of nicotine. Nicotine did not induce Akt phosphorylation by itself, but instead promoted the HGF‑induced phosphorylation of Akt. It was also observed that nicotine had no effect on ERK1/2 phosphorylation.Figure 1
Conclusion:
These results indicate that nicotine, when alone, does not have a pro‑migratory function, but instead enhances responsiveness to the pro‑migratory stimulus emitted by HGF. This study provides an insight into the mechanism of tumor promotion by demonstrating that nicotine and α7‑nAchRs act in synergy with the HGF‑induced PI3K/Akt signaling pathway, increasing the sensitivity of lung cancer cells to HGF, and thereby promoting cell migration, a vital step in invasion and metastasis.
