Virtual Library
Start Your Search
A. Hara
Author of
-
+
P2.06 - Poster Session with Presenters Present (ID 467)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Scientific Co-Operation/Research Groups (Clinical Trials in Progress should be submitted in this category)
- Presentations: 1
- Moderators:
- Coordinates: 12/06/2016, 14:30 - 15:45, Hall B (Poster Area)
-
+
P2.06-047 - LRRK2-In-1 Inhibit Proliferation of Doublecortin and CaM Kinase-Like-1 (DCLK1)-Positive Lung Cancer Cells (ID 4847)
14:30 - 14:30 | Author(s): A. Hara
- Abstract
Background:
Doublecortin and CaM kinase-like-1 (DCLK1) is a kinase that regulates microtubule polymerization in migrating neurons. DCLK1 is also suggested to be a tumor stem cell marker in colon and pancreatic cancer. The expression status of DCLK1 and its role in lung cancer remain largely unknown. LRRK2-IN-1, a potent therapeutic agent for the treatment of Parkinson’s disease, has shown to inhibit DCLK1 kinase activity.
Methods:
DCLK1 expression status in human non-small cell lung cancer (NSCLC) cell lines was examined by quantitative real-time RT-PCR and western blotting. Cell proliferation assay was made after treatments with either si-DCLK1 or LRRK2-IN-1.
Results:
DCLK1 was expressed in most of the cell lines examined in various degrees. In DCLK1-expressing cell lines, si-DCLK1 treatment showed growth inhibition. LRRK2-IN-1 treatment also showed growth inhibition, in a dose-dependent manner.
Conclusion:
DCLK1 can be a target molecule for NSCLC treatment. LRRK2-IN-1 might be therapeutic for DCLK1-expressing lung cancer, through inhibition of its kinase activity.
-
+
P3.03 - Poster Session with Presenters Present (ID 473)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Mesothelioma/Thymic Malignancies/Esophageal Cancer/Other Thoracic Malignancies
- Presentations: 1
- Moderators:
- Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)
-
+
P3.03-043 - Trimodality Therapy with Extrapleural Pneumonectomy, Radiation Therapy, and Chemotherapy for Epithelioid Malignant Pleural Mesothelioma (ID 3987)
14:30 - 14:30 | Author(s): A. Hara
- Abstract
Background:
Malignant pleural mesothelioma (MPM) is a dreadful disease, and the treatment strategy of it has not been established yet. Our experience of trimodality therapy with extrapleural pneumonectomy (EPP), radiation therapy, and chemotherapy for epithelioid MPM is reported.
Methods:
26 consecutive EPP for epithelioid MPM which were performed from June 2006 to December 2015 in our hospital were reviewed. We have instituted a trimodality therapy protocol consisting of EPP, adjuvant 45-50.4 Gy hemithoracic radiation therapy, and adjuvant CDDP plus PEM chemotherapy. 21 patients have been treated with this protocol. However, 5 patients were given induction CDDP plus PEM chemotherapy, and referred to us. They were scheduled to undergo EPP and adjuvant hemithoracic radiation therapy. Overall survival was calculated using Kaplan-Meier method. This was one institutional retrospective study.
Results:
Median age at EPP was 61 years old. Female was 7, and male was 19. Right side was 15, and left side was 11. Median EPP time was 7 hours 22 minutes. No blood transfusion during EPP was 12 cases (46%). 30 day mortality was zero. Atrial fibrillation was the most common morbidity, and developed in 9 patients (35%). IMIG pathological stage was stage IV in 1, stage III in 18, stage II in 3, and stage Ib in 4. Adjuvant 45-50.4 Gy radiation therapy was completed for 21 patients (81%). 5 patients (19%) could not undergo chemotherapy. 18 patients (69%) underwent trimodality therapy. Postoperative median follow-up period was 5 years and 2 months. Five year survival, two year survival, and median survival of all 26 patients were 40%, 55%, and 30.4 months.Figure 1
Conclusion:
The five year survival and median survival of trimodality therapy with EPP, 45-50.4 Gy hemithoracic radiation therapy, and CDDP plus PEM chemotherapy for epithelioid MPM is 40% and 30.4 months. This treatment strategy is feasible, and the prognosis has been very improved.
