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P. Martin Acosta
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P3.01 - Poster Session with Presenters Present (ID 469)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)
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P3.01-010 - Primary Giant Cell Carcinomas of the Lung: Study of Seven Cases (ID 4741)
14:30 - 14:30 | Author(s): P. Martin Acosta
- Abstract
Background:
Giant cell carcinoma (GCC) of the lung is a subtype of sarcomatoid carcinoma (2015 WHO classification) traditionally associated with a highly aggressive clinical behavior. The histology consists in giant cells without differentiated carcinomatous elements. The aim of this study is to analyze the clinical, pathological and molecular features of seven GCC cases diagnosed in our hospital.
Methods:
Twenty-nine sarcomatoid carcinoma diagnosed in our hospital during the years 2009-2016 were reviewed and 7 cases with GCC histology were selected for the study. Immunohistochemical staining with antibodies targeting TTF1, napsinA, p40, and β-HCG were performed. ALK and MET status were assessed by FISH. EGFR mutations were performed using real-time PCR.
Results:
The patients were 4 men and 3 women with a mean age of 61 years (range 45-79). At the moment of diagnosis three patients were current smokers and 4 former smokers. Five cases were peripheral tumors, six in the left lung, and one in the right lung. Complete resection was achieved in all patients. Tumor staging showed 3 cases pT1; 3 with pT2 stage and one case pT3. Histopathologically, all were pure GCC and immunohistochemical stains revealed that the giant cells were negative for β-HCG in all cases except one who could not be analyzed. Two cases showed null phenotype (TTF1 and p40-negative), two cases were TTF1-negative and p40-positive, two cases co-expressed TTF1 and p40 and one case was TTF1-positive and p40-negative. NapsinA was positive in two cases. Molecular analysis was done in 6 cases and no EGFR mutation was detected. FISH results for c-MET probe showed a MET/CEN7 ratio <2 in all cases, polysomy with ≥5 MET signals without amplification was found in 5 cases. No ALK rearrangement was observed in the series. Five cases showed ALK copy number gain (3 to 5 fusion signals) and one case had two fusion signals. With a median follow-up of 38 months (5-130 months), two patients died due to brain metastases (both with vascular-lymphatic invasion and nodal metastases at the time of surgery), and five patients are alive at the moment of analysis.
Conclusion:
Pure GCC is a very rare lung cancer subtype and there are few series reported. Lymphovascular invasion and lymph node involvement at diagnosis can predict a worse outcome in this subtype. GCC in our series do not have a specific immunohistochemical profile. Neither EGFR nor ALK were potential molecular targets, nevertheless c-MET status could be an interesting biomarker in GCC tumors.
