Virtual Library
Start Your Search
Teresa García Manrique
Author of
-
+
P2.03 - Chemotherapy/Targeted Therapy (ID 704)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Chemotherapy/Targeted Therapy
- Presentations: 1
- Moderators:
- Coordinates: 10/17/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
-
+
P2.03-051 - The Impact of EGFR Mutations. Treatment with ITKs in Non Small Cell Lung Cancer Patients (ID 10302)
09:30 - 16:00 | Presenting Author(s): Teresa García Manrique
- Abstract
Background:
Patients with advanced stage of non small cell lung cancer (NSCLC) have been historically treated with a limited number of cycles of first-line chemotherapy, with platinum-doublets as the most commonly used regimen, after which, those with tumour response or stable disease are observed for evidence of disease progression; progression is followed by second-line therapy in proper patients. In patients with advanced NSCLC harboring EGFR mutations, the use of EGFR TKIs in first-line treatment has shown a large PFS benefit with almost no toxicity when compared with chemotherapy. For patients with lung adenocarcinoma and activating EGFR mutations who received EGFR TKIs median overall survival (OS) ranges between 24 and 30 months contrasts with the plateau of 10 months reached with first line platinum-based chemotherapy in populations not selected by molecular profiling.
Method:
We analyze all patients attended in our hospital with NSCLC, who had received EGFR-TKI since 2010 to 2015 when hoarbouring EGFR mutation. For descriptive purposes, continuous variables were summarized as arithmetic means, medians and standard deviations, and categorical variables were reported as proportions with 95% confidence intervals (95% CI). PFS and OS were measured from the day of EGFR TKI treatment to the date of progression or death, respectively, and analyzed with the Kaplan-Meier technique.
Result:
The amount of patients were 46. Six types of EGFR gene mutations were found: delection in exon 19, exon 18 (G719), exon 20 (T790 and S768I ) and in exon 21 (L861Q and L858R). Two patients were combinations of G719 and L861Q, the third was a combination of G719 plus S768I, and the fourth was a combination of delection in 19 exon and T790 mutation. 13 patients (24.5%) could recieve second and furthers lines of therapy after EGFR ITKs, including: chemotherapy, immunotherapy and second generation EGFR TKIs. PFS was 9,98 months [4,7-15,25; IC95%.] OS was 23,45 months [11,26-35,6; IC 95%]
Conclusion:
The outcome of this study is to describe patient population receiving EGFR-TKIs. As expected most of them harbored the common sensitizing EGFR mutations L858R and delection in exon 19;both were higher in women and specially L858R mutation in non smokers. Nowadays treatment of patients with advanced NSCLC should be individualized, based on the molecular and histological features of their tumour. When harbouring an activating EGFR mutation, first-line treatment should be with an EGFR TKI.
-
+
P3.02 - Biology/Pathology (ID 620)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
-
+
P3.02-047 - Testing EGFR and ALK in Large Cell Neuroendocrine Carcinoma of the Lung. Looking for Biological Features in Rare Tumors (ID 9612)
09:30 - 16:00 | Presenting Author(s): Teresa García Manrique
- Abstract
Background:
Large-cell neurodendocrine carcinoma (LCNEC) of the lung is a high-grade carcinoma. It is a very rare tumor, approximately 3% of all lung malignancies. Despite LCNEC responds to cisplatin-based chemotherapy prognosis remains poor. We try to Identify positive cases for EGFR mutations and ALK rearrangement by using fluorescence in situ hybridization (FISH) as gold standard and its correlation with immunohistochemistry (IHC) in LCNEC aming to find new therapeutic options for those patients.
Method:
Patients with LCNEC in our Hospital between 1998 and 2017 were included; classification were originally performed according to the WHO2004 scheme and updated to the WHO2015 scheme. EGFR mutation was determined on DNA extracted from formalin-fixed paraffin-embedded (FFPE) tissue with the cobas® EGFR Mutation Test v2. ALK FISH testing was performed using the Vysis ALK break-apart FISH kit (Abbott Molecular). At least 50 non-overlapping nuclei were scored by two FISH assays expert pathologists. A higher number of nuclei (100) was counted in cases with the results close to cut-off values.Tumours were interpreted as positive if a split pattern and/or single orange signal without a corresponding green signal were identified in at least 15% of tumour cells ALK IHQ test was performed retrospectively on freshly cut 4-lm thick FFPE tissue sections using anti-ALK (D5F3 clone) rabbit monoclonal antibody on a BenchMark XT autostainer with the Ultraview diaminobenzidine (DAB) detection kit. Staining was positive if tumour cells showed moderate or strong multifocal or diffuse expression. Positive cases showed granular cytoplasmic pattern. Cases were considered concordant if ALK FISH and ALK IHC results were identical.
Result:
27 cases, all of them with enough samples for additional EGFR, ALK FISH and ALK IHC testing were identified. Although 4 cases were positive for ALK staining with IHC only one showed expression in more than 90% of tumor cells and it was also positive for ALK rearrangement with FISH. As reported in literature, we have observed some moderate stippling staining in alveolar and peritumoral macrophages with IHC . Only one was EGFR mutated in exon 20, harboring G719X mutation
Conclusion:
To our knowledge very few LCNEC carrying EGFR mutation or ALK rearrangement have been reported. It highlights the possibility of treating those patients with targeted therapy Although we have found good correlation between FISH and IHC, we dare to recommend still as gold standar test, FISH to assess ALK gene rearrangement.
