贝伐珠单抗联合TP化疗方案治疗晚期NSCLC的疗效及预后观察

目的探讨贝伐珠单抗联合TP(紫杉醇+顺铂)化疗方案治疗晚期非小细胞肺癌(NSCLC)的疗效及对预后的影响。方法选取晚期NSCLC患者78例,随机分为A组(39例,予以TP化疗方案)和B组(39例,予以TP化疗方案+贝伐珠单抗)。比较2组的客观缓解率(ORR)、疾病控制率(DCR)和血清肿瘤标志物[血管内皮生长因子(VEGF)、细胞角蛋白19片段(CYFRA21-1)、癌胚抗原(CEA)]水平。记录治疗期间肝肾功能损害、白细胞减少、中性粒细胞减少、血小板减少、胃肠道反应等不良反应发生情况。自实施治疗日始对患者进行随访,统计2组患者的5年生存率、无进展生存期(PFS)和总生存期(OS)。结果B组ORR、DCR分别为58.97%、89.74%,分别高于A组的35.90%、71.79%(P<0.05)。治疗后2组血清VEGF、CYFRA21-1、CEA水平均降低,且B组低于A组(P<0.05)。2组肝、肾功能损害,白细胞减少,中性粒细胞减少,血小板减少,胃肠道反应发生率均无明显差异(P>0.05)。B组5年生存率为20.51%,与A组(12.82%)相比无明显差异(P>0.05)。Kaplan-Meier生存曲线显示,B组的中位PFS长于A组(8.9 vs 7.2个月)(P<0.05);B组的中位OS长于A组(25.6 vs 17.9个月)(P<0.05)。结论相比于TP化疗方案治疗晚期NSCLC,联合贝伐珠单抗可提高ORR和DCR,延长PFS和OS,且可降低VEGF、CYFRA21-1、CEA肿瘤标志物水平。

盐酸安罗替尼对晚期NSCLC患者生存质量的影响分析

目的探究盐酸安罗替尼对晚期非小细胞肺癌(Non-small-cell Lung Carcinoma,NSCLC)患者生存质量的影响。方法方便选择2022年1—10月新沂市人民医院收治的122例NSCLC患者作为研究对象,采用随机双盲法将患者分成对照组(n=61)和观察组(n=61)。对照组进行常规化疗,观察组采用常规化疗联合盐酸安罗替尼治疗。对比两组肿瘤标志物水平、生活质量和不良反应。结果治疗前,两组癌胚抗原(Carcinoembryonic Antigen,CEA)、神经特异性烯醇化酶(Neuro-specific Enolase,NSE)、胃泌素释放肽前体(Gastrin-releasing Peptide Precursors,ProGRP)水平对比,差异无统计学意义(P均>0.05);治疗后,两组CEA、NSE、ProGRP水平均有下降,观察组分别为(17.36±2.17)ng/mL、(10.06±1.57)μg/L、(9.74±1.81)ng/L,低于对照组的(18.92±2.15)ng/mL、(11.14±1.54)ng/L、(11.15±1.73)μg/L,差异有统计学意义(t=3.989、3.836、4.398,P均<0.001);治疗前,两组肺癌治疗功能评价量表(Functional Assessment Lung Cancer Therapy,FACT-L)和生活质量评估量表(Quality of Life,QOL)评分对比,差异无统计学意义(P均>0.05),治疗后,两组FACT-L、QOL评分均有升高,且观察组高于对照组,差异有统计学意义(t=6.295、7.057,P均<0.001);治疗后,观察组患者不良反应的发生例数较对照组高,但差异无统计学意义(P>0.05)。结论安罗替尼能有效降低晚期NSCLC患者肿瘤标志物水平,控制疾病发展进程,提升患者生存质量,使用后产生的不良反应较小,用药安全性能得到保障。

Treatment with Intensity-Modulated Radiation Therapy (IMRT) and Chemotherapy in Advanced Inoperable Non-Small Cell Lung Cancer (NSCLC): Toxicity, Survival and Patterns of Failure in Relation to Treatment with High and Low Radiation Dose

Purpose: To investigate the toxicity, survival and patterns of failure in patients with advanced lung cancer treated with intensity modulated radiation therapy (IMRT) and chemotherapy. Methods and Materials: Retrospective chart review of 68 total patients: 46 academic and 22 community center. Endpoints: Grade ≥ 3 pneumonitis, Grade ≥ 2 esophagitis, local, regional and distant failure, progression-free survival (PFS) and overall survival (OS). Results: For the academic center patients, median follow-up was 19.2 months. Esophagitis: 0% Grade 3, 35% Grade 2, no significant difference between dose bins: <70 Gy vs. 70 Gy, 25% vs. 45% (p = 0.22), <66 Gy vs. 66 - 70 Gy, 28% vs. 39% (p = 0.53). Lung dose metrics and PTV size were not associated with Grade ≥ 3 pneumonitis. Esophageal V35, V50, and mean dose but not PTV size was associated with Grade 2 esophagitis. 1 year local, regional and distant failure = 6.5%, 6.5%, and 30.4%. No endpoint differences were seen between dose bins, though patients with smaller PTVs treated with 70 Gy did demonstrate improved OS (ns) when compared to those treated with <70 Gy. Community Center: Median follow-up 6.2 months with 15% Grade 2 esophagitis, no Grade 3 esophagitis. Two patients (9%) experienced Grade ≥ 3 pneumonitis. Conclusions: IMRT chemoradiation was well tolerated in a population with advanced NSCLC both in the academic and community settings. Severe pneumonitis rates were low and comparable to other series using IMRT and chemotherapy. Esophagitis was mild and associated with V35, V50 and mean dose. No significant benefit was seen for higher doses regarding survival, local, regional or distant control despite that higher dose bins had smaller tumors. Though not statistically significant, we did find a trend toward worse OS for <70 Gy when the PTV was less than the median PTV.

The clinical effects of DC-CIK cells combined with chemotherapy in the treatment of advanced NSCLC

Objective: The aim of the study was to evaluate the safety and therapeutic effects of autologous dendritic cells co-cultured with cytokine-induced killer cells (DC-CIK) combined with chemotherapy in advanced non-small cell lung cancer (NSCLC) patients. Methods: Fifty patients with advanced NSCLC (stages III to IV), who had received therapies in our Center (Department of Biotherapy, Affiliated to Cancer Hospital of Shanxi Medical University, Taiyuan, China) from August 2008 to January 2010, were treated by DC-CIK + chemotherapy as the combined treatment group; fifty advanced NSCLC patients treated with chemotherapy at the same time served as controls. The immunologic function, short-term therapeutic effects, the 1-year survival rate, the life quality, the chemotherapy side effects were compared between the two groups, the safety and therapeutic effects of DC-CIK cells therapy were observed too. Results: There was no obvious change of subsets of T cells in peripheral blood before and after therapy in DC-CIK + chemotherapy group, and IFN-γ was improved after therapy in this group (P < 0.05); in chemotherapy alone group, the ratios of CD3+CD4+, CD3+CD8+, CD3-CD56+ cells and the secretion of IL-2, TNF-α decreased significantly after therapy (P < 0.05); the ratios of CD3+CD8+, CD3+CD56+ were improved after cell culture (P < 0.05). The disease control rate (DCR) of DC-CIK + chemotherapy group was higher than that in the chemotherapy alone group (78.0% vs 56.0%, P < 0.05); the 1-year survival rates of DC-CIK + chemotherapy group and chemotherapy alone group were 50% and 44% respectively, had no significant difference. Compared with chemotherapy alone group, the occurrence of chemotherapy side effects (including bone marrow suppression, nausea and vomiting, peripheral nerve toxicity) was less in the DC-CIK + chemotherapy group (P < 0.05). The physical and appetite were better in DC-CIK + chemotherapy group after therapy. Conclusion: To compare with simple chemotherapy, DC-CIK + chemotherapy for advanced NSCLC is safe and effective, and it can improve patients' life quality and remission rate, and prolong their survival time.

First-line cemiplimab monotherapy and continued cemiplimab beyond progression plus chemotherapy for advanced non-small-cell lung cancer with PD-L150%or more(EMPOWER-Lung 1):35-month follow-up from a multicentre,open-label,randomised,phase 3 trial

肺癌是全球癌症相关死亡的主要原因,非小组胞肺癌(NSCLC)占所有肺癌病例的80%-85%。随着分子生物学的发展,针对驱动基因突变(如EGFR、ALK等)的靶向药物治疗已成为晚期NSCLC的标准一线治疗。但大多数NSCLC并没有可检测到的驱动基因突变,传统的铂类化疗效果不佳。免疫检查点抑制剂的出现极大地改变了这一领域的治疗格局。PD-1/PD-L1抑制剂已被证实可以显著提高NSCLC患者的疗效和生存期,特别是PD-L1表达阳性率≥50%的人群。

Exploration of Kras Mutations and Their Potential for Being a Target Molecule in Cancer Chemotherapy

The Rat sarcoma virus (RAS) family of proteins, which includes the Kristen Rat sarcoma virus (KRAS), is linked to nearly one-fourth of all human cancers. KRAS mutations, in particular, are associated with Non-Small Cell Lung Carcinoma (NSCLC), colorectal cancer, adenocarcinomas, ovarian carcinoma, and endometrial tumors. KRAS activates 80 different signaling pathways, including Mitogen-activated protein kinases (MAPK) and Phosphoinositide 3-kinase (PI3K), and up-regulates transcription factors such as ETS like Protein (ELK), Jun Proto-Oncogene (JUN), and Myelocytomatosis (MYC), which are involved in cell differentiation, proliferation, transformation, and survival. KRAS mutations are also known to cause autocrine function, which further exacerbates the situation. In NSCLC, KRAS mutations have a strong positive correlation with the disease, particularly in patients with a smoking history. In pancreatic cancer, KRAS mutations are a dominant pathological basis, with most mutations being G12D, G12V, G13D, G13C, G13S, and G13R. These mutations serve as initial markers in tumorigenesis and are associated with poor prognosis and high mortality rates. In colorectal cancer, KRAS mutations contribute to 4/5 of cases, with cellular mechanisms involving the MAPK pathway, which resists anti-epidermal growth factor antibodies. In Low-grade Serous Ovarian Cancer (LGSOC), KRAS mutations are associated with altered signaling in the MAPK pathway and drug resistance. However, treatments such as Selumetinib, a down regulator of RAS/Rapidly Accelerated Fibrosarcoma (RAF)/Mitogen-activated protein kinase (MEK) pathways, and a combination of trametinib and buparlisib have shown promise in managing LGSOC when diagnosed early through KRAS mutation markers. Although KRAS mutations are commonly associated with many types of cancer, their use in clinical practice is limited due to the lack of accurate methods to identify them. It is needed to further isolate the KRAS mutation products and correlate the cancer-causing genes to make it a promising approach for cancer chemotherapy.

Neoadjuvant nivolumab with or without platinum-doublet chemotherapy based on PD-L1 expression in resectable NSCLC(CTONG1804):a multicenter open-label phase II study

This prospective multicenter phase II study evaluated the clinical efficacy of neoadjuvant nivolumab-exclusive(N)and nivolumab–chemotherapy(N/C)combinations based on PD-L1 expression.Eligible patients exhibited resectable clinical stage IIA–IIIB(AJCC 8th edition)NSCLC without EGFR/ALK alterations.Patients received either mono-nivolumab(N)or nivolumab+nabpaclitaxel+carboplatin(N/C)for three cycles based on PD-L1 expression.The primary endpoint was the major pathological response(MPR).Key secondary endpoints included the pathologic complete response(pCR),objective response rate(ORR),and event-free survival(EFS).Baseline PD-L1 expression and perioperative circulating tumor DNA(ctDNA)status were correlated with pCR and EFS.Fifty-two patients were enrolled,with 46 undergoing surgeries.The MPR was 50.0%(26/52),with 25.0%(13/52)achieving pCR,and 16.7%and 66.7%for patients with PD-L1≥50%in N and N/C groups,respectively.Thirteen(25.0%)patients experienced grade 3 or higher immune-related adverse events during neoadjuvant treatment.Patients with post-neoadjuvant ctDNA negativity was more likely to have pCR(39.1%)compared with those remained positive(6.7%,odds ratio=6.14,95%CI 0.84-Inf,p=0.077).With a median follow-up of 25.1 months,the 18-month EFS rate was 64.8%(95%CI 51.9–81.0%).For patients with ctDNA–vs.ctDNA+,the 18m-EFS rate was 93.8%vs 47.3%(HR,0.15;95%CI 0.04,0.94;p=0.005).Immunochemotherapy may serve as an optimal neoadjuvant treatment even for patients with PD-L1 expression≥50%.ctDNA negativity following neoadjuvant treatment and surgery could help identify superior pathological and survival benefits,which requires further confirmation in a prospective clinical trial(NCT04015778).

新辅助免疫联合化疗在非小细胞肺癌中的初步疗效观察

目的观察新辅助程序性死亡受体1(programmed receptor 1,PD-1)单抗免疫治疗联合化学药物治疗(以下简称化疗)在非小细胞肺癌(non-small cell lung cancer,NSCLC)中的近期疗效。方法纳入接受新辅助免疫联合化疗的IB~Ⅲ期NSCLC患者176例,之后159例(90.34%)患者接受手术治疗,包括腺癌42例、鳞癌115例和混合癌2例。结果所有患者接受新辅助治疗的中位周期数为2个周期,4例(2.5%)患者术前达到完全缓解(complete response,CR),115例(72.3%)患者达到部分缓解(partial response,PR),40例(25.2%)患者评估为疾病稳定(stable disease,SD)且仅有2例病灶增大;术后96例(60.4%,95%CI:52.7%~68.1%)患者达到显著病理缓解(major pathological response,MPR),74例(46.5%,95%CI:38.7%~54.4%)患者达到病理完全缓解(pathological complete response,pCR);多因素分析显示,性别和程序性死亡配体1(programmed ligand 1,PD-L1)显著影响MPR率和pCR率。结论新辅助免疫联合化疗在IB~Ⅲ期NSCLC治疗中初现疗效,PD-L1的表达水平可能是MPR和pCR的预测因素。

XPD751基因多态性与晚期NSCLC对GP方案化疗的敏感性

目的:研究DNA修复基因XPD751基因多态性与晚期非小细胞肺癌(NSCLC)对吉西他滨/顺铂(GP)方案化疗敏感性的关系。方法:收集经病理学确诊的晚期NSCLC116例,所有病例化疗前抽静脉血,提取白细胞DNA,用多聚酶链反应—限制性片段长度多态性(PCR-RFLP)分析技术检测XPD751基因型,所有患者均为GP方案化疗。结果:①在肺癌患者中,XPD751Lys/Lys、Lys/Gln和Gln/Gln基因型分别为94例(81.0%)、20例(17.2%)和2例(1.8%)。经化疗后,44例患者有效,总有效率37.9%。②XPD751Lys/Lys、Lys/Gln和Gln/Gln基因型有效率分别为39.4%、25.0%、100.0%,三者相比差异无统计学意义(χ2=4.775,P=0.093)。与携带Lys/Gln基因型患者相比,Lys/Lys基因型者对GP方案化疗效果无显著增加,调整性别、年龄、临床分期和细胞学类型后的OR=1.09,95%CI:0.95～1.51。③携带Lys/Lys基因型患者的恶心呕吐反应和脱发程度均高于Lys/Gln和Gln/Gln基因型患者(χ2=4.032,P=0.045;χ2=4.344,P=0.037)。结论:XPD751基因多态性与晚期NSCLC对GP方案化疗的敏感性无显著相关,但可作为预测GP方案化疗毒副反应的指标。

EGFRTKIs联合化疗的给药顺序对NSCLC细胞促凋亡的影响

目的探究表皮生长因子受体络氨酸激酶抑制剂(EGFR TKIs)与化疗药物单用、联用,以及顺序给药时,对获得性TKI耐药的非小细胞肺癌(NSCLC)细胞系凋亡的影响。方法选用存在TKI耐药基因突变(T790M,c MET)的NSCLC细胞系PC9ER、H1975和HCC827GR,以及TKI敏感基因突变(19外显子突变)的细胞系PC9和HCC827。采用MTS法检测化疗药物顺铂和紫杉醇,以及TKI厄洛替尼单用、联用,或者顺序给药干预各NSCLC细胞系时的细胞活性状态,并利用集落形成试验加以验证。采用Western blot检测各处理组蛋白裂解液中细胞凋亡标志物c PARP含量变化。结果 MTS法和集落形成试验结果发现,EGFR TKIs联合化疗能协同增加NSCLC细胞系的细胞毒性。同时给予EGFR TKIs和化疗或先化疗再用EGFR TKIs,可获得最佳干预效果。Western bolt检测结果表明,联合用药后c PARP蛋白表达升高。而且先化疗后EGFR TKIs干预比两者顺序颠倒的促凋亡作用更强。结论先化疗后EGFR TKIs干预的最优给药顺序可使对获得性TKI耐药的NSCLC细胞系产生最强的促凋亡作用。

肺积1号联合化疗治疗中晚期NSCLC疗效分析

目的探讨肺积1号在中晚期非小细胞肺癌(NSCLC)化疗中的治疗作用。方法将2009～2010年60例NSCLC患者随机分为对照组和实验组各30例。对照组予PP方案化疗,实验组在化疗基础上联合肺积1号治疗,观察两组近期临床疗效、生活质量及其化疗毒副反应。结果与对照组比较,实验组可明显改善患者的生活质量,差异有统计学意义(P<0.05)。实验组在白细胞减少、贫血、消化道损伤等化疗副作用方面与对照组相比,有明显改善,差异有统计学意义(P<0.05)。在近期疗效、化疗引起的肝肾功能损害等方面两组无统计学差异(P>0.05)。结论肺积1号联合化疗能够显著改善患者的生活质量,减轻化疗副反应。

康莱特联合化疗对NSCLC患者生活质量改善的临床研究

目的 探讨康莱特注射液对联合化疗与单纯化疗改善晚期非小细胞肺癌 (NSCL C)患者的生活质量临床意义。方法 采取随机对照分组 ,治疗组 30例为康莱特联合化疗 ;对照组 30例为单纯化疗。结果 治疗组有效率为 36 .7% ,对照组为 2 3.3% ,有显著性差异 (P<0 .0 5 ) ,在控制疼痛、体重及 karnofsky评分等方面治疗组均优于对照组 ,差异有显著性。结论 康莱特注射液联合化疗可提高化疗疗效。

紫杉醇和铂剂联合治疗NSCLC的临床研究

目的 比较紫杉醇 -卡铂 (TAX CBP)方案和紫杉醇 -顺铂 (TAX DDP)方案治疗非小细胞肺癌(NSCLC)的疗效。方法 12 6例NSCLC病例被随机分入TAX CBP组和TAX DDP组。TAX CBP方案 :TAX175mg/m2 静脉滴注第 1天 ,CBP 35 0mg/m2 静脉滴注第 1天。TAX DDP方案 :TAX 175mg/m2 静脉滴注第 1天 ,DDP 10 0mg/m2 静脉滴注第 1天 (需水化 )。 2 8天为一周期 ,对连续使用三个周期者进行疗效评估。结果 TAX CBP组化疗有效率为 36 % (2 2 /6 1) ,1年生存率为 34.1% ,TAX DDP组化疗有效率为 33 .9% (2 1/6 2 ) ,1年生存率为 33 .1% ,二组疗效无显著性差异 (P >0 .0 5 ) ,但中位生存期TAX CBP组 (11.2个月 )优于TAX DDP组(9个月 ) (P <0 .0 5 )。副作用依次为脱发、骨髓抑制、胃肠道反应和肌肉 (关节 )疼痛。TAX CBP组血小板减少发生率显著高于TAX DDP组 (P <0 .0 5 ) ,而TAX DDP组消化道反应、肌肉 (关节 )痛发生率显著高于TAX CBP组 (P <0 .0 5 )。结论 TAX CBP方案和TAX CDDP方案均可作为NSCLC的一线化疗方案。

DC+CIK联合常规化疗对延长晚期NSCLC患者生存期、提高生活质量的作用

目的探讨晚期NSCLC患者生存期、生活质量受DC＋CIK联合常规化学治疗（化疗）的影响.方法：随机选取2012年5月～2015年5月我院收治的120例晚期非小细胞肺癌（NSCLC）患者,依据随机数字表法分这些患者为两组,即研究组（n=60）和对照组（n=60）.给予对照组患者单纯常规化疗治疗,给予研究组患者DC＋CIK联合常规化疗治疗,然后对两组患者的临床疗效、免疫功能、PFS、OS及1年、2年生存率、生活质量进行统计分析.结果：研究组患者的DCR90.0%（54/60）显著高于对照组73.3%（44/60）（P〈0.05）,PFS显著长于对照组（P〈0.05）,1年、2年生存率均显著高于对照组（P〈0.05）,KPS评分显著高于对照组（P〈0.05）,但两组患者的ORR11.7%（7/60）、5.0%（3/60）,CD3^＋、CD3^＋ CD4^＋、CD3^＋ CD8^＋T细胞、CD4^＋/CD8^＋T细胞比值、CD3^-CD56^＋NK细胞,OS之间的差异均不显著（P〉0.05）.结论：DC＋CIK联合常规化疗能够有效延长晚期NSCLC患者生存期、提高生活质量.

HMVP、MVP和HVP方案治疗晚期NSCLC的前瞻性随机研究

背景与目的:非小细胞肺癌(non-smallcelllungcancer,NSCLC)对常用的一、二线化疗方案敏感性较低,在化疗中联用喜树碱类衍生物已引起国内外的研究兴趣。本研究旨在观察羟基喜树碱(hydroxycamptothecin,HCPT)联合丝裂霉素(mitomycin,MMC)、长春花碱酰胺(vindesine,VDS)和顺铂(cisplatin,DDP)组成的HMVP、MVP和HVP方案治疗晚期NSCLC的近期、远期疗效和不良反应。方法:134例晚期NSCLC患者随机分为HMVP组(46例)、MVP组(44例)和HVP组(44例),接受相应方案的化疗,观察各组的近期及远期疗效、不良反应和生存情况。结果:HMVP、MVP和HVP三组的有效率分别为39.54%、36.59%和26.19%,三组之间无显著性差异(P>0.05);三组的中位缓解期、中位生存期、1年及2年生存率亦无明显差别。三组之间的Ⅲ～Ⅳ度白细胞减少、Ⅲ～Ⅳ度血小板减少、Ⅲ～Ⅳ度恶心/呕吐及Ⅲ～Ⅳ度便秘发生率均无显著性差异(P>0.05)。结论:MVP方案治疗晚期NSCLC的疗效略低于HMVP方案,但后者未显示出明显的疗效优势,且可能增加白细胞抑制、恶心/呕吐和便秘的发生率。MVP方案疗效略高于HVP方案。

含铂方案治疗进展期NSCLC与p53、p16、bcl-2表达的关系

目的 :化疗耐药是影响非小细胞肺癌 (NSCLC)预后的主要原因 ,本研究旨在探讨进展期NSCLC化疗耐药与凋亡相关基因p5 3、p16和bcl- 2的关系。方法 :用免疫组化方法检测进展期NSCLCp5 3、p16和bcl- 2的表达 ,同时收集患者的临床资料及化疗方案 ,比较p5 3、p16和bcl- 2表达与化疗疗效的关系。结果 :共有 14 1患者纳入研究 ,男性 12 1例 ,平均年龄 6 3岁 ;Ⅲ期 6 7例 ,Ⅳ期 76例 ;p5 3阳性 72例 (5 1% ) ,p16阴性 83例(5 9% ) ,bcl- 2阳性 15例 (10 % )。p5 3阳性组患者化疗有效率为 2 6 % ,p5 3阴性组化疗有效率为 5 7% ,两者相关显著 (P =0 0 0 4 )。结论 :本研究探讨了以顺铂为基础的联合化疗与p5 3表达的关系 ,对指导进展期NSCLC治疗及判断预后有一定意义。

化疗交替靶向药物治疗对EGFR突变阳性的晚期NSCLC患者PFS及OS的影响

目的观察化疗交替靶向药物治疗对EGFR突变阳性的晚期非小细胞肺癌患者PFS及OS的影响。方法选取100例EGFR突变阳性的晚期NSCLC患者作为研究对象,将患者分为2组,A组为吉西他滨+顺铂/卡铂化疗交替吉非替尼组,B组为单用吉非替尼组。比较患者治疗过程中的耐受情况、不良反应的发生率和总缓解率(ORR);对比A、B组患者的肿瘤无进展生存期(PFS)、总生存期(OS)和患者生活质量评分(Qo L)。结果 2组患者的不良反应发生率无统计学差异(P>0.05),治疗期间A组5例患者因无法耐受不良反应而退出,B组4例患者退出。A组患者ORR为68.89%,B组ORR为47.86%,差异具有统计学意义(P<0.05)。A组患者的PFS、OS和Qo L高于B组,差异具有统计学意义(P<0.05)。结论化疗交替靶向药物在晚期EGFR突变阳性的NSCLC的治疗中具有显著的临床疗效,值得在临床上进行推广和应用。

洛铂联合长春瑞滨对NSCLC术后辅助化疗疗效及安全性研究

目的探讨非小细胞肺癌术后患者联用洛铂(LBP)与长春瑞滨(NVB)的有效性和安全性。方法对60例非小细胞肺癌患者采用长春瑞滨联合洛铂方案治疗,21天为1个治疗周期,治疗两个周期以上。结果 60例患者中53例可进行疗效评价,完全缓解、部分缓解、无变化和进展的例数分别为18例、21例、11例和2例。总治疗有效率和疾病控制率分别为37.7%和75.5%。主要不良反应为可逆性的骨髓抑制和胃肠道反应,治疗过程中未出现肝肾毒性作用。结论洛铂联合长春瑞滨作为NSCLC患者术后的辅助化疗疗效尚可,不良反应在耐受范围,可对患者生活质量提升有一定的效果。

微小RNA-21与NSCLC放化疗抵抗的研究新进展

近年研究发现,微小RNA(microRNAs,miRNAs)家族成员miRNA-21与非小细胞肺癌(non-small cell lung cancer,NSCLC)的化疗、放疗抵抗及EGFR-TKI耐药密切相关,提示其可作为NSCLC放化疗的潜在新靶标。本文就其相关研究最新进展作一综述。

NSCLC术前化疗后“T”降期的临床评价

目的 :研究NSCLC术前化疗后临床、组织学缓解率和化疗前后“T”分期变化及中数生存期的关系。方法 :自 1995年 2月～ 1997年 2月 ,5 6例经诱导化疗后手术的非小细胞肺癌 ,以铂类为基础的联合化疗 1～ 2个疗程 ,按TNM分期系统评价期别、“T”降期。结果 :期别降期发生率为 2 1.4% ,“T”降期发生率 2 3.2 %。化疗 2个周期的“T”降期比例明显高于 1个周期 (P<0 .0 5 ) ,“T”降期与化疗临床缓解率和组织学缓解率相关 (P <0 .0 5 ) ;“T”降期组的中数生存期高于“T”无变化和“T”升期组 ,分别为 45 .2 8个月、33.30个月和 2 4.0 3个月 ,但差异无统计学意义 ,P =0 .142 3。进一步分析 ,在N2中“T”降期组MST较长 ,但P =0 .0 6 86。同样在腺癌中 ,“T”降期组MST较“T”无变化和升期组延长。P =0 .0 5 94。结论 :化疗后降期和“T”降期分别是反映化疗疗效因素之一 ;可延长生存期。