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Yanjun Xu
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P1.12 - Small Cell Lung Cancer/NET (Not CME Accredited Session) (ID 944)
- 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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P1.12-01 - A Single-Arm Multi-Center Phase II Study of Apatinib in Patients with ES-SCLC After Second/Third-Line Chemotherapy (ID 12960)
16:45 - 18:00 | Author(s): Yanjun Xu
- Abstract
Background
The survival of patients (pts) with extensive-stage small-cell lung cancer (ES-SCLC) was poor. And the standard treatment strategies have not yet been established for those who failed from second/third-line chemotherapy. Apatinib, a vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor, has been shown anti-cancer activity and manageable toxicities in several solid cancers.
a9ded1e5ce5d75814730bb4caaf49419 Method
A single-arm multi-center phase II study was designed to determine the efficacy and safety of apatinib in pts with ES-SCLC after second/third-line chemotherapy (clinical trial information: NCT02945852). The inclusion criteria mainly included aged 18-75 years; pathologically confirmed SCLC; received chemotherapy with two or three regimens previously, including first-line platinum-based regimen. Pts were treated with afatinib 500 mg/day p.o. until tumor progression or lack of tolerability. One treatment cycle was 28 days long. The full analysis set included patients who received at least one cycle of treatment. Treatment interruptions or dose reductions were allowed when ≥grade 3 hematologic or grade 2 nonhematologic toxicities occurred. The primary endpoint is progression-free survival(PFS); secondary endpoint includes the safety of afatinib, overall survival (OS), objective response rate (ORR) and disease control rate (DCR).
4c3880bb027f159e801041b1021e88e8 Result
As of Mar 2018, 40 pts from 3 institutions were recruited into the trial. Median age was 60 years, and 37 pts were male (92.5%). 17/40 (42.5%) pts experienced dose reduction or treatment interruptions. Followed up to Apr 26, 2018, the median during time of afatinib treatment was 80 days and 36 pts were eligible for assessing tumor responses. In the 36 pts, 8 (22.2%) pts achieved partial responses [PR], 20 (55.5%) pts achieved stable disease [SD] and 8 (22.2%) pts were assessed as progressive disease [PD]. The ORR was 22.2% (8 pts PR) and the DCR was 77.8% (8 pts PR, 20 pts SD). During the follow-up, a total of 25 pts died. The median PFS and OS was 86 days and 105 days, respectively. The most common adverse events were anemia (69.4%, 25/36), hand-foot syndrome (61.1%, 22/36), urine protein (55.6%, 20/36), hypertension (52.8%, 19/36) and fatigue (44.4%, 16/36). The related grade 3-4 toxicities included hypertension (47.2%, 17/36), hand-foot syndrome (5.6%, 2/36), Oral ulcer (5.6%, 2/36) and elevated aminotransferase (5.6%, 2/36).
8eea62084ca7e541d918e823422bd82e Conclusion
In this prospective phase II trial, apatinib showed encouraging durable response rates and survival in patients with ES-SCLC after second/third-line chemotherapy, with an acceptable safety profile.
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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P2.01-30 - Applicability of Lung-molGPA Index in Non-Small Cell Lung Cancer Patients with Different Gene Alterations and Brain Metastases (ID 12734)
16:45 - 18:00 | Author(s): Yanjun Xu
- Abstract
Background
The Lung-molGPA was based on the original Diagnosis-Specific Graded Prognostic Assessment (DS-GPA) by incorporating recently reported gene alteration data for non-small cell lung cancer (NSCLC) patients with brain metastases (BM). However, the prognostic prediction value of DS-GPA and Lung-molGPA models remains undetermined, especially in patients with different molecule types.
a9ded1e5ce5d75814730bb4caaf49419 Method
A total of 1184 NSCLC patients with BM analyses for clinical factors and outcomes were identified at Zhejiang Cancer Hospital, China. All prognostic factors were weighted for significance by hazard ratios. The applicability of DS-GPA and Lung-molGPA were reappraised in NSCLC patients with BM and various genetic profiles. Additionally, a modified Lung-molGPA, was newly developed for mutant NSCLC patients.
4c3880bb027f159e801041b1021e88e8 Result
8eea62084ca7e541d918e823422bd82e Conclusion
The NSCLC patients in the present study had a median survival of 14.0 months from the time of BM diagnosis. Both DS-GPA and Lung-molGPA models could predict the outcomes (P<0.001), while Lung-molGPA model appeared to exhibit better accurate prediction. Furthermore, Lung-molGPA scores performed a discrimination capability in patients with gene variations (3.5-4.0 vs 2.5-3.0 vs 1.5-2.0 vs 0-1.0=62.0 vs 32.0 vs 17.7 vs 3.2 months, P<0.001). However, no significant difference was reached in wild-type patients (P=0.133). Regarding to the oncogene-positive NSCLC patients with BM, a modified Lung-molGPA index had been established derived from the prognostic factors with the C-index of 0.73 (95% CI: 0.73-0.80) to accurately calculate the survival probability (P<0.001).
In an era of precision medicine, Lung-molGPA could precisely predict the prognosis of mutant NSCLC patients with BM, while not work in wild-type patients.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P2.09 - Pathology (Not CME Accredited Session) (ID 958)
- 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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P2.09-31 - Cisplatinum Suppressed Metastasis of NSCLC by Inhibiting Macrophage M2-Like Polarization (ID 12542)
16:45 - 18:00 | Presenting Author(s): Yanjun Xu
- Abstract
Background
Although M2-like tumor-associated macrophages (TAMs) have been considered as a vital therapeutic target in cancer therapy due to their role in promoting tumor progression and metastasis by inducing expression of CCR2 and CX3CR1 through IL-10 secretion, few compounds have been identified to inhibit M2-like polarization of TAMs.
a9ded1e5ce5d75814730bb4caaf49419 Method
In vitro analysis of cisplatinum in preventing macrophage M2-like polarization was conducted. Expression of cell surface marker CD206 and CDH1, CCR2, CCL2 and CX3CR1 genes were detected.The migration of non-small lung cancer cells promoted by the conditioned medium from M2-like macrophages was conducted by Transwell migration assay. The percentage of M2-like macrophages in tumor and normal lung tissues were analysised after the administration of cisplatinum for one week.
4c3880bb027f159e801041b1021e88e8 Result
Here, we showed that cisplatinum significantly prevented macrophage M2-like polarization induced by IL-10 in vitro, as illustrated by reduced expression of cell surface marker CD206 and CDH1, CCR2, CCL2 and CX3CR1 genes. Furthermore, the migration of non-small lung cancer cells promoted by the conditioned medium from M2-like macrophages could be restrained by cisplatinum. Furthermore, cisplatinum reduced the number of metastasis of lung cancer without affecting tumor growth. Both in tumor and normal lung tissues, the percentage of M2-like macrophages decreased after the administration of cisplatinum for one week.
8eea62084ca7e541d918e823422bd82e Conclusion
Taken together, these data suggest that cisplatinum is able to inhibit macrophage M2-like polarization, which plays a vital role in cisplatinum suppressed metastasis of NSCLC.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P2.13 - Targeted Therapy (Not CME Accredited Session) (ID 962)
- 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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P2.13-15 - Short-Term Responders of NSCLC to EGFR-TKIs Display High Prevalence of TP53 Mutations and Primary Resistance Mechanisms (ID 12540)
16:45 - 18:00 | Author(s): Yanjun Xu
- Abstract
Background
Non-small cell lung cancer (NSCLC) with activating EGFR mutations in exon 19 and 21 usually responds to EGFR tyrosine kinase inhibitors (TKI), but sometimes the responses can only be maintained for a few months. The underlying mechanisms of such short responses have not been fully elucidated.
a9ded1e5ce5d75814730bb4caaf49419 Method
The genomic profiles of sixteen short-term responders (SR) that had progression free survival (PFS) of less than 6 months on the first-generation EGFR TKI were interrogated, in comparison to twelve long-term responders (LR) that had more than 24 months of PFS. All patients were diagnosed with advanced lung adenocarcinoma and harbored EGFR 19del or L855R mutation before treatment. Paired tumor samples collected before treatment and after relapse (or at the last follow-up) were subjected to next-generation sequencing of 416 cancer-relevant genes.
4c3880bb027f159e801041b1021e88e8 Result
SR patients were significantly younger than LR patients (p<0.001). 88% of SR patients have TP53 variations compared to 13% in LR patients (p<0.001), and 37.5% SR patients carry EGFR amplification, which is much higher than LR patients (8%). In addition, 12 SR patients (75%) were identified with other potential primary resistance mechanisms in pre-treatment samples, including PTEN loss, BIM deletion polymorphism, amplifications of EGFR, ERBB2, MET, HRAS and AKT2. Comparatively, only 3 LR patients (25%) were detected with EGFR or AKT1 amplification that could possibly exert resistance.
8eea62084ca7e541d918e823422bd82e Conclusion
The diversified pre-existing resistance mechanisms in SR patients revealed the complexity of defining treatment strategies even for EGFR sensitive mutations.
6f8b794f3246b0c1e1780bb4d4d5dc53
