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EP1.01 - Advanced NSCLC (ID 150)
- Event: WCLC 2019
- Type: E-Poster Viewing in the Exhibit Hall
- Track: Advanced NSCLC
- Presentations: 1
- Now Available
- Coordinates: 9/08/2019, 08:00 - 18:00, Exhibit Hall
EP1.01-61 - iSEND Model as a Predictor of Efficacy in Immune Checkpoint Inhibitors for Non-Small Cell Lung Cancer: Fukushima Cohort (Now Available) (ID 1689)
08:00 - 18:00 | Author(s): Masayuki Watanabe
The expression of PD-L1 in tumor tissue and the number of gene mutations (TMB) in tumor tissue have been investigated as predictors of the efficacy of PD-1/PD-L1 inhibitors in non-small cell lung cancer. However. In actual clinical practice, it is difficult to perform these tests in all cases.
Therefore, we are searching for an effect prediction marker that can be done easily and inexpensively. Wungki Park et al. constructed the iSEND model as a therapeutic effect predictor and showed its usefulness. We examined the usefulness of iSEND model for non-small cell lung cancer patients who received PD-1 / PD-L1 inhibitor at our institution.Method
We retrospectively examined the usefulness of the iSEND model in 56 patients with non-small cell lung cancer who were treated with PD-1/PD-L1 inhibitor in our department after the second treatment. The iSEND model uses patient background and blood tests. Calculated and scored using gender, ECOG performance status, NLR before treatment and after treatment (Neutrophi-to-Lymphocyte Ratios), and divided into three group. For each group, we statistically compared the clinical course such as overall survival and recurrence-free survival.Result
In the analysis by Wungki Park et al. , The iSEND Poor group has a median overall survival of 4.0 months and 15.9 months, respectively, compared with the iSEND Good group (p = 0.0002), and the median recurrence free period is 1.6 months and 2.6 months, respectively. Months (p = 0.0045), and each showed a significant difference. In our study, no statistically significant difference was found, but a trend similar to the analysis of Wungki Park et al.Conclusion
In this study, it is suggested that the iSEND model may be useful as a predictor of the effect of PD-1/PD-L1 inhibitor.
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P2.06 - Mesothelioma (ID 170)
- Event: WCLC 2019
- Type: Poster Viewing in the Exhibit Hall
- Track: Mesothelioma
- Presentations: 1
- Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
P2.06-20 - Characterization of Claudin15 as a New Diagnostic Marker for Malignant Pleural Mesotheliomas (ID 1770)
10:15 - 18:15 | Presenting Author(s): Masayuki Watanabe
Malignant pleural mesotheliomas (MPMs) is a fatal disease mainly caused by past exposure to asbestos. MPMs are classified into three main histological subtypes: epithelioid, sarcomatoid, and biphasic type. There have been known several immunopathological markers for diagnosing MPMs, but there are not enough reliable markers, which often makes it difficult to diagnose MPMs correctly. In the present study, we investigated whether Claudin15 serves as a diagnostic and therapeutic target for MPMs. Claudins are four-transmembrane proteins and form a protein family consisting 27 members in humans. Specific combination of claudins are differentially expressed in different organs and form tight junctions with different permeability. Expression of Claudin15 has been known to be increased at mRNA level in MPMs.Method
Since 2003 to 2018, 34 patients were diagnosed with MPMs in our hospital. We made a new anti-Claudin15 rat monoclonal antibody, and established a hybridoma clone suitable for IHC. We immunostained 34 tissues with newly established anti-Claudin15 antibody, and compared the staining intensity and occupation with those of Calretinin, a known marker for MPMs. We also immunostained poorly differentiated lung adenocarcinomas, which are sometimes hardly distinguishable with MPMs, with anti-Claudin15 antibody to examine whether Claudin15 staining can distinguish MPMs from adenocarcinomas.Result
Of the 34 cases, the epithelial type was 27 cases, the sarcomatoid type was 1 case, and the biphasic type was 6 cases. The overall expression rate was 53% for Claudin15 and 59% for Calretinin. In terms of histology type, Claudin15 was 50% and Calretinin was 65% in the epithelial type, while Claudin15 was 80% and Calretinin was 40% in the biphasic type. There was only one sarcomatoid type, neither was expressed. Poorly differentiated adenocarcinomas showed no or very low-level expression of Claudin15.Conclusion
Our results suggest that Claudin15 could be a novel diagnostic marker for MPMs, especially for biphasic type. Greater number of cases and further analyses would be required to establish Claudin15 as a diagnostic impact for MPMs in clinical use.