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An observational study on the efficacy of targeted therapy for pulmonary sarcomatoid carcinoma
Takeshi Tsuda1, Tomomi Ichikawa2, Masahiro Matsumoto3
1Department of Respiratory Medicine, Toyama Prefectural Central Hospital, Toyama City, Japan.
Background:
Pulmonary sarcomatoid carcinoma is a rare tumor that is resistant to cytotoxic agents. This observational study aimed to evaluate the detection rate of driver gene alteration and the efficacy of targeted therapy for pulmonary sarcomatoid carcinoma.
Methods:
We established a database of patients with pulmonary sarcomatoid carcinoma and their clinical information, including EGFR mutation, ALK fusion gene, ROS1 fusion gene, BRAF mutation, and MET exon 14 skipping mutation. The present study retrieved and analyzed the data of patients with pulmonary sarcomatoid carcinoma in whom driver gene alterations were evaluated, and the survival duration after the initiation of treatment with targeted therapy was examined.
Results:
A total of 44 patients were included in the present study. The EGFR mutation, ALK fusion gene, and MET exon 14 skipping mutation were detected in 2/43 patients (4.7%), 2/34 patients (5.9%), and 2/16 patients (12.5%), respectively. The ROS1 fusion gene (0/18 patients) and BRAF mutation (0/15 patients) were not detected. Female patients (P = 0.063, Fisher's exact test) and patients without smoking history (P = 0.025, Fisher's exact test) were the dominant groups in which any driver mutation was detected. Five patients with driver gene alterations were treated with targeted therapy. Progression-free survival (PFS) was 1.3 months and 1.6 months in 2 of the patients treated with gefitinib. Two patients with the ALK fusion gene showed 2.1 and 14.0 months of PFS from the initiation of treatment with crizotinib, and a patient with the MET exon 14 skipping mutation showed 9.7 months of PFS from the initiation of treatment with tepotinib.
Conclusion:
The EGFR mutation, ALK fusion gene, and MET exon 14 skipping mutation were detected in patients with pulmonary sarcomatoid carcinoma in clinical practice, and some patients achieved long survival times after receiving targeted therapy. Further investigation is necessary to evaluate the efficacy of targeted therapy for pulmonary sarcomatoid carcinoma.
Insights
This study found driver gene alterations like EGFR, ALK, and MET mutations in pulmonary sarcomatoid carcinoma. Targeted therapies showed varied efficacy, with some patients experiencing prolonged progression-free survival, indicating potential treatment avenues.
Area of Science:
- Oncology
- Genetics
- Pulmonology
Background:
- Pulmonary sarcomatoid carcinoma (PSC) is a rare and aggressive lung cancer subtype.
- PSC exhibits resistance to conventional cytotoxic chemotherapy.
- Identifying actionable genetic alterations is crucial for developing effective treatments.
Purpose of the Study:
- To determine the detection rate of driver gene alterations in PSC.
- To evaluate the clinical efficacy of targeted therapies in PSC patients with identified mutations.
- To analyze progression-free survival (PFS) in response to specific targeted agents.
Main Methods:
- Retrospective analysis of a database of 44 PSC patients.
- Evaluation of common driver gene alterations including EGFR, ALK, ROS1, BRAF, and MET exon 14 skipping.
- Assessment of PFS following targeted therapy initiation for patients with detected mutations.
Main Results:
- Driver gene alterations were detected in a subset of patients: EGFR (4.7%), ALK (5.9%), and MET exon 14 skipping (12.5%).
- ROS1 fusion and BRAF mutations were not detected.
- Targeted therapy demonstrated variable PFS, with examples including gefitinib (1.3–1.6 months), crizotinib (2.1–14.0 months), and tepotinib (9.7 months).
Conclusions:
- EGFR, ALK, and MET exon 14 skipping mutations are present in PSC and can be targeted.
- Some PSC patients achieve meaningful PFS with targeted therapies.
- Further research is warranted to optimize targeted treatment strategies for PSC.
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