RESUMO
Background: Lung cancer is a malignant tumor with high morbidity and mortality worldwide. At present, the main treatment methods for patients with advanced non-small cell lung cancer (NSCLC) include molecular targeted therapy and immunotherapy. The efficacy rate of immune checkpoint inhibitor (ICI) monotherapy is relatively low. Studies have confirmed that some combination therapies have better anti-tumor efficacy and higher response rates, such as PD-1/PD-L1 inhibitors combined with chemotherapy or targeted therapy. Poly (ADP-ribose) polymerase (PARP) inhibitors have become a new line of cancer therapy in ovarian and breast cancer, but it's not approved in lung cancer. Some reports show that homologous recombination repair (HRR) gene variants may be potential biomarkers for immunotherapy. However, whether lung cancer with HRR gene variants can be benefit from ICIs combined with PARP inhibitors is unknown. Case Description: We present a case of a 30-year-old man who was admitted to hospital with several months of cough and the chest computed tomography (CT) scan showed a mass about 2.6 cm × 2.1 cm in the left lung. Then he was diagnosed with lung adenocarcinoma (LUAD). Next generation sequencing (NGS) revealed that he harbors ROS1 fusion and NBN germline mutation. So, he received platinum-based chemotherapy and ROS1 inhibitors, but the disease continued to progress. Ultimately, the patient was switched to sintilimab combined with niraparib and the efficacy was evaluated as stable disease (SD), with a progression-free survival (PFS) of more than 12 months, and the overall survival (OS) is 23 months up to now. During the treatment, the major adverse events (AEs) observed were lymphopenia, nausea, vomiting, and edema. The AEs were tolerable. Conclusions: This case shows that the combination of small-molecule inhibitors and immunotherapy may improve survival in NSCLC patients with driver genes, and sintilimab combined with niraparib provides a successful clinical case for the treatment of refractory tumors HRR gene mutation, which can be used as a reference for personalized treatment. Of course, more clinical trials are needed to confirm this combination treatment strategy.
RESUMO
BACKGROUND: Ovarian cancer (OC) is a common malignancy in the gynecological tumor. Standard treatment for ovarian cancer is surgery and chemotherapy based on paclitaxel and platinum. However, traditional chemotherapy for ovarian cancer is limited by drug resistance and systemic side effects. It is imperative to explore effective treatment options for refractory ovarian cancer. CASE PRESENTATION: A 52-year-old female initially presented with lower abdominal distension and migratory pain. After the laparoscopic exploration and biopsy, immunohistochemistry showed poorly differentiated adenocarcinoma originated from ovarian (cT3NxM1, stage IV, peritoneal and abdominal wall metastasis). The next generation sequence detected ERRFI1 (T187A, exon4) mutation. RESULTS: The patient received first-line chemotherapy (paclitaxel, nedaplatin plus avastin), followed by maintenance therapy with gefitinib, achieving a 15-month progression-free survival (PFS). After disease progression and second-line treatment failure, endostar plus apatinib was administered for 14 cycles and she obtained a PFS of 14 months without long-term adverse events. CONCLUSION: We believe that the ERRFI1 gene may be a potential target of gefitinib. Importantly, endostar combined with apatinib is worth recommending for maintenance treatment in refractory ovarian cancer.
