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A. Martinez
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P3.02c - Poster Session with Presenters Present (ID 472)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)
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P3.02c-063 - Lactate Dehydrogenase (LDH) as a Surrogate Biomarker to Checkpoint-Inhibitors for Patient with Advanced Non–Small-Cell Lung Cancer (NSCLC) (ID 5073)
14:30 - 14:30 | Author(s): A. Martinez
- Abstract
Background:
Effectiveness of immunotherapy has been observed in around 20% of cases, nowadays there is no accurate biomarker to select those patients (pts) who will benefit the most.
Methods:
We evaluated retrospectively pretreatment (baseline) and post-treatment (every 2 months) serum-LDH in 94 pts with NSCLC treated with anti-PD1/PDL1. Repeated measures ANOVA, Kaplan-Meier and the proportional COX model were used to examine the association of LDH with overall survival (OS). The cutoff level of LDH was 400 based on the median of the sample. (normal range 105-333 UI/L).
Results:
From July 2013 to February 2016, 94 pts were treated with immunotherapy based in anti-PD1 (77,6%) and anti-PDL1 (22,4 %), in trials at VHIO. Median age was 62 (39-86). Histological subtypes were: adecocarcinoma 53.2%, squamous 42.5%, others 4.2 %. The OS was significantly different in pts treated with immunotherapy according to baseline LDH, if LDH ≥ 400 median OS was 8.2 months, while in pts with LDH <400 median survival was not reached (Figure 1) Figure 1 There were statistically significant differences in the evolution of LDH, with better responses if there was a downward trend in LDH levels. In long responding pts (45 of 94 pts), defined as ≥ 3 evaluations (6 months), a LDH level at the time of 6 months treatment below than the baseline LDH predicts better responses (22/45 pts): 68.2% partial response (RP); 18.2% stable disease (SD); 13.6% disease progression (PD). In contrast, when LDH at third evaluation was higher than baseline LDH (23/45 pts): 39.1% PR; 56.5% SD; 4.3% PD, (p=0.022). There were differences between the level of LDH pre and post-progression. 66.67% of patients who progressed had a higher level of LDH at the time of progression than at the previous assessment (p=0.03).
Conclusion:
LDH may be a potential predictive biomarker of survival benefit conferred by immunotherapy in patients with NSCLC.
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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)
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P3.03-019 - Molecular Characterization of Malignant Pleural Mesothelioma (MPM) by next Generation Sequencing (ID 4881)
14:30 - 14:30 | Author(s): A. Martinez
- Abstract
Background:
Malignant pleural mesothelioma (MPM) is a highly aggressive pleural tumor associated with asbestos exposure and with limited survival despite treatment. Chromosomal abnormalities are abundant in MPM and the most frequently mutated genes are BAP1, NF2 and CDKN2A. Expanded molecular profile in MPM may provide targetable molecular aberrations and improve treatment options for these patients (p).
Methods:
Thirty two MPM patients who progressed to standard chemotherapy underwent genetic tumor profiling in a molecular prescreening program at our institution between 2006 and 2015. Paraffin-embedded biopsies were used for the analysis. Mass detection (MassARRAY, Sequenom) including analysis of mutations in 25 oncogenes was used and since June 2014 multiplexed amplicon sequencing (AmpliSeq, Illumina) was implemented assessing mutations in 59 oncogenes. No patients received systemic treatment prior to obtain the tumor sample.
Results:
Demographics: male/female (22/10); median age 60.5 (range 32-83 years); histology epithelial/no epithelial (24/8); PS 0/1 (15/17); stage III/IV (14/13). All patients were treated with chemotherapy. Sequenom was performed in 21 p and AmpliSeq in 11 p. Median follow up was 23.3 months and median overall survival (OS) for entire cohort was 30.2 months. The median OS for patients with epitheliod and no-epithelioid histology was 31.5 vs 21.4 months (p=0.033). Genetic alterations were detected in 5 patients (4 p with AmpliSeq and 1 p with Sequenom).The mutations detected were RNF43/ZNRF3 (2p), PI3KCA (1p), APC (1p) and P53 (1p). We did not identify significant association between mutations with histology, gender and clinical stage (p>0.05). Median survival for patients with mutations was not reached and for patients without mutations was 30.2 m (p=0.462)
Conclusion:
This study shows genetic alterations are not frequent in MPM and AmpliSeq detected more genetic alterations than Sequenom. With a limited number of patients, we suggest further investigations about the role of mutations in Wnt pathway in MPM
