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B. Han



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    P1.11 - Poster Session 1 - NSCLC Novel Therapies (ID 208)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Medical Oncology
    • Presentations: 1
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      P1.11-036 - The efficacy and safety of sunitinib in EGFR-TKI pretreated advanced non-small cell lung cancer: a retrospective review from Chinese patients at a single institution (ID 2534)

      09:30 - 09:30  |  Author(s): B. Han

      • Abstract

      Background
      Sunitinib is an oral, selective multi-targeted tyrosine kinase inhibitor (TKI) with antiangiogenic and antitumor activities. The result from a previous study suggested that the treatment of sunitinib might present favorable survival outcomes for the EGFR-TKI pretreated NSCLC Chinese patients. This study was therefore to evaluate the efficacy and toxicity of this therapeutic strategy.

      Methods
      This is a retrospective review of 30 stage IV NSCLC patients who received sunitinib as salvage therapy in Shanghai Chest hospital, from January 2009 until August 2011. All of the patients had previously been treated with EGFR-TKIs. Kaplan-Meier method was employed to estimate the median progression-free survival (PFS) and overall survival (OS). Univariate and multivariate Cox proportional hazard regression analyses were carried out to determine the important prognostic risk factors influencing NSCLC survival.

      Results
      The median PFS of all 30 treated patients was 1.25 months (95% CI: 0.90-1.9 months), and the median OS was 3.40 months (95% CI: 3.00-6.80 months). Of the 29 patients eligible for efficacy evaluation, none achieved partial response. Cox regression analysis suggested that Eastern Cooperative Oncology Group (ECOG) performance status (PS) is predictive of both PFS (p=0.001) and OS (p<0.001). Hand-foot syndrome (53.3%), mucositis (40.0%), rash (36.7%) and diarrhea (33.3%) were most commonly reported adverse events.

      Conclusion
      In this study, the sunitinib treatment did not demonstrate overall clinical benefits to the EGFR-TKI pretreated NSCLC Chinese patients. Most side effects were mild to moderate. These results need further validation in prospective studies.

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    P2.12 - Poster Session 2 - NSCLC Early Stage (ID 205)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Medical Oncology
    • Presentations: 1
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      P2.12-002 - Clinical characteristics and prognosis of lung adenocarcinoma driver mutations from Chinese population (ID 1292)

      09:30 - 09:30  |  Author(s): B. Han

      • Abstract

      Background
      Driver gene mutation in lung adenocarcinoma varies greatly among different populations, and lacks of large sample study on Chinese population. The purpose of this study was to identify driver gene mutations or translocations, and to evaluate their association with clinicopathological features and prognosis in Chinese lung adenocarcinoma.

      Methods
      Gene mutations or translocations were detected by fluorescence quantitative PCR in tumor tissues of 762 lung adenocarcinoma patients, including mutations of EGFR, KRAS and BRAF, and translocations of ALK and RET. The correlation of gene mutations/translocations with clinicopathological features was retrospectively analyzed by Chi-square test and logistic regression. Kaplan-Meier survival curves were used to evaluate the correlation of these genes with disease-free survival(DFS) in 314 patients and overall survival(OS) in 564 patients respectively.

      Results
      In the 762 patients with lung adenocarcinoma, the positive rate of gene mutations/translocations involving EGFR, KRAS, ALK, RET and BRAF was 49.6%, 10.0%, 4.5%, 1.7%, 0.5%, respectively, among which there was no mutations of polygenes. This study showed that EGFR mutations were more common in non-smokers or light smokers, lepidic predominant invasive adenocarcinoma subtype, and patients without distant metastasis. KRAS mutations were more common in heavy smokers, mucinous invasive adenocarcinoma subtype, and early stage patients. ALK translocations were more common in patients younger than 55 years old, with solid predominant invasive adenocarcinoma subtypes. RET translocations were more common in patients younger than 52 years old, with solid predominant invasive adenocarcinoma subtypes and patients who have family history of lung cancer. BRAF mutations were more common in mucinous invasive adenocarcinoma subtype. The survival analysis showed that the median OS of EGFR-mutant group was shorter than wild-type group among stage IIIB-IV paitents without targeting therapy(P=0.019); Although KRAS gene mutations in patients with early stage was not related to disease recurrence and survival either, KRAS mutations in stage IIIA patients do contribute to shorter DFS and OS(P=0.018, 0.039); ALK translocations in each stage subgroup were not related to recurrence and survival; Patients with mutations of either EGFR, KRAS, or translocations of ALK as a group showed no significant difference in DFS and OS as compared to those without involvement of any of these genes.

      Conclusion
      The overall driver gene positive rate in this series detected by Q-PCR is 66.3%. Each type of drive gene corresponds to different clinical and pathological features. Patients with ALK or RET gene translocations are more younger, and more likely to be solid predominant invasive adenocarcinoma. EGFR-mutant group has shorter OS than wild-type group among stage IIIB-IV paitents without targeting therapy. KRAS mutations implicate poor prognosis only in patients with stage IIIA.

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    P3.18 - Poster Session 3 - Pathology (ID 177)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Pathology
    • Presentations: 1
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      P3.18-010 - 5 Driver genes in Chinese Female Lung Adenocarcinoma (ID 1898)

      09:30 - 09:30  |  Author(s): B. Han

      • Abstract

      Background
      Currently, 5 driver genes (EGFR, K-RAS, B-RAF, ALK, RET) related to lung cancer have been widely explored and become new targets of NSCLC, however no report has been found in Chinese female lung adenocarcinoma, who were prone to EGFR mutations and therefore, are the targeted populations for TKIs therapy.

      Methods
      FFPE-tissues from 310 female lung adenocarcinoma adopted in Hunan province or Henan province between 2000 and 2012 were investigated. Oncogenic alterations in newly found 5 driver genes were analyzed. For EGFR, K-RAS and B-RAF mutation detection, ARMS was performed. The reverse transcription and real-time PCR were performed either to detect all ALK and RET fusions using primers specific to known rearrangement or to detect ALK and RET expression by primers specific to TK domain. Sequencing was further applied to confirm the subtypes of fusions.

      Results
      Among 310 samples, 149 (48.1%) EGFR mutations, 16 (5.2%) KRAS mutations, 0 (0%) BRAF mutations, 23 (7.4%) ALK fusions and 5 (1.6%) RET fusions were detected. Deletions in exon 19 and L858R in exon 21 account for the major EGFR mutations, representing 97 (65.1%) and 41 (27.5%), respectively. Only EML4-ALK fusion but no other ALK fusions were found. Further research demonstrated that cases (22, 95.6%) with high ALK expression were often accompanied by EML4-ALK fusion and poorly differentiated adenocarcinoma. Two RET fusions, namely, KIF5B-RET and CCDC6-RET were found, with 2 cases and 3 cases, respectively. The ratio of RET/ABL mRNA levels was significantly higher in CCDC6-RET samples with poorly differentiated adenocarcinoma. However, with KIF5B-RET fusion, the situation was more complex. Relatively high RET/ABL mRNA expression was detected in one KIF5B-RET sample with moderately differentiated adenocarcinoma, while no RET expression was detected in other two KIF5B-RET samples with highly differentiated adenocarcinoma.

      Conclusion
      This is the first research about the oncogenic alterations of 5 important driver genes in Chinese female lung adenocarcinoma, as well as the correlation between ALK fusion and ALK expression or between RET fusion and RET expression, thus laying good foundation for understanding the genetic mutation spectrum in female lung adenocarcinoma.

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    P3.22 - Poster Session 3 - Epidemiology, Etiology (ID 168)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Prevention & Epidemiology
    • Presentations: 1
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      P3.22-005 - XPA gene rs1800975 single nucleotide polymorphism and lung cancer risk: a meta-analysis (ID 2359)

      09:30 - 09:30  |  Author(s): B. Han

      • Abstract

      Background
      No clear consensus has been reached on the XPA gene A23G (rs1800975) polymorphism and lung cancer risk. We performed a meta-analysis in an effort to systematically explore the possible association.

      Methods
      Case-control studies in English and Chinese publications performed with human subjects were identified by searching MEDLINE, EMBASE, Wanfang and CNKI databases prior to June 2013. References of retrieved articles were also screened. According to the inclusion criteria, 10 articles (12 studies) were finally included. The fixed-effects model and the random-effects model were applied for dichotomous outcomes to combine the results of the individual studies.

      Results
      Overall, statistical association could be found between A23G polymorphism and lung cancer risk in recessive genetic model (AA vs. (AG+GG)) (P=0.001, OR=1.21, 95%CI [1.08–1.35], P~heterogeneity~=0.11, fixed-effects model) and in the homozygote comparison (AA vs. GG) (P=0.03, OR=1.15, 95%CI [1.01–1.31], P~heterogeneity~=0.14, fixed-effects model). In East Asians, significant association was found in allele comparison model (A vs. G) (P=0.03, OR=1.13, 95%CI [1.01–1.26], P~heterogeneity~=0.39, fixed-effects model), in recessive genetic model (AA vs. (AG+GG)) (P=0.005, OR=1.30, 95%CI [1.08–1.56], P~heterogeneity~=0.58, fixed-effects model) and in the homozygote comparison (AA vs. GG) (P=0.02, OR=1.30, 95%CI[1.04–1.63], P~heterogeneity~=0.39, fixed-effects model). No evidence suggested that A23G polymorphism might associate with lung cancer risk in the Caucasians or African-Americans. Stratification analysis was performed by histologic types and indicated that AA genotype might represent a risk factor for squamous cell carcinoma (AA vs. (AG+GG)) (P=0.01, OR=1.42, 95%CI [1.08–1.86], P~heterogeneity~=0.27, fixed-effects model); (AA vs. GG) (P=0.03, OR=1.43, 95%CI[1.04–1.96], P~heterogeneity~=0.21, fixed-effects model). No association was observed in adenocarcinoma subgroup. Stratification analysis performed by gender shown that A allele might increase the lung cancer risk in male (A vs. G) (P=0.02, OR=1.18, 95%CI [1.02–1.37], P~heterogeneity~=0.48, fixed-effects model), but did not found association in female subgroup. Figure 1 Figure – Meta-analysis for the association between XPA gene rs1800975 polymorphism and lung cancer risk in the contrast of AA vs. (AG+GG) in overall. “Events” indicates the number of the AA genotype; “Total” indicates the total number of the AG+GG genotype plus the AA genotype.

      Conclusion
      XPA gene A23G polymorphism might associate with lung cancer risk in Overall and East Asians. This polymorphism might also associate with lung cancer risk in male and in the squamous cell carcinoma subgroup.