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Zhengbo Song
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P3.01 - Advanced NSCLC (Not CME Accredited Session) (ID 967)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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P3.01-104 - EGFR-RAD51 Fusion Variant in Lung Adenocarcinoma and Response to Erlotinib: A Case Report (ID 11102)
12:00 - 13:30 | Author(s): Zhengbo Song
- Abstract
Background
The most frequent epidermal growth factor receptor (EGFR) mutations of lung cancer include exon 19 in deletion and the exon 21 L858R mutation. And EGFR-tyrosine kinase inhibitor (TKI) as the standard first line treatment show good response to classical/sensitizing EGFR mutations. With the development of detection methods, some uncommon genomic mutation events such as exon 18-25 kinase domain duplications (KDD) and EGFR rearrangements (EGFR-RAD51 or EGFR-PURB) are found. We reported a case of EGFR-RAD51 fusion in non-small-cell lung cancer(NSCLC) and the efficacy of erlotinib to this type fusion of NSCLC patients.
a9ded1e5ce5d75814730bb4caaf49419 Method
A 48-year-old male diagnosed with adenocarcinoma (IV, T1N2M1), who was shown to have EGFR fusion by next generation sequencing.
4c3880bb027f159e801041b1021e88e8 Result
The patient with right lung tumor and multiple brain metastases NSCLC. Histological examination of surgical specimens from the brain tumor showed lung adenocarcinoma metastasis. By using next generation sequencing assay, we found that tumor had EGFR-RAD51 fusion rather than the most common kind of EGFR mutations. Then the patient experienced a remarkable tumor response to erlotinib. Considering this rare EGFR fusion and remarkable response to TKI treatment, we conclude that the incidence of EGFR fusions in NSCLC patients should be attentive. NSCLC patients with EGFR-RAD51 fusion gene response to treatment with EGFR inhibitor.
8eea62084ca7e541d918e823422bd82e Conclusion
With the guidance of precise diagnosis, it is important that we should realize other rare EGFR gene mutations and novel diagnostic method.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P3.CR - Case Reports (Not CME Accredited Session) (ID 984)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 2
- Moderators:
- Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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P3.CR-09 - MET-UBE2H fusion as a novel mechanism of acquired EGFR resistance in<br /> lung adenocarcinoma" with "MET fusion as a novel mechanism of acquired EGFR resistance in<br /> lung adenocarcinoma (ID 11219)
12:00 - 13:30 | Author(s): Zhengbo Song
- Abstract
Background
As we all known, the most common mechanism of acquired resistance to EGFR-TKIs treatment is the development of the EGFR T790M mutation, which occurs almost one half of cases of acquired resistance. Other previously described resistance mechanisms include HER2 amplification, MET amplification, PIK3CA mutation, epithelialmesenchymal transition (EMT), and small cell transformation.
a9ded1e5ce5d75814730bb4caaf49419 Method
A 43-year-old female diagnosed with adenocarcinoma including brain and bone metastases, who was shown to have MET fusion after erlotinib acquired resistance by next generation sequencing.
4c3880bb027f159e801041b1021e88e8 Result
The patient with left lung tumor. Cytological examination of sepecimens from primary focus show adenocarcinoma." with "A bronchoscopic biopsy sepecimens from primary foucus show adenocacrcinoma. By next generation sequencing we found EGFR 19 exon E746_S752delinsV and MET-UBE2H fusion after erlotinib acquired resistance, and the patient experienced a remarkable tumor response to crizotinib remains at 6 months on therapy.
8eea62084ca7e541d918e823422bd82e Conclusion
We report the occurrence of MET-UBE2H fusion along with EGFR 19del at disease progression after treatment with erlotinib. Hence we attribute the emergence of MET-UBE2H fusion as a possible mechanism of acquired resistance to first generation EGFR-TKI in EGFR mutated NSCLC.
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P3.CR-11 - ROS1 Fusion and MET Amplification Dual Drive Coexistence in Lung Adenocarcinoma and Response to Crizotinib: A Case Report (ID 11212)
12:00 - 13:30 | Author(s): Zhengbo Song
- Abstract
Background
The c-ros oncogene 1 (ROS1) fusion is almost mutually exclusive to MET amplication in non-small cell lung cancer (NSCLC), and it is not seen in the literature for patients to exhibitthree mutations.
a9ded1e5ce5d75814730bb4caaf49419 Method
A 66-year-old female diagnosed with IV stage adenocarcinoma, who was shown to have ROS1 fusion and MET amplication by fluorescence in situ hybridization (FISH), and verified by next generation sequencing.
4c3880bb027f159e801041b1021e88e8 Result
The patient with right lung tumor and brain metastases NSCLC. Histological examination of surgical sepecimens from primary focus show adenocarcinoma. By fluorescence in situ hybridization (FISH), we found ROS1 fusion and MET amplication. Then we verified a novel ROS1fusion: ZCCHC8-ROS1, and the patient experienced a remarkable tumor response to crizotinib for 6 months (PFS).
8eea62084ca7e541d918e823422bd82e Conclusion
To the best of to our knowledge, this is the first case report of a patient with concurrent ROS1 fusion and MET amplication, and ZCCHC8-ROS1. This patient had an excellent response to crizotinib, suggesting that concurrent ROS1 fusion and MET amplication response to crizotinib was less than ROS1 fusion single driver.
6f8b794f3246b0c1e1780bb4d4d5dc53
