Objective To investigate the effect and safety of Sintilimab combined with Endostar injection in the treatment of programmed cell death ligand-1(PD-L1)positive lung squamous cell carcinoma(LSCC)in elderly patients.Methods A total of 94 elderly patients with PD-L1 positive LSCC diagnosed and treated from November 2019 to November 2021 were selected as the research subjects,and they were divided into the observation group(n=47)and the control group(n=47)by random number table method.The observation group was treated with Sintilimab combined with Endostar injection,and the control group was treated with Sintilimab.Twenty-one days constituted one treatment cycle,and they were treated for 3 consecutive cycles.The clinical efficacy and improvement rate of Karnofsky performance status(KPS)score in the two groups were statistically analyzed,as well as the tumor markers[carcinoembryonic antigen(CEA),cancer antigen 125(CA125),cytokeratin 19 fragment(CYFRA21-1)],angiogenesis factors[endostatin,insulin-like growth factor-1(IGF-1),vascular endothelial growth factor(VEGF),basic fibroblast growth factor(bFGF),and platelet-derived growth factor(PDGF)],apoptosis factor[B-cell lymphoma-2 gene(Bcl-2),Bcl-2-associated X protein(Bax),Livin protein,programmed cell death 5(PDCD5)]before and after treatment.The toxic and side effects during treatment,progression-free survival(PFS)and median survival time at 2-year follow-up were compared between the two groups.Results After treatment,the objective remission rate and disease control rate of the observation group were higher than those of the control group(P<0.01);after treatment,the improvement rate of KPS score in the observation group was higher than that in the control group(P<0.01).After treatment,the levels of serum CEA,CA125,and CYFRA21-1 in both groups decreased,and which were lower in the observation group than in the control group(P<0.05,P<0.01).After treatment,the levels of endostatin increased in both groups,while IGF-1,VEGF,bFGF,and PDGF decreased;the levels of endostatin in the observation group were higher than those in the control group,while the levels of IGF-1,VEGF,bFGF,and PDGF were lower than those in the control group(P<0.05,P<0.01).After treatment,the levels of Bcl-2 and Livin decreased in both groups,while Bax and PDCD5 increased;the levels of Bcl-2 and Livin in the observation group were lower than those in the control group,while the levels of Bax and PDCD5 were higher than those in the control group(P<0.05,P<0.01).There was no significant difference in toxic and side effects between the two groups during treatment(P>0.05).The 2-year survival rate and median survival time of the observation group were higher or longer than those of the control group(P<0.05).Conclusion The treatment of PD-L1 positive LSCC in elderly patients with Sintilimab combined with Endostar injection can improve the therapeutic effect and the survival status of patients,inhibit tumor angiogenesis,induce tumor apoptosis,prolong the survival time of patients,and has good safety.

Objective To investigate the effect and safety of Sintilimab combined with Endostar injection in the treatment of programmed cell death ligand-1(PD-L1)positive lung squamous cell carcinoma(LSCC)in elderly patients.Methods A total of 94 elderly patients with PD-L1 positive LSCC diagnosed and treated from November 2019 to November 2021 were selected as the research subjects,and they were divided into the observation group(n=47)and the control group(n=47)by random number table method.The observation group was treated with Sintilimab combined with Endostar injection,and the control group was treated with Sintilimab.Twenty-one days constituted one treatment cycle,and they were treated for 3 consecutive cycles.The clinical efficacy and improvement rate of Karnofsky performance status(KPS)score in the two groups were statistically analyzed,as well as the tumor markers[carcinoembryonic antigen(CEA),cancer antigen 125(CA125),cytokeratin 19 fragment(CYFRA21-1)],angiogenesis factors[endostatin,insulin-like growth factor-1(IGF-1),vascular endothelial growth factor(VEGF),basic fibroblast growth factor(bFGF),and platelet-derived growth factor(PDGF)],apoptosis factor[B-cell lymphoma-2 gene(Bcl-2),Bcl-2-associated X protein(Bax),Livin protein,programmed cell death 5(PDCD5)]before and after treatment.The toxic and side effects during treatment,progression-free survival(PFS)and median survival time at 2-year follow-up were compared between the two groups.Results After treatment,the objective remission rate and disease control rate of the observation group were higher than those of the control group(P<0.01);after treatment,the improvement rate of KPS score in the observation group was higher than that in the control group(P<0.01).After treatment,the levels of serum CEA,CA125,and CYFRA21-1 in both groups decreased,and which were lower in the observation group than in the control group(P<0.05,P<0.01).After treatment,the levels of endostatin increased in both groups,while IGF-1,VEGF,bFGF,and PDGF decreased;the levels of endostatin in the observation group were higher than those in the control group,while the levels of IGF-1,VEGF,bFGF,and PDGF were lower than those in the control group(P<0.05,P<0.01).After treatment,the levels of Bcl-2 and Livin decreased in both groups,while Bax and PDCD5 increased;the levels of Bcl-2 and Livin in the observation group were lower than those in the control group,while the levels of Bax and PDCD5 were higher than those in the control group(P<0.05,P<0.01).There was no significant difference in toxic and side effects between the two groups during treatment(P>0.05).The 2-year survival rate and median survival time of the observation group were higher or longer than those of the control group(P<0.05).Conclusion The treatment of PD-L1 positive LSCC in elderly patients with Sintilimab combined with Endostar injection can improve the therapeutic effect and the survival status of patients,inhibit tumor angiogenesis,induce tumor apoptosis,prolong the survival time of patients,and has good safety.

Patients with operable non-small cell lung cancer (NSCLC) receiving neoadjuvant or adjuvant chemotherapy have a very limited improvement in 5-year survival rate. Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKI) have made a breakthrough in the treatment of EGFR-mutant advanced NSCLC, which shed light for the exploration of perioperative targeted therapy in NSCLC patients. Significant progress has been made in the research of targeted therapy of the first and third generation EGFR-TKI in perioperative patients. The availability of novel potent and less toxic targeted therapy has brought new treatments for the operable NSCLC. This article reviews the progress and existing problems of adjuvant and neoadjuvant targeted therapy in NSCLC harboring EGFR mutation.

Non-small cell lung cancer (NSCLC) is a malignant tumor with rapid progress and high malignancy, accounting for 85% of all lung cancers. Treatment has shifted from traditional surgery, radiotherapy and chemotherapy to targeted therapy. Targeted therapy can prolong the survival of patients with positive driver gene fusion. With the continuous progress of biological research, targets related to NSCLC have gradually been discovered. Among the many driving genes of NSCLC, RET fusion is an important emerging target discovered in recent years. It has been confirmed to have a high incidence in non-smoking, young and low-differentiated NSCLC patients. This article reviews RET gene fusion in NSCLC, the relationship between the two and the treatment progress.

KRAS mutation is one of the most frequent driver gene mutations found in patients with non-small cell lung cancer (NSCLC). KRAS-mutant NSCLC is highly heterogeneous. Various mutation types and different co-mutational signatures affect tumor biological behavior and therapeutic responses. NSCLC patients with KRAS mutations could relatively benefit from immunotherapy, while the effects of KRAS mutations on chemotherapy are still controversial. The treatment methods of KRAS-mutant lung cancer have followed the therapy of NSCLC without driver gene mutation for a long time. With the introduction of novel KRAS G12C inhibitors in the clinic, the therapeutic landscape has begun to change and has made the preliminary advance, and the combined therapies resulted in encouraging signals of efficacy both in preclinical and early phase trials. This paper reviews the biological and clinical characteristics as well as the latest treatment progress of KRAS-mutant NSCLC.

Immune checkpoint inhibitor (ICI) has been proven to be a major breakthrough in the treatment of various tumor types. Despite the favorable results in terms of oncological outcomes, these treatments have been associated with a variety of immune-related adverse events (irAEs). Myasthenia gravis (MG) is one of rare but life-threatening irAEs, with acute onset and rapid progression after ICI initiation. Early diagnosis and active treatment are crucial. Herein, we review recent literatures to provide guidance to frequently asked questions concerning the diagnosis and management of ICI-MG.

Background and objective Kirsten rat sarcoma viral oncogene (KARS) mutation is one of the major driver genes of non-small cell lung cancer (NSCLC). KARS is a resistant predictor of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), which raises controversy because of its role in chemotherapy sensitivity and prognosis. hTe aim of this study is to accumulate clinical experience in treating NSCLC patients harboringKARSmutation.MethodsA total of 107 NSCLC patients harboringKARSmutation were analyzed retrospectively. hTe effcacy was analyzed in terms of ifrst-line chemotherapy or EGFR-TKIs therapy.Results hTe objective response rate (ORR) to ifrst-line chemotherapy of 52 pa-tients with advanced disease harboringKARS mutation was 9.6%. hTe disease control rate (DCR) was 53.8%, and the median progression-free survival (PFS) was 3 months. hTe ORR to EGFR-TKIs therapy in 21 patients harboringKARS mutation and EGFR/KARS co-mutation was 9.5%; the DCR was 23.8%, and the median PFS was 1 month. hTe ORR and DCR to EGFR-TKIs therapy of patients withEGFR/KARS co-mutation were signiifcantly higher than those of patients withKARS mutation (50%vs 0,P=0.029; 75%vs 11.8%,P=0.043); the median PFS was also signiifcantly longer (3 monthsvs 1 month,P=0.004). Conclusion hTe effcacy to ifrst-line chemotherapy and EGFR-TKIs therapy in NSCLC patients harboringKARS mutation was poor; thus, new drugs should be developed. Furthermore, the existence ofEGFR/KARS co-mutation was conifrmed. Hence, EGFR-TKIs therapy should be administered to patients withEGFR/KARS co-mutation.

Background and objective Status of epidermal growth factor receptor (EGFR) gene is a predictor of response to EGFR tyrosine kinase inhibitor (TKI). However, lile is know about the relationship between EGFR status and response to chemotherapy. We evaluated the prediction value of EGFR mutation status on response to first-line chemotherapy in patients with advanced non-small-cell lung cancer (NSCLC). Methods e data of 181 patients with stage IIIb/IV NSCLC who diagnosed by histopathology from January 10, 2006 to December 20, 2013 in Beijing Chest Hospital, Capital Medical University were collected. e relationships between EGFR gene status, clinical characteristics and response and progression-free survival (PFS) were analyzed. Results All of the 181 patients’ EGFR statuses were determined. 75 (41.4%) patients har-bored EGFR-activating mutations and 106 (58.6%) patients were EGFR wild-type. All patients received first-line chemother-apy. e objective response rate (ORR) was 26.0% and disease control rate (DCR) was 70.2%. Patients with EGFR-activating mutations had a higher DCR than patients with EGFR wild-type (84.0% vs 60.4%, P=0.001) did. Subgroup analysis showed that the ORR and DCR in patients with EGFR exon 19 deletions were remarkably higher than those with EGFR wild-type (P= 0.049, 0.002, respectively). e DCR in patients with EGFR exon 21 L858R mutation was significantly higher than that in patients with EGFR wild-type (P=0.010). 168 patients were available for response evaluation in all of 181 patients and median PFS was 4.3 mo. e PFS of patients with adenocarcinoma was significantly higher than that patients with squamous cell carci-noma (4.7 mo vs 3.0 mo, P=0.036). e PFS in patients harbored EGFR-activating mutations was significantly higher than that in the patients with EGFR wild-type (6.3 mo vs 3.0 mo, P=0.002). e PFS of patients with a performance status (PS) of 0-1 was significantly higher than that in patients with a PS of 2 (4.4 months vs. 0.7 months, P= 0.016). Cox multivariate analysis indicates the EGFR-activating mutation is an independent factor aecting PFS (HR=0.654, 95%CI: 0.470-0.909, P=0.012). Conclusion EGFR-activating mutation is a predictor for PFS of first-line chemotherapy in advanced NSCLC patients.

Background and objective Activating mutations in epidermal growth factor receptor (EGFR) and KARS are important markers in non-small cell lung cancer. However, EGFR and KARS gene mutations in lung squamous cell carcinoma are rarely reported. hTe aim of this study was to analyze EGFR and KARS gene mutation rate and their relationship with clinical features in patients with lung squamous cell carcinomas. Methods A total of 139 patients undergoing treatment for na?ve lung squamous cell carcinomas with tumor tissue samples available for testing were recruited. EGFR and KARS mutation statuses of the tumor samples were detected using a mutant enriched liquid chip. Results Of the 139 cases of lung squamous cell carcinoma, EGFR mutations were detected in 25 cases (18%), KARS mutations were detected in 7 cases (5%), and the pres-ence of both EGFR and KARS mutations was detected in 1 case (0.7%). EGFR mutations occurred more otfen in females than in males (33.3%vs 16.5%) and in patients that never smoked than in those who smoke (29.6%vs 16.1%). However, the differ-ence did not reach statistical signiifcance (P>0.05). No signiifcant differences were observed in age, stage, and different biopsy type. KARS mutations occurred more otfen in males than in females (5.5%vs 0%), but the difference did not reach statistical signiifcance (P>0.05). No signiifcant differences were observed in age, stage, different biopsy type, and smoking status (P>0.05). Conclusion EGFR and KARS mutations were low in lung squamous cell carcinomas, and had no signiifcant correlation with clinical features. Before using tyrosine kinase inhibitor targeted therapy, EGFR and KARS mutations should be detected in pa-tients with lung squamous cell carcinomas.

Background and objectiveMutations in epidermal growth factor receptor (EGFR) andKARS are im-portant markers in non-small cell lung cancer, which are closely related to the clinical therapeutic effect. To analysis theEGFR andKARS gene mutation rate and its relationship with clinical features in patients with lung adenocarcinoma.Methods395 patients with treatment na?ve lung adenocarcinoma, tumor tissue samples were available for testing. Tumor sampleEGFR and KARS mutation status were detected using mutant enriched liquidchip.Results 395 cases of lung adenocarcinoma,EGFR mutations were detected in 192 cases (48.9%),KARS mutations were detected in 29 cases (7.8%), and the presence ofEGFR andKARS mutation were detected in 1 case (0.3%).EGFR mutations were found to occur signiifcantly more otfen in female than in male patients (62.0%vs 37.1%,P<0.001) and in never smokers than in smokers (61.9%vs 30.3%,P<0.001), no sig-niifcant differences were observed in age, stage and different biopsy type.KARS mutations were not found to have statistical signiifcance (P>0.05) in each clinical factors, only occurred in the wild typeEGFR gene in patients (13.5%, 27/200) was sig-niifcantly higher than that of patients withEGFR mutation (1.0%, 2/192), the difference was statistically signiifcant (P<0.001). ConclusionIn lung adenocarcinomas,EGFR mutation was higher in female and non-smoking patients,KARS mutation only in patients with wild-typeEGFR gene was higher. Before using TKI targeted therapy,EGFR andKARS mutations should be detected.