Virtual Library

 x 
My Library Virtual Library FAQ

Start Your Search

R.E. Martins



Author of

  • +

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

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

      P3.22-003 - EGFR genotyping and epidemiology, clinical and pathological features in 191 patients with metastatic pulmonary adenocarcinoma in Sao Paulo - Brazil. (ID 1026)

      09:30 - 09:30  |  Author(s): R.E. Martins

      • Abstract

      Background
      EGFR activating mutations in pulmonary adenocarcinoma does confer better prognosis and are also predictive of higher response rates to both chemotherapy and EGFR-tyrosine kinase inhibitors. Therefore, EGFR genotyping in these patients (pts) is a very helpful biomarker for treatment selection. Here we aimed to report the results of consecutive EGFR genotyping in our Institution in Sao Paulo - Brazil.

      Methods
      It is a prospective, observational study on all consecutively tested samples from pts diagnosed with pulmonary adenocarcinoma and treated at ICESP. All samples were formalin-fixed and paraffin-embedded. Tumor areas were selected and macrodissected, followed by whole DNA extraction and amplification by PCR. EGFR genotyping was performed through DNA sequencing (exons 18, 19, 20 and 21) by Sanger´s methodology.

      Results
      191 pts had tumor samples genotyped between Aug/2011 and Apr/2013. Median age was 64 y (17-90), 106 (56%) female. According to ethnicity, 154 pts were Caucasian (81%), 26 African-American (14%) and 11 Asian (6%). Seventy pts were classified as never-smokers (37%), 23 (12%) as light-smokers (≤ 10 p.y.) and 95 as current smokers (51%). EGFR activating mutations could be identified in 54 out of 191 samples (28%): 35 were exon 19 deletions (65%), 15 were L858R mutation in exon 21 (30%), and three were rare mutations (G719S and G719A in exon 18, and V774M in exon 20). These mutations were found to be more frequent in females than in males (56% vs. 45%, p=0.035), and in never-smokers and light-smokers than in current smokers (77% vs. 20%, p<0.0001). It is noteworthy to mention that 11 mutations were detected in current smokers. All tumors harboring EGFR activating mutations presented TTF-1 expression by immunohistochemistry, and among those seven TTF-1-negative adenocarcinomas, no mutation was detected (p=0.0969). In a mean follow-up of 12 months, 77 pts were dead. Median overall survival was not reached in those pts whose tumors harboring EGFR-activating mutations, versus 19 months in pts with wild-type EGFR tumors (HR 0.40; 95%CI 0.29-0.78, p=0.003).

      Conclusion
      In this group of pts, the frequency of EGFR activating mutations was 28%, being more frequent in females, and never-smokers or light smokers, as previously described. Indeed, the presence of EGFR activating mutations was a favorable prognostic factor. The data here presented does reinforce the importance of testing EGFR activating mutations in all pts with TTF-1-positive, pulmonary adenocarcinoma.

  • +

    P3.24 - Poster Session 3 - Supportive Care (ID 160)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Supportive Care
    • Presentations: 1
    • +

      P3.24-051 - Primary Thoracic Angiosarcoma: Treatment and outcomes of 5 patients (ID 3280)

      09:30 - 09:30  |  Author(s): R.E. Martins

      • Abstract

      Background
      Angiosarcomas (AS) are rare aggressive tumors that represent about 1-2% of all soft-tissue sarcomas; 9.5% of them arise in the thorax. We describe five patients diagnosed with thoracic AS who were treated at ICESP.

      Methods
      It is a case series descriptive study with review of the medical files from five consecutively registered patients with AS confirmed by immunohistochemistry at our institution between June 2010 and March 2013.

      Results
      Case 1: A 49-year-old woman was admitted with pulmonary AS presenting progressive dyspnea and a recent hemoptysis. Pneumonectomy was performed in April 2011 and she was treated with adjuvant doxorubicin (every 3 weeks, 4 cycles) and paclitaxel (12 weeks). After 7 months, she developed progressive disease (PD) in liver, bones and lymph nodes. Weekly paclitaxel was restarted, but she had hepatic PD. Since May 2013 she has been treated with liposomal doxorubicin. She is alive after 26 months of diagnosis. Case 2: A 62-year-old woman was diagnosed with metastatic paracardiac AS after cardiac tamponade. She was treated with weekly paclitaxel and developed PD in liver and lungs. She died 3 months after diagnosis. Case 3: A 32-year-old man, was diagnosed with a primary AS in the right ventricle, metastatic to lungs, was admitted with recurrent pericardial effusion for 6 months. The tumor was considered unresectable and he was treated with doxorubicin and ifosfamide (only one cycle), temporarily interrupted due to febrile neutropenia grade 4, but with a partial response. He is alive after 3 months of diagnosis. Case 4: A 31-year-old man was diagnosed with unresectable AS in the right atrium after developing a superior vena cava syndrome. Weekly paclitaxel was started, with initial clinical improvement, but PD was detected after 6 cycles (24 weeks). As a second-line treatment, doxorubicin and ifosfamide were administered, with PD in lungs after 5 cycles. He died 13 months after the beginning of chemotherapy. Case 5: A 58-year-old woman was diagnosed with a right infraclavicular unresectable AS with local pain and edema in the upper right arm for one year. No response was seen after two cycles of doxorubicin and ifosfamide. Palliative radiotherapy followed by weekly paclitaxel was attempted as a second-line therapy with no response. Best supportive care was started and she is alive 6 months after diagnosis.

      Conclusion
      We concluded that thoracic AS presents a very dismal prognosis, due to the primary location and the high incidence of metastatic disease. For those patients with resectable disease and curative intent, surgery must always be considered. Weekly paclitaxel and the combination of doxorubicin and ifosfamide are both active in thoracic AS, but responses usually were not long-lasting. Oral tyrosine kinase inhibitors with antiangiogenic properties may be an option to be better explored.