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Ruifen Tian
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P1.13 - Targeted Therapy (Not CME Accredited Session) (ID 945)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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P1.13-21 - Clinical Efficacy and Safety of Apatinib Combined with EGFR - TKIs in Advanced Non-Small Cell Lung Cancer with EGFR - TKIs Resistance (ID 13638)
16:45 - 18:00 | Presenting Author(s): Ruifen Tian
- Abstract
Background
Acquired resistance to EGFR-TKIs frequently occurs in advanced non-small cell lung cancer (NSCLC) patients with sensitizing EGFR mutations. Previous studies have shown that apatinib (a TKI against VEGFR-2) combined with EGFR-TKIs might improve the survival of EGFR-TKIs resistant NSCLC patients. We conducted this trial to investigate the efficacy and safety of apatinib combined with EGFR-TKIs compared with traditional chemotherapy for EGFR-TKIs resistant NSCLC patients.
a9ded1e5ce5d75814730bb4caaf49419 Method
This prospective study enrolled advanced NSCLC patients who acquired resistance to the EGFR-TKIs therapy. Patients received apatinib combined with EGFR-TKIs (apatinib in start dose of 250 mg+pior EGFR-TKIs dose) or chemotherapy ( pemetrexed or vinorelbine with platinum). Efficacy was evaluated every 6 weeks based on RECIST 1.1. This study was registered on Chinese Clinical Trail Registry, and the registration number was ChiCTR-OIN-17012051.
4c3880bb027f159e801041b1021e88e8 Result
From Mar 2017 to May 2018, 24 patients were enrolled, including 18 patients received apatinib combined with EGFR-TKIs, 6 patients received chemotherapy. In the apatinib group, 83.33%(15/18) patients were available evaluated. The objective response rate was 20% (3/15) and the disease control rate was 100% (15/15). All patients have different degrees of lesion shrinkage. Till May 1, 2018, the median duration of apatinib group treatment was 187 days, and the median PFS has not researched. The most common adverse events in the apatinib group were hypertension, proteinuria, weakness. Five (27.78%) grade 3 hypertension, 3 (16.67%) grade 3 proteinuria and 1 (5.56%) grade 3 diarrhea were observed. Two patients who failed treatment with osimertinib received osimertinib combined with apatinib, got lesions decreased after one cycle. One of the two patients was treated as fifth line treatment. Two patients with brain metastases in the apatinib group got metastases lesions decreased. Two progressive patients got lesions decreased after apatinib dose increasing to 500mg. Of the 7 patients receiving chemotherapy, 6 patients were available evaluated. The objective response rate was 16.67%(1/6) and the disease control rate was 100% (6/6). Major adverse reactions were digestive tract reaction and myelosuppression.
8eea62084ca7e541d918e823422bd82e Conclusion
Apatinib combined with EGFR-TKIs may provide a new therapy strategy for NSCLC patients with acquired EGFR-TKIs resistance. Both drugs are oral, which is advantageous in improving the patient's quality of life and the compliance of therapy. Further study with lager samples are needed to validate our findings. Moreover, We will further explore the correlation between genetic mutations, biomarkers and therapeutic efficacy.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P2.01 - Advanced NSCLC (Not CME Accredited Session) (ID 950)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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P2.01-93 - The Analysis of the Soluble Programmed Death-1 of Lung Cancer Patients with Different Characteristics (ID 13760)
16:45 - 18:00 | Author(s): Ruifen Tian
- Abstract
Background
Programmed death 1 ligand-1(PD-L1) is important regulators in cancer immunity. The aim of this study was to evaluate the values of the expression of the soluble programmed death-1(sPD-L1) in the plasma of patients with lung cancer, and to investigate the associations between the expression level of sPD-L1 and clinicopathological features as well as effective and survival outcomes.
a9ded1e5ce5d75814730bb4caaf49419 Method
A total of 200 patients with non-small cell lung cancer(NSCLC)(n=188) and small cell lung cancer(SCLC)(n=12) treatment naive were explored, 96 samples of healthy subjects and 13 samples of benign tumours were studied as control. The sPD-L1 expression was scored by the way of anenzyme-linked immunosorbent assay (ELISA). We followed up 67 patients with NSCLC before and after standard treatment, and blood samples were taken every two months. We compared sPD-L1 expression with clinicopathological features and patients outcomes.
4c3880bb027f159e801041b1021e88e8 Result
The Expression of sPD-L1 in patients of lung cancer was significantly higher than benign tumour group and healthy group (3.01±3.00ng/ml, 1.76±1.74ng/ml, 1.82±1.20ng/ml, P=0.002). The level of sPD-L1 in lung cancer was not associated with gender, age, smoking history, and histologic subtypes(P＞0.05). The level of sPD-L1 was significantly higher in patients of worse PS(performance status)(PS≥2) than better PS(PS<2) (6.40±6.53 vs. 2.68±2.06 P=0.005). The level of sPD-L1 with later stages were remarkable higher than earlier stages(P<0.001) in NSCLC patients. The expression of sPD-L1 of the patients with epidermal growth factor(EGFR) mutated adenocarcinoma was higher than EGFR-wild group(4.30±1.82ng/ml vs. 3.76±1.57ng/ml, P=0.271). The decline of the level of sPD-L1 was correlated with the effects of good response and progressive disease(PD)(0.49±1.48ng/ml vs. 0.11±0.52ng/ml, P=0.307). As for survival, there was no difference between the decline of level of sPD-L1 and the progress free survival(PFS).
8eea62084ca7e541d918e823422bd82e Conclusion
Our results indicated that the elevated expression of sPD-L1 of patients with NSCLC was associated with later stages and worse life conditions, and which may correlated with bad clinical response and poor prognosis. EGFR mutation status may affect the expression of sPD-L1. Further studies are needed to determine the role of sPD-L1 as a molecular prognosis marker for the treatment and prognosis of patients with lung cancer.
6f8b794f3246b0c1e1780bb4d4d5dc53
