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Edgardo S. Santos
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P2.01 - Advanced NSCLC (ID 618)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Advanced NSCLC
- Presentations: 2
- Moderators:
- Coordinates: 10/17/2017, 09:00 - 16:00, Exhibit Hall (Hall B + C)
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P2.01-014 - ABOUND.PS2: Safety and Efficacy of Nab-Paclitaxel–Based Therapy in Patients with NSCLC and ECOG PS 2 (ID 8186)
09:00 - 09:00 | Author(s): Edgardo S. Santos
- Abstract
Background:
Patients with advanced NSCLC with poor ECOG PS can benefit from platinum-based doublet chemotherapy, although limited data exist from recent, randomized prospective trials. ABOUND.PS2 evaluated the safety and efficacy of nab-paclitaxel/carboplatin induction followed by nab-paclitaxel monotherapy in patients with advanced NSCLC and ECOG PS 2.
Method:
Chemotherapy-naive patients with histologically/cytologically confirmed stage IIIB/IV NSCLC and ECOG PS 2 received 4 cycles of nab-paclitaxel 100 mg/m[2] on days 1 and 8 plus carboplatin AUC 5 on day 1 q3w. Patients not progressing could receive monotherapy with nab-paclitaxel 100 mg/m[2] on days 1 and 8 q3w until progression or unacceptable toxicity. Primary endpoint: percentage of patients discontinuing within the first 4 cycles due to treatment-emergent adverse events (TEAEs). Other endpoints: progression-free survival (PFS), disease control rate (DCR), overall survival (OS), overall response rate (ORR), and quality of life (QoL) by Lung Cancer Symptom Score (LCSS).
Result:
Forty patients were treated. Median age was 67.5 years, 60.0% were male, 92.5% were white, and 62.5% had nonsquamous histology. During induction, 11 of 40 patients (28%) discontinued due to TEAEs (primary endpoint). In total, 16 of 40 patients (40.0%) received nab-paclitaxel as monotherapy. In all treated patients, the median percentage of per-protocol dose of nab-paclitaxel was 78.3% and the median nab-paclitaxel dose intensity was 52.2 mg/m[2]/week (planned, 66.7 mg/m[2]/week). See table for additional safety, efficacy, and QoL results.
Conclusion:
These results support the role of this nab-paclitaxel–based regimen in patients with NSCLC and ECOG PS 2. The regimen was well tolerated and appears to have resulted in a clinically meaningful improvement in QoL. Compared with historical data, this regimen is active in patients with stage IIIB/IV NSCLC and ECOG PS 2. NCT02289456
[a] A ≥ 10-mm improvement was considered clinically meaningful.All Treated Patients N = 40 Safety Grade ≥ 3 TEAEs of special interest, n (%) Neutropenia Anemia Thrombocytopenia Peripheral neuropathy 9 (22.5) 7 (17.5) 2 (5.0) 1 (2.5) Efficacy PFS, median (95% CI), months 4.4 (2.99-7.00) OS, median (95% CI), months 7.66 (4.93-13.17) ORR (RECIST v1.1), n (%) 12 (30.0) DCR, % Complete response Partial response Stable disease Progressive disease, % Patients with no postbaseline tumor assessment 30 (75.0) 0 12 (30.0) 18 (45.0) 2 (5.0) 8 (20.0) QoL Mean maximum improvement from baseline LCSS Global QoL item, mm[a] 16.91
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P2.01-015 - Longitudinal Assessment of Performance Status (PS) in Patients with NSCLC and ECOG PS 2 on Nab-Paclitaxel–Based Therapy (ID 8187)
09:00 - 09:00 | Author(s): Edgardo S. Santos
- Abstract
Background:
ABOUND.PS2 evaluated nab-paclitaxel/carboplatin induction followed by nab-paclitaxel monotherapy in patients with advanced NSCLC and ECOG PS 2. Concordance between patient- and physician-reported PS as well as change in PS with chemotherapy were assessed longitudinally.
Method:
Chemotherapy-naive patients with histologically/cytologically confirmed stage IIIB/IV NSCLC and ECOG PS 2 received 4 cycles of nab-paclitaxel 100 mg/m[2] on days 1 and 8 plus carboplatin AUC 5 on day 1 q3w. Patients not progressing could receive monotherapy with nab-paclitaxel 100 mg/m[2] on days 1 and 8 q3w until progression or unacceptable toxicity. Primary endpoint was the percentage of patients discontinuing within the first 4 cycles due to treatment-emergent adverse events. ECOG PS was assessed by patients on day 1 of each cycle and at treatment discontinuation, and ECOG PS and spirometry were assessed by physicians at screening, on day 1 of each cycle, and at treatment discontinuation.
Result:
Forty patients were treated. Baseline ECOG PS was reported as 2 by 48% and 95% of patients and physicians, respectively. Only 53% of patients rated their ECOG PS the same as the physician at cycle 1 day 1. For patients with both pre- and post-treatment ECOG assessments, 14 of 33 patients (42%) and 12 of 38 physicians (32%) reported an improvement from baseline at least once during treatment (Figure). At baseline, physicians believed that ECOG PS would be reversible with treatment in the majority of patients (80%). Mean FEV1 was 1.29 L and mean PEF was 2.66 L/s at baseline; exploratory investigations of spirometry data indicate that lung function (FEV1 and PEF) remained stable over the course of treatment.
Conclusion:
These results from the ABOUND.PS2 study suggest that patient-reported PS assessments may differ from physician assessments. Improvements in ECOG PS were reported by both patients and physicians during treatment. NCT02289456Figure 1
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P3.02 - Biology/Pathology (ID 620)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P3.02-004 - Analysis of MET in Liquid Biopsy and Tissue Biopsy in Patients with Advanced NSCLC: Incidence and Pattern. (ID 8726)
09:30 - 09:30 | Presenting Author(s): Edgardo S. Santos
- Abstract
Background:
MET pathway is dysregulated in several cancers, having three types of alterations: overexpression, amplification and mutation. MET amplification has been reported in 2-4% of NSCLC while MET exon 14 skipping mutation has been found in 3-4% of lung adenocarcinoma. Increased MET expression is associated with higher malignancy, and acts as a negative prognostic factor. To date, several MET inhibitors are in development. Hence, the importance of understanding MET biology, its incidence, patterns of appearance, and which type of genomic abnormality. Is MET a trunchal genomic abnormality or does it appear as a result of mechanism of resistance of tumor cells once exposed to therapeutic agents? In the past, MET inhibitors have failed to improve OS in clinical trials; lack of benefit from this approach was the fact that there was no standard method for detecting MET related anomalies that allowed an adequate patient (pt) selection.
Method:
A search for MET alterations was performed in a retrospective analysis from November 2014 until May 2017. A total of 142 liquid biopsies (LBx) from pts with advanced NSCLC using NGS were identified. Once pts with a MET genomic alteration were identified by LBx, we proceed to review their initial tumor biopsy (TBx) genetic analyses and assess for the presence of MET alterations. Data regarding histologic subtypes, therapy received in each case, and timing of LBx analysis were collected.
Result:
A total of 142 LBx were identified in our cohort of patients with advanced NSCLC from November 2014 until May 2017. These samples came from 127 pts; 20 pts (15.7%) had MET alterations identified by LBx. Characteristics of these 20 pts were: median age was 72 (range, 62-85); 15 pts (75%) were females; all patients had adenocarcinoma histology. Genomics alterations in LBx were distributed as: 5 amplifications and 15 mutations. Genetic analyses from the TBx of these 20 pts done at initial diagnosis were reviewed. There were 8 pts who had TBx and LBx done at the same time and at initial diagnosis; only 2 pts out of these 8 had MET alterations in both tests (amplifications). The other 6 pts (with both TBx and LBx done simultaneously) had MET alterations identified only by LBx despite other genetic abnormalities concordance found between TBx and LBx in 5/6 pts. In these pts, median number of alterations identified by LBx and TBx were 7 and 0.5, respectively. There were 12 pts who had LBx done after progression of disease. All these pts had MET alterations identified in LBx however, none of them had MET genomic abnormalities in their TBx at initial diagnosis. One pt who had MET exon 14 skipping mutation in LBx (at progression of disease) did not have TBx genetic analysis due to insufficient tumor tissue.
Conclusion:
In this pt sample, we were able to identify more sensitivity from LBx than TBx for detection of MET alteration at initial diagnosis when both tests were done simultaneously. Our pts had metastatic disease with lesions outside the lung parenchyma. This will increase the diagnostic yield of LBx. Also, tumor heterogeneity plays a major role for discrepancies between TBx and LBx. The median number of genomic alterations identified by LBx was also higher than the one reported by TBx. Interestingly, 12 pts with MET alterations at progression of disease did not have these anomalies at TBx (initial diagnosis). Many questions remain unanswered. A prospective clinical trial using NGS in both tissue and blood at initial diagnosis will help us to identify and understand the biology of MET. It seems that LBx could be a complimentary tool at initial assessment of pt with metastatic NSCLC.
