Virtual Library

 x 
My Library Virtual Library FAQ

Start Your Search

L. Xiong



Author of

  • +

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

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Medical Oncology
    • Presentations: 1
    • +

      P2.12-001 - Erlotinib as neoadjuvant treatment in patients with stage IIIA-N2 non-small cell lung cancer (NSCLC) with activating Epidermal Growth Factor Receptor (EGFR) mutation (NCT01217619, EASTERN): study update (ID 260)

      09:30 - 09:30  |  Author(s): L. Xiong

      • Abstract

      Background
      Approximately 15% of patients with NSCLC are diagnosed with stage IIIA-N2 disease, the treatment modalities of which are not clearly defined due to its heterogeneous character. Patients with stage IIIA N2 NSCLC have poor outcomes with 5-year survival rate of approximately 15% after treatment with surgical resection or chemo-radiotherapy. Tyrosine kinase inhibitor mono-therapy as the first line treatment could significantly improve tumor response rate and disease progression free survival (PFS) for metastatic NSCLC patients with activating EGFR mutation. The objective of this trial is to explore the efficacy and safety profile of erlotinib as neoadjuvant treatment in patients of stage IIIA-N2 NSCLC with activating EGFR mutation.

      Methods
      This is a prospective, single arm, phase Ⅱ clinical trial. Patients with Endobronchial Ultrasound(EBUS) confirmed stage ⅢA-N2 NSCLC with activating EGFR mutation in exon 19 or 21 will be enrolled into the study. All the recruitment patients will be treated by erlotinib 150mg orally per day for 56 days for neoadjuvant period. Patients will be assessed after erlotinib treatment and those who get response from neoadjuvant therapy and are technically resectable will undergo surgery treatment. The adjuvant regime is decided by the investigator taking patients’ benefits into consideration. The primary endpoint is radical resection rate. The secondary endpoints are pathological complete resection rate(pCR), objective response rate(ORR), disease free survival(DFS), overall survival(OS), quality of life(QoL) and safety profile. Patients after surgery and therapy will receive long-term follow-up including regular chest CT and ultrasound examination.

      Results
      Eighty-eight(88) patients have been screened and 15 patients have been enrolled since first patients in (FPI) on 30th April, 2011. Excluded reasons including ineligible pathological diagnosis (n=23), ineligible stage (n=36), without EGFR mutation (n=10) and poor compliance (n=4). Ineligible stage including T1-3N0M0 (n=11), T1-3N1M0 (N=8), T1-3N3M0 (N=8), T1-3N2M1 (N=7) and T4N2M0 (N=2). 41% patients who were diagnosed with stage IIIA-N2 non-small cell lung cancer when in chest CT examinations were not in the stage after endobronchial ultrasound(EBUS) , and became the main reason for screening failure in this study. Seven patients had partial response, 3 patients with stable disease and 2 patients were still on treatment (DCR 66.6%). 3 patients with progress disease. Due to active hepatitis and technical infeasibility, 2 patients with partial disease didn’t receive surgery. However, one stable disease patient and five partial response patients (40%) received R0 surgery.

      Conclusion
      Neoadjuvant erlotinib therapy might be a promising treatment for IIIA-N2 NSCLC patients with EGFR activating mutation. EBUS helps the judgment of mediastinal lymph node metastasis and is better than CT scan.

  • +

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

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Prevention & Epidemiology
    • Presentations: 1
    • +

      P3.22-005 - XPA gene rs1800975 single nucleotide polymorphism and lung cancer risk: a meta-analysis (ID 2359)

      09:30 - 09:30  |  Author(s): L. Xiong

      • 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.