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Tianqing Chu



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    P1.01 - Advanced NSCLC (Not CME Accredited Session) (ID 933)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 2
    • Moderators:
    • Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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      P1.01-29 - Crizotinib in Advanced Lung Adenocarcinoma Patients with ALK or ROS-1 Rearrangement: Is it the Same? (ID 12929)

      16:45 - 18:00  |  Author(s): Tianqing Chu

      • Abstract
      • Slides

      Background

      Crizotinib is an orally taken tyrosine kinase inhibitor (TKI) targeting both ALK and ROS1 rearrangement, which have defined two different molecular subgroup patients. The aim of the study was to compare the therapeutic efficacy of crizotinib in advanced lung adenocarcinoma patients diagnosed with ALK or ROS1 mutation.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      Patients diagnosed with ALK (Group A) or ROS1 (Group B) mutation were identified from our standardized registration system. The effectiveness of crizotinib in eligible patients was retrospectively analyzed.

      4c3880bb027f159e801041b1021e88e8 Result

      A total of 5348 and 4695 patients were screened and 393 (7.3%, 95% CI, 6.6%-8.0%) and 105 (2.2%, 95% CI, 1.8%-2.7%) positive patients were identified among the two groups, respectively. There were 141 and 32 eligible patients were included for survival analysis. The ORR is 53.0% (95% CI, 43.0%-63.0%) in group A, without statistical significance compared with group B (71%, 95% CI, 51.2%-90.4%, P=0.11). Similar result was also observed in terms of DCR (86%, [95% CI, 79.1%-92.9%] vs. 92.0%, [95%, CI, 80.0%-100.0%], P=0.74). The median PFS in group A was 12.4 months (95% CI, 10.2 -14.7 months), which was statistically worse than patients in group B (18.2 months, 95% CI, 6.3 -29.0 months, P=0.02). The OS was too immature to analyze.

      8eea62084ca7e541d918e823422bd82e Conclusion

      Patients harboring ROS1 rearrangement derived better prognosis compared with these who had ALK rearrangement when treated with crizotinib.

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      P1.01-30 - Crizotinib in Advanced Non-Adenocarcinoma, NSCLC (NA-NSCLC) Patients with ALK Rearrangement: A Retrospective Study and Literature Review (ID 12942)

      16:45 - 18:00  |  Author(s): Tianqing Chu

      • Abstract
      • Slides

      Background

      The aim of the study was to investigate the prevalence of anaplastic lymphoma kinase (ALK) rearrangement in non-adenocarcinoma, non-small cell lung cancer (NA-NSCLC) patients and therapeutic efficacy of crizotinib in these patients.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      From January 2013 to January 2017, NA-NSCLC patients who were diagnosed with ALK rearrangement were screened. The effectiveness of crizotinib in positive patients was retrospectively analyzed. A literature review was performed and eligible cases were analyzed combined with our data.

      4c3880bb027f159e801041b1021e88e8 Result

      A total of 1212 NA-NSCLC patients were screened during the period with 25 positive patients identified (2.1%, 95% CI, 1.3%-2.9%). A statistically higher percentage of female patients (40.0% vs. 10.4%, P< 0.01), non-smoker (72.0% vs.43.2%, P< 0.01), containing adenocarcinoma component (36.0% vs. 7.1%, P< 0.01) and advanced stage (68.0% vs. 45.6%, P=0.03) were observed in ALK positive group. The median PFS of the 9 eligible patients in our institution was 7.0 months (95% CI, 0-15.6 months). We combined our data with the sporadic cases from 10 previous case reports (total n=19) and found that the median PFS was 7.0 months (95% CI, 5.6-8.4 months).

      8eea62084ca7e541d918e823422bd82e Conclusion

      Our study suggested the opportunity to test ALK rearrangement in NA-NSCLC patients, especially in female, non-smoker and patients containing adenocarcinoma component. Crizotinib provides an option for the treatment of NA-NSCLC patients who diagnosed with ALK rearrangement.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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    P1.03 - Biology (Not CME Accredited Session) (ID 935)

    • 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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      P1.03-16 - Anlotinib Inhibits Angiogenesis of Refractory Advanced Non-Small Cell Lung Cancer via Blocking CCL2 Expression (ID 12406)

      16:45 - 18:00  |  Author(s): Tianqing Chu

      • Abstract
      • Slides

      Background

      Anlotinib has been demonstrated to be effective in prolonging progression free survival (PFS; Anlotinib: 5.37 months vs Placebo: 1.40 months) and overall survival (OS; Anlotinib: 9.63 months vs Placebo: 6.30 months) of refractory advanced Non-Small Cell Lung Cancer (NSCLC) patients in clinical trials. Clinical evidences suggested that Anlotinib-induced anti-tumor efficacy could be attributed to anti-angiogenesis. However, the underlying molecular mechanisms and predictive biomarker of Anlotinib are still unclear.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      437 patients with advanced NSCLC enrolled in clinical study, and 294 patients received Anlotinib therapy. Retrospectively analysis of the Anlotinib-administrated 294 NSCLC patients was performed to screen out underlying biomarker for Anlotinib-responsive patients. Transcriptome and functional assays were performed to understand the anti-tumor molecular mechanism of Anlotinib in vitro. CCL2 levels and their roles in angiogenesis were evaluated by ELISA detection, RT-qPCR quantification, and immunofluorescence assay, in vivo. Changes in serum CCL2 levels were analyzed to reveal the correlation of Anlotinib response between responders and non-responders.

      4c3880bb027f159e801041b1021e88e8 Result

      Anlotinib therapy is more beneficial to prolong OS for NSCLC patients harboring positive driver gene mutations, especially for patients harboring EGFRT790M mutation. Moreover, our data indicated that Anlotinib-induced cell viability downregulation, cell apoptosis induction, cell invasion inhibition, cell cycle arrest, and cell migration inhibition are associated with CCL2 levels in vitro. We demonstrated that Anlotinib inhibits angiogenesis of NCI-H1975 derived xenografts model via inhibiting CCL2 in vivo. Lastly, we found that Anlotinib-induced serum CCL2 level decreases are associated with the benefits of PFS and OS, in refractory advanced NSCLC patients (n = 28).

      8eea62084ca7e541d918e823422bd82e Conclusion

      Our study reports a novel anti-angiogenesis mechanism of Anlotinib via inhibiting CCL2 in NCI-H1975 derived xenografts model, and suggests the changes in serum CCL2 levels may be used to monitor and predict clinical outcome in Anlotinib-administered refractory advanced NSCLC patients. The biomarker of serum CCL2 alteration may guide precision therapy of Anlotinib for NSCLC patients at third-line or over third-line.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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    P1.11 - Screening and Early Detection (Not CME Accredited Session) (ID 943)

    • 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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      P1.11-19 - Expression of TNFRII in Serum is Correlated with the Significant Risk of Subcentimeter Lung Adenocarcinoma (ID 12954)

      16:45 - 18:00  |  Author(s): Tianqing Chu

      • Abstract
      • Slides

      Background

      With the rapid advances of low-dose computed tomography (LDCT) screening for lung cancer, the opportunity to detect subcentimeter non-small cell lung cancer (NSCLC) is gradually increasing. The results of many previous studies have shown that even subcentimeter NSCLCs are not always in the early stage. Thus, it is quite important for us to judge the possibility of malignancy for these patients, even the tumor size is less than 10mm. However, subcentimeter lung cancer is hard to diagnose only via biopsy and imaging features because of its tinny size. Chronic inflammation is well established as a hallmark in lung carcinogenesis. In our previous study, B lymphocyte chemoattractant (BLC), is found to be slightly associated with the risk of subcentimeter lung adenocarcinoma. The aim of the present study is to evaluate the correlation between TNF receptor type II (TNFRII) and the risk for subcentimeter lung adenocarcinoma, and the efficacy of diagnosing subcentimeter lung cancer after combining TNFRII and BLC.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      Inflammatory biomarkers were measured in 71 subcentimeter lung adenocarcinoma patients and 71 age-, sex- and smoking-matched healthy controls by using the Luminex bead-based assay.

      4c3880bb027f159e801041b1021e88e8 Result

      The mean (standard deviation or SD) age of patients was 56.01 (8.91) years, and 73.20% of them were female patients (n=52). Never smokers accounted for 85.96% of patients (n=57). The expression level of TNFRII is significantly down-regulated in subcentimeter lung adenocarcinoma patients compared with the healthy controls (P<0.001). And the results were validated by oncomine data mining analysis.

      Elevated levels of TNFRII were associated with an 89% reduced risk for subcentimeter lung adenocarcinoma. (OR=0.11, 95% CI: 0.04-0.30, P=2.4*10-5). BLC was associated with a 2.70-fold (95% CI: 1.31-5.58, P=7.0*10-3) increased risk of subcentimeter lung adenocarcinoma for the comparison of patients in the higher-level group with the lower-level group. To yield more information, the BLC/TNFRII ratio was created to examine their prediction for the risk of subcentimeter lung adenocarcinoma, and as expected there was a 35- fold increased risk for patients in the higher-level group relative to patients in the lower-level group. Further ROC curve analysis revealed that TNFRII was a significant diagnostic biomarker for subcentimeter lung adenocarcinoma, with the area under the curve of 0.73 (95% CI: 0.65-0.82, P=2.0*10-6). The sensitivity, specificity and accuracy were 0.75, 0.72 and 0.73, respectively.

      8eea62084ca7e541d918e823422bd82e Conclusion

      Our findings demonstrated that TNFRII was associated with the significant risk of subcentimeter lung adenocarcinoma, and could be a promising biomarker for accessorily diagnosing subcentimeter lung adenocarcinoma.

      6f8b794f3246b0c1e1780bb4d4d5dc53

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    P2.12 - Small Cell Lung Cancer/NET (Not CME Accredited Session) (ID 961)

    • 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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      P2.12-17 - Prophylactic Cranial Irradiation Can Not Provide Survival Benefits for Resected Small Cell Lung Cancer Without Lymph Node Involvement (ID 13996)

      16:45 - 18:00  |  Author(s): Tianqing Chu

      • Abstract

      Background

      Currently, prophylactic cranial irradiation (PCI) was recommended for all patients after resection small-cell lung cancers, even those without lymph node metastasis. However, there is no directly evidence supporting this recommendation. The purpose of the present study is to assess the role of PCI for this subset of patients.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      We retrospectively identified completely resected SCLC without lymph node involvement (N0M0) at the Shanghai Chest Hospital between January 2006 and May 2017.

      4c3880bb027f159e801041b1021e88e8 Result

      A total of 146 patients (44 patients received PCI, 102 patients did not) were identified in the study. During the observation period, 8.8 % (9/102) patients in the non-PCI-treated cohort and 11.4 % (5/44) patients in the PCI-treated cohort developed brain metastases. There was no significant difference in the risk of cerebral recurrence between the two cohorts with regard to the time to recurrence (P = 0.677). What is more, neither overall survival benefit (HR = 0.88, 95% CI: 0.47–1.65, P = 0.700) nor disease-free survival (HR = 0.95, 95% CI: 0.55–1.62, P = 0.835) was significant between the PCI-treated and non-PCI-treated cohorts.

      8eea62084ca7e541d918e823422bd82e Conclusion

      The present study did not support using PCI in surgically resected small cell lung cancer without lymph node involvement. A relatively lower risk of brain metastasis in this particular subset might explain the inferior efficacy of PCI.

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