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目的 分析辽宁省肿瘤医院2020-2022年小分子酪氨酸激酶抑制剂的使用情况以及变化趋势,为临床安全合理经济用药提供参考依据。方法 收集2020-2022年辽宁省肿瘤医院小分子酪氨酸激酶抑制剂使用数据,分析销售金额、用药频度(DDDs)、限定日费用(DDC)以及排序比(B/A)。结果 2020-2022年小分子酪氨酸激酶抑制剂销售金额逐年增长。奥希替尼连续3年销售金额稳居第1位。仑伐替尼销售金额大幅增长,而吉非替尼销售金额大幅下降。奥希替尼、埃克替尼、吉非替尼的DDDs近3年稳居前3位。仑伐替尼DDDs大幅上升,而索拉非尼DDDs大幅下降。普拉替尼、赛沃替尼和洛拉替尼的DDC值偏高。埃克替尼、吉非替尼、厄洛替尼、索拉非尼和达可替尼DDC值较低。从B/A可以看出,2022年埃克替尼和吉非替尼的B/A>1,赛沃替尼、培唑帕尼和阿来替尼的排序比<1。结论 2020-2022年辽宁省肿瘤医院小分子酪氨酸激酶抑制剂的使用总体上较为合理,但仍需进一步加强监管力度,保障患者用药的安全、有效和经济。 相似文献
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Hongfu Cai Longfeng Zhang Na Li Shen Chen Bin Zheng Jing Yang Lizhu Weng Mao-Bai Liu 《Clinical therapeutics》2019,41(2):280-290
Purpose
This study aimed to evaluate the cost-effectiveness of osimertinib with gefitinib or erlotinib as first-line and sequential therapy for epidermal growth factor receptor (EGFR) mutation–positive non–small cell lung cancer (NSCLC) in China.Methods
The Markov model was used, and the study included 3 health states over a 10-year period. Transition probabilities and safety data were collected from the FLAURA (AZD9291 versus gefitinib or erlotinib in patients with locally advanced or metastatic Non-small Cell Lung Cancer) trial. Cost and utility values were derived from local charges and literature. Sensitivity analyses were performed to observe model stability.Findings
: The strategy with gefitinib or erlotinib first-line therapy and second-line gene-guided osimertinib therapy (GE-T790M) resulted in a gain of 0.31 quality-adjusted life year (QALY) at a cost of $15,200.95 per patient compared with the gefitinib or erlotinib first-line therapy and second-line chemotherapy (GE-chemotherapy). The incremental QALY and incremental cost values for first-line osimertinib therapy compared with GE-chemotherapy was 0.96 and $69,420.76, respectively. Compared with the GE-T790M strategy (0.96 QALY and $29,223.33), first-line osimertinib was estimated to be more effective (1.61 QALYs) and more costly ($83,443.14). Relative to the GE-chemotherapy strategy, the incremental cost-effectiveness ratios were $47,873.96 and $71,954.08 per QALY gained with GE-T790M and the osimertinib first-line strategy. The incremental cost-effectiveness ratio for first-line osimertinib versus GE-T790M was estimated to be $83,766.61. The results were found to be robust for univariate and multivariable sensitivity analyses.Implications
Gefitinib or erlotinib first-line and chemotherapy second-line strategies were the most cost-effective first-line treatments for EGFR mutations in patients with NSCLC. Gefitinib or erlotinib first-line and gene-guided osimertinib second-line strategies were more cost-effective than osimertinib first-line treatment for patients who preferred osimertinib administration in China. 相似文献45.
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Koji Fukuda Sakiko Otani Shinji Takeuchi Sachiko Arai Shigeki Nanjo Azusa Tanimoto Akihiro Nishiyama Katsuhiko Naoki Seiji Yano 《Cancer science》2021,112(9):3784-3795
Leptomeningeal carcinomatosis (LMC) occurs frequently in non–small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations and is associated with acquired resistance to EGFR tyrosine kinase inhibitors (EGFR-TKIs). However, the mechanism by which LMC acquires resistance to osimertinib, a third-generation EGFR-TKI, is unclear. In this study, we elucidated the resistance mechanism and searched for a novel therapeutic strategy. We induced osimertinib resistance in a mouse model of LMC using an EGFR-mutant NSCLC cell line (PC9) via continuous oral osimertinib treatment and administration of established resistant cells and examined the resistance mechanism using next-generation sequencing. We detected the Kirsten rat sarcoma (KRAS)-G12V mutation in resistant cells, which retained the EGFR exon 19 deletion. Experiments involving KRAS knockdown in resistant cells and KRAS-G12V overexpression in parental cells revealed the involvement of KRAS-G12V in osimertinib resistance. Cotreatment with trametinib (a MEK inhibitor) and osimertinib resensitized the cells to osimertinib. Furthermore, in the mouse model of LMC with resistant cells, combined osimertinib and trametinib treatment successfully controlled LMC progression. These findings suggest a potential novel therapy against KRAS-G12V–harboring osimertinib-resistant LMC in EGFR-mutant NSCLC. 相似文献
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回顾性分析中南大学湘雅医学院附属株洲医院1例晚期肺腺癌患者的临床资料,并进行相关文献复习。该患者经胸腔穿刺术及左侧淋巴结活检确诊为肺腺癌,头部MRI及上腹部增强CT示头、肝、脾、胰腺及左侧肾上腺多发转移,表皮生长因子受体扩增阻滞突变系统(epidermal growth factor receptor-amplification refractory mutation system,EGFR-ARMS)检测提示EGFR 21外显子突变(L858R),给予第1代EGFR抑制剂(tyrosine kinase inhibitors,TKIs;吉非替尼)治疗11个月后,病情出现进展,再次基因检测EGFR T790M突变为阳性,二线给予第3代EGFR-TKIs(奥西替尼)治疗,病情得到缓解。说明初次EGFR-TKIs治疗后,部分晚期肺腺癌患者耐药后仍然可在EGFR-TKIs治疗中受益。以奥西替尼为代表的第3代EGFR-TKIs治疗耐药后出现T790M突变的患者疗效显著,给晚期肺癌患者带来更多的生存获益。 相似文献
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目的:通过体外细胞学实验初步探究奥希替尼联合两种不同机制的抗血管靶向治疗药物(贝伐珠单抗或阿帕替尼)治疗表皮生长因子受体(EGFR)敏感突变和T790M耐药突变肺腺癌细胞的抗肿瘤活性及其作用机制。方法:培养人肺腺癌细胞PC-9(E19 del)和H1975(E21 L858R/E20 T790M),CCK-8法检测奥希替尼及抗血管靶向治疗药物(贝伐珠单抗或阿帕替尼)单药或联合处理肺腺癌细胞48 h后的抑瘤率;蛋白质印迹法检测EGFR及其下游AKT和ERK信号通路蛋白表达情况。结果:PC-9和H1975肺腺癌细胞对奥希替尼敏感且呈剂量依赖性。奥希替尼联合抗血管生成靶向药物(贝伐珠单抗,阿帕替尼)较同等浓度的单药奥希替尼可增加对PC-9和H1975细胞株的抑瘤率(P<0.05)。低浓度奥希替尼联合高浓度阿帕替尼(1 000 nmol/L)的抑制作用与高浓度奥希替尼相当(P>0.05)。随着联合的阿帕替尼浓度的升高,对PC-9和H1975细胞抑瘤率也有一定程度的提高(P<0.05)。不同处理因素对PC-9细胞的抑制率均高于对H1975细胞(P<0.01)。随着奥希替尼浓度的上升,p-EGFR、p-AKT、p-ERK磷酸化蛋白表达逐渐降低。结论:奥希替尼联合贝伐珠单抗或阿帕替尼会进一步增强对EGFR敏感突变或T790M突变肺腺癌细胞的杀伤作用。奥希替尼与阿帕替尼联合使用具有很强的抑瘤活性,具有很好的应用前景。奥希替尼单药或与抗血管形成药联合作用可能是进一步下调EGFR及其下游AKT和ERK信号通路的活化。 相似文献
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Rationale:Leptomeningeal metastasis (LM) is a fatal complication of advanced non-small cell lung cancer (NSCLC) with a poor prognosis. Osimertinib is a promising option for NSCLC with LM harboring epidermal growth factor receptor (EGFR) mutation. However, therapeutic approaches remain a challenge for osimertinib resistant NSCLCs with LM. Although studies have reported that the first/second-generation EGFR-tyrosine kinase inhibitors were active against osimertinib-resistant NSCLC with EGFR C797S and sensitive mutation (SM), the resistance inevitably occurred due to the development of the EGFR SM/C797S/T790M triple mutations.Patient concerns:A 48-year-old woman was diagnosed with stage IV lung adenocarcinoma harboring the EGFR mutation in the combination of chest computed tomography, biopsy and amplification refractory mutation system-polymerase chain. One year and a half after oral administration of osimertinib, the patient progressed to extensive LM.Diagnoses:Magnetic resonance images of the brain showed extensive LM. Exfoliated tumor cells from cerebrospinal fluid (CSF) were positive detected by lumbar puncture and the cytology examination. EGFR mutations (exon19 E746_T751delinsI and exon20 C797S) in CSF circulating tumor DNA were detected by next-generation sequencing (NGS).Interventions:Pemetrexed (800 mg day 1), cis-platinum (40 mg day 1-3) combined with bevacizumab (400 mg day 1) every 3 weeks were administered to the patient. After 1 cycle, due to optic nerve invasion, erlotinib was applied 150 mg/d combined with previous regimen. The patient continued erlotinib monotherapy after 6 cycles.Outcomes:After LM, erlotinib combined with pemetrexed, cis-platinum and bevacizumab were administered to the patient for 4.25 months based on the CSF NGS. Then, the patient continued erlotinib monotherapy and appeared disease progression after 10 months. The overall survival is 35 months.Lessons:LM is a fatal complication of advanced NSCLC with a poor prognosis. NGS profiling of CSF circulating tumor DNA is important in NSCLC patients with LM and erotinib plus bevacizumab and chemotherapy is a promising option for patients with LM harboring EGFR C797S/SM. 相似文献