BACKGROUND Kirsten rat sarcoma viral oncogene homolog(KRAS)is a commonly identified oncogenic driver in solid tumors,especially in non-small cell lung cancer.Until recently,KRAS was believed to be impossible to target...BACKGROUND Kirsten rat sarcoma viral oncogene homolog(KRAS)is a commonly identified oncogenic driver in solid tumors,especially in non-small cell lung cancer.Until recently,KRAS was believed to be impossible to target because it lacks adenosine triphosphate-binding domains or other regions that allow specic small-molecule inhibitors to act.In this report,we described using KRAS at glycine 12 to cysteine(G12C)inhibitors as posterior line therapy in a patient with relapsed metastatic lung adenocarcinoma carrying KRAS G12C mutation.CASE SUMMARY A 53-year-old Chinese man was treated with radical surgical resection for lung cancer in June 2014.Re-examination in June 2015 indicated postoperative rec-urrence with metastasis.The patient completed several courses of antitumor therapy,including pemetrexed and nedaplatin,bevacizumab with docetaxel and cisplatin,bevacizumab and pemetrexed,sintilimab and anlotinib,sintilimab and albumin-bound paclitaxel,and cadonilimab and docetaxel.In early May 2023,the patient developed a cough productive of bloody sputum and shortness of breath after exercise.The main adverse reactions associated with KRAS G12C inhibitor therapy were gastrointestinal reactions,which could be alleviated by daily oral ondansetron tablets.CONCLUSION After multiple-line treatment including chemotherapy,targeted therapy,and immunotherapy,disease control was achieved in a case of advanced pulmonary adenocarcinoma carrying the KRAS G12C mutation by mutation-specific inhibitor therapy,and the adverse reactions to the therapy were tolerable.展开更多
基金Supported by National Natural Sciences Foundation of China,No.81803553.
文摘BACKGROUND Kirsten rat sarcoma viral oncogene homolog(KRAS)is a commonly identified oncogenic driver in solid tumors,especially in non-small cell lung cancer.Until recently,KRAS was believed to be impossible to target because it lacks adenosine triphosphate-binding domains or other regions that allow specic small-molecule inhibitors to act.In this report,we described using KRAS at glycine 12 to cysteine(G12C)inhibitors as posterior line therapy in a patient with relapsed metastatic lung adenocarcinoma carrying KRAS G12C mutation.CASE SUMMARY A 53-year-old Chinese man was treated with radical surgical resection for lung cancer in June 2014.Re-examination in June 2015 indicated postoperative rec-urrence with metastasis.The patient completed several courses of antitumor therapy,including pemetrexed and nedaplatin,bevacizumab with docetaxel and cisplatin,bevacizumab and pemetrexed,sintilimab and anlotinib,sintilimab and albumin-bound paclitaxel,and cadonilimab and docetaxel.In early May 2023,the patient developed a cough productive of bloody sputum and shortness of breath after exercise.The main adverse reactions associated with KRAS G12C inhibitor therapy were gastrointestinal reactions,which could be alleviated by daily oral ondansetron tablets.CONCLUSION After multiple-line treatment including chemotherapy,targeted therapy,and immunotherapy,disease control was achieved in a case of advanced pulmonary adenocarcinoma carrying the KRAS G12C mutation by mutation-specific inhibitor therapy,and the adverse reactions to the therapy were tolerable.
