2004年至2005年MRSA调查分析

目的调查龙岩市第一医院2004年至2005年各病区各类标本MRSA分离率及对常用抗生素耐药率。方法用VITEK 32细菌仪GPI卡鉴定及Slidex Staph-k it、MRSA胶乳凝集试验确认,用VITEK 32细菌仪GPS101做药敏,并统计分析。结果共检查229株SA,其中2004年MRSA为56.6%,耐药率苯唑西林、青霉素G为100%,优力新、头孢噻吩为100%,红霉素79%,四环素73%,环丙沙星71%,氯洁霉素36%,万古霉素0%;2005年MRSA为59.4%,耐药率苯唑西林、青霉素G、优力新、头孢唑啉为100%,红霉素94%,环丙沙星89%,氧氟沙星88%,四环素76%,氯洁霉素50%,利福平43%,万古霉素0%。结论该院SA耐药性监测显示临床分离SA的耐药性和交叉耐药性已相当严重,必须采取相应的措施严密监测、控制和预防MRSA感染,严格执行院内消毒隔离制度,防止MRSA扩散,定期对临床分离菌株的耐药性进行分析,避免万古霉素过度使用,防止耐万古霉素SA产生。     

1例别嘌醇致慢性肾衰患者重症药疹的护理

正别嘌醇是一种黄嘌呤氧化酶抑制剂,可减少尿酸的产生,降低血尿酸水平,是临床常用于治疗高尿酸血症和痛风病的药物。据报道约0.4%使用别嘌醇的患者出现不良反应[1],主要不良反应有皮疹、胃肠道反应、发热、骨髓抑制、肝肾功能损害等。重症药疹的类型较多,病情严重、发展迅速,常见有大疱性表皮松解型药疹、多形红斑型药疹以及剥脱型皮炎型[2]。若治疗护理不当,易造成严重的后果。2015年8     

热毒灵过敏致大泡表皮松解型药疹伴全身感染死亡相关问题的研究

目的:对1例热毒灵致大泡表皮松解型药疹伴全身感染和血气胸死亡的相关问题进行讨论分析。方法:详细报道1例热毒灵致大泡表皮松解型药疹伴全身感染和血气胸死亡的案例,并对该案例的相关性理论进行回顾性分析,对案例进行详细的尸体检验与死亡原因的鉴定。结果:本案结合案情资料、尸体检验及包括病理组织学检查在内的其他相关法医学检验证实因大泡表皮松解型药疹伴皮肤及全身感染和血气胸死亡,最终导致多器官功能障碍而死亡。结论:热毒灵致大泡表皮松解型药疹伴全身感染和血气胸死亡的法医学鉴定应根据案情资料并结合用药史、有关病历资料、生前临床表现、解剖发现、病理组织学检验、法医毒化检验并参考特殊检查结果等多种因素进行综合评定。     

15 例重症药疹患者临床特征及激素联合免疫球蛋白的疗效分析

目的:探讨15例重症药疹患者的临床特点及采用激素联合免疫球蛋白治疗改病的临床效果。方法:回顾性分析2012年12月至2014年12月在我院就诊的15例重症药疹患者的临床资料,患者采用激素联合免疫球蛋白进行治疗,观察患者的发病类型、致敏药物及疗效,分析血常规、肝功能、肾功能指标与与预后的关系。结果:15例患者中,中毒表皮坏死松解8例,占53.33%,药疹重型4例,占26.67%,中毒表皮坏死松解并支气管炎患者、史蒂文斯并支气管肺炎患者及重症药疹并重症肝炎患者各1例,占6.67%。致敏药物主要是中药、卡马西平、柳氮磺吡啶、头孢他啶、布洛芬、青霉素、别嘌呤醇、感冒药。治疗总有效率86.67%。白细胞、中性比、总胆红素(TBIL)、谷丙转氨酶、胆碱酯酶、胱抑素、肌酐(Cr)、乳酸脱氢酶(LDH)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)与重症药疹患者治愈预后有关(P0.05)。结论:重症药疹以中毒表皮坏死松解患者为主,对不同致敏药物引起的重症药疹患者应进行区别治疗,重症药疹患者的预后与患者内脏受累程度密切相关,临床采用激素联合丙种球蛋白持续治疗,可提高治愈率,改善患者临床症状及预后,     

外周血Th1/Th2比值、IL-23/Th17轴与中重度斑块状银屑病患者颈动脉粥样硬化和临床疗效的关系

摘要 目的：探讨外周血辅助T细胞（Th）1/Th2比值、白介素（IL）-23/Th17轴与中重度斑块状银屑病（PP）患者颈动脉粥样硬化和临床疗效的关系。方法：选取2021年1月～2022年1月徐州医科大学附属医院收治的97例中重度PP患者为中重度PP组,根据颈动脉内中膜厚度（CIMT）分为增厚组39例和正常组58例,根据甲氨蝶呤（MTX）治疗是否应答有效分为无应答组和应答组,另选取同期50例体检健康志愿者为对照组。采用流式细胞术检测外周血Th1、Th2百分比和Th1/Th2比值,酶联免疫吸附法检测外周血IL-23、IL-17A水平。采用Pearson相关性分析中重度PP患者外周血Th1、Th2、Th1/Th2比值和IL-23/Th17轴相关因子与CIMT的相关性,多因素Logistic回归分析中重度PP患者MTX治疗无应答的影响因素。结果：与对照组比较,中重度PP组外周血Th1、Th1/Th2比值、IL-23和IL-17A水平升高,Th2比例降低（P均＜0.001）。97例中重度PP患者颈动脉粥样硬化发生率为40.21%（39/97）。与正常组比较,增厚组外周血Th1、Th1/Th2比值、IL-23和IL-17A水平升高,Th2比例降低（P均＜0.001）。Pearson相关性分析显示,中重度PP患者外周血Th1、Th1/Th2比值、IL-23、IL-17A与CIMT呈正相关,Th2与CIMT呈负相关（r=0.695、0.706、0.688、0.650、-0.639,P均＜0.001）。97例中重度PP患者MTX治疗无应答率为21.65%（21/97）。多因素Logistic回归分析显示,重度PP和Th1、Th1/Th2比值、IL-23、IL-17A升高为中重度PP患者MTX治疗无应答的独立危险因素,Th2升高为独立保护因素（P均＜0.05）。结论：中重度PP患者外周血Th1/Th2比值和IL-23/Th17轴相关因子升高,与颈动脉粥样硬化和MTX治疗无应答有关,可能成为中重度PP患者颈动脉粥样硬化和临床疗效评估指标。     

犬猫常见药物过敏反应及其防治

犬猫常见的药物过敏反应包括皮疹、荨麻疹、皮炎、发热、血管神经性水肿、哮喘、过敏性休克等,其中以荨麻疹最为常见,以过敏性休克最为严重。1992-1998上半年,我中心动物医院发生药物过敏性休克多例,其中青霉素致死1例,链霉素致死3例,洁霉素致死4例,庆大霉素致死3例,银黄注射液致死1例。引起犬猫过敏反应的药物有:青霉素、链霉素、庆大霉素、卡拉霉素、洁霉素、维生素Ｂ1、地塞米松、维丁胶性钙、柴胡、红花、银黄、板蓝根、维生素Ｋ、疫苗等。由于动物本身的生理特性,毛长、皮厚、肤色多样等特点,不适宜做皮肤过敏试验。所以在给动物注射各…     

多原发癌

目的:探讨多原发癌的病因、临床特点及其诊治。方法:回顾性总结分析了一组普通外科多原发癌病人的资料,并结合文献进行了分析。结果:本组77例多原发癌,占同期普通外科住院病人的1.33%(77/5768),半数以上发生于65岁及以上的老年人。胃肠道多原发癌占81.8%。其发生主要与下列因素有关:基因缺陷因素(遗传易感性)、环境因素、治疗所致(如放、化疗)、免疫缺陷、老龄。结论:多原发癌近年呈增加趋势,对于肿瘤病人的诊治,不要忽略了同时性癌的可能;手术仍是多原发癌实体瘤主要而有效的治疗手段。     

左旋氨氯地平与氨氯地平治疗原发性轻中度高血压的临床分析

目的:本文就左旋氨氯地平和氨氯地平治疗轻、中度高血压的临床疗效进行了浅显的研究和探讨。方法:选择我院自2012年11月至2013年11月期间收治的80例中轻度原发性高血压患者,将其随机平均分为A组合和B组(每组40人),在饮食控制、运动等常规治疗基础上,A组患者使用左旋氨氯地平治疗,B组患者使用氨氯地平治疗,对比两组患者的治疗效果病观察不良反应。结果:发现A组和B组均能有效降低血压,左旋氨氯地平的不良反应明显低于氨氯地平。结论:左旋氨氯地平和氨氯地平在治疗高血压方面有相似的疗效,左旋氨氯地平降压效果更理想,不良反应更轻微,是较理想的抗高血压药。     

乌司他丁与沐舒坦治疗严重烧伤伴吸入性损伤的疗效分析

目的:探讨严重烧伤伴中重度吸入性损伤患者早期联合使用大剂量乌司他丁与沐舒坦的临床疗效。方法:选择2003年5月~2013年5月在我院接受治疗的185例严重烧伤伴中重度吸入性损伤患者,随机分为两组,治疗组93例,对照组92例。两组患者在确诊为中重度吸入性损伤后,立即给予传统常规治疗:吸氧、视情尽早预防性气管切开、湿化气道及气道灌洗、翻身拍背吸痰、呼吸机辅助呼吸等。治疗组在常规治疗的基础上给予乌司他丁40万单位,每隔8h静脉滴注,沐舒坦450 mg,每隔12h微泵静推;对照组给予乌司他丁10万单位,每隔8h静滴,沐舒坦30 mg,每隔8h静滴,疗程为10天,比较两组患者急性肺损伤(ALI)的发生率、急性呼吸窘迫综合征(ARDS)的发生率、呼吸机使用时间、死亡率。结果:治疗组93例患者,治愈92例,死亡1例,死亡率为1.08%(1/93),治疗过程中发生ALI34例,ARDS12例,呼吸机使用时间为(4.2±2.1)d。对照组92例患者治愈88例,死亡4例,死亡率率为4.35%(4/92),治疗过程中发生ALI43例,ARDS17例,呼吸机使用时间为(8.2±2.7)d。两组患者ALI发生率、ARDS发生率、呼吸机使用时间、治愈率差异均有统计学意义(P0.05)。结论:对于严重烧伤伴中重度吸入性损伤的患者,在气管切开的前提下,给予常规传统治疗的同时,采用大剂量乌司他丁与沐舒坦早期联合使用给药,能够明显的提高治愈率,降低并发症,值得在临床上广泛推广应用。     

百令胶囊联合信必可对中重度稳定期慢性阻塞性肺疾病患者肺功能及免疫功能的影响

目的:探讨百令胶囊联合信必可对中重度稳定期慢性阻塞性肺疾病(COPD)患者肺功能及免疫功能的影响,为临床用药提供依据。方法:选取我院于2015年8月至2017年1月收治的104例COPD患者作为研究对象。采用随机数字表法将其分为单药组与联合组各52例。单药组患者单独给予信必可治疗及常规健康教育,联合组患者在单药组的基础上联用百令胶囊治疗。治疗前及治疗12周后对所有患者的用力肺活量(FVC)、第1秒用力呼气容积(FEV1)及两者之比(FEV1/FVC)进行测定,同时测定患者CD3~+,CD4~+T细胞,并计算CD4~+/CD8~+比值。观察并比较两组患者的临床疗效。结果:治疗12周后,两组患者FVC、FEV1、FEV1/FVC均明显升高(均P0.05),且与单药组比较,联合组患者FVC、FEV1、FEV1/FVC均明显更高(均P0.05)。治疗12周后,两组患者CD3~+、CD4~+及CD4~+/CD8~+均明显升高(均P0.05),且与单药组比较,联合组患者CD3~+CD4~+及CD4~+/CD8~+均明显更高(均P0.05)。联合组总有效率为86.54%,明显高于单药组的67.31%(P0.05)。结论:百令胶囊联合信必可治疗中重度稳定期COPD患者疗效确切,能有效改善患者肺功能并提高免疫功能,值得在临床上推广。     

The results and characteristics of the mupirocin (Bactroban) sanative treatment of intranasal Staphylococcus carriers in a large hospital]

The action of mupirocin as a nasal ointment (Bactroban) was studied on intranasal carriers of the hospital staphylococcal strains. The study included 37 medical workers from different and mainly problem units of the large general hospital. The tolerability of the ointment was good. After the Bactroban use no complications of the patients were recorded. The efficacy of Bacroban by the microbiological criteria in total amounted to 100 per cent. The eradication of methicillin resistant Staphylococcus aureus (MRSA) was observed in 93 per cent of the cases. A decrease of the level of the nasal passages dissemination by MRSA and methicillin resistant coagulase-negative staphylococci (MRSC) up to such low titers as 100 and 90 per cent was stated. No difference in the action of Bactroban on MRSA, MSSA and MRSC was noted. The bacteriological monitoring for 3 to 4 months revealed a change of the staphylococcal strains in 94 per cent of the cases, recolonization by the same staphylococcal strain in 19 per cent, recolonization by some another staphylococcal strains in 33 per cent and no recolonization in 14 per cent. A stable decrease of staphylococcal strains was possible with simultaneous Bactroban sanitation of all the bacterial carriers of the hospital or its isolated unit.     

Targeted combinatorial therapy of non-small cell lung carcinoma using a GST-fusion protein of full-length or truncated MDA-7/IL-24 with Tarceva

Melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24), a cytokine belonging to the IL-10 family, displays cancer-specific apoptosis-inducing properties when delivered by a replication-incompetent adenovirus (Ad.mda-7) or as a GST-tagged recombinant protein (GST-MDA-7). Previous studies demonstrated that an adenovirus expressing M4, a truncated version of MDA-7/IL-24 containing amino acid residues 104-206, also induced similar cancer-specific apoptosis. We generated recombinant GST-M4 proteins and examined the potency of GST-MDA-7 and GST-M4 on a panel of epidermal growth factor receptor (EGFR) wild type and mutant non-small cell lung carcinoma (NSCLC) cells either as a single agent or in combination with a reversible EGFR inhibitor, Tarceva. The combination of either GST-MDA-7 or GST-M4 ( approximately 0.1 microM) and Tarceva (10 microM), at sub-optimal apoptosis-inducing concentrations synergistically enhanced growth inhibition and apoptosis induction over that observed with either agent alone. The combination treatment also augmented inhibition of EGFR signaling, analyzed by phosphorylation of EGFR and its downstream effectors AKT and ERK1/2, over that with single-agent therapy. Tarceva enhanced GST-MDA-7 and GST-M4 toxicity in cells expressing mutated EGFR proteins that are resistant to the inhibitory effects of Tarceva. In total, these data suggest that combined treatment of NSCLC cells with an EGFR inhibitor can augment the efficacy of GST-MDA-7 and GST-M4 and that the EGFR inhibitor Tarceva may mediate this combinatorial effect by inhibiting multiple tyrosine kinases in addition to the EGFR. This approach highlights a potential new combinatorial strategy, which may prove beneficial for NSCLC patients with acquired resistance to EGFR inhibitors.     

Overcoming Acquired Resistance to Iressa/Tarceva with Inhibitors of a Different Class

Small molecule kinase inhibitors of the epidermal growth factor receptor (EGFR) have recently been found to exhibit clinical efficacy in the setting of non-small cell lung cancers that harbor activating EGFR mutations. However, the remissions induced by these drugs (Iressa and Tarceva) are typically short-lived, presumably due to acquired drug resistance. We recently reported findings demonstrating that a distinct class of EGFR inhibitors may overcome some mechanisms of secondary drug resistance in these tumors and may therefore be useful in treating lung cancer patients that initially responded to Iressa or Tarceva and eventually relapsed.     

Specific method for determination of OSI-774 and its metabolite OSI-420 in human plasma by using liquid chromatography-tandem mass spectrometry

A new simple and specific method was developed and validated for the quantitative determination of OSI-774 (Tarceva, Erlotinib) and its metabolite, OSI-420, in human plasma. Sample pretreatment involved a single protein precipitation step with acetonitrile. The analytes were separated on Waters X-Terra C(18) (50 x 2.1 mm I.D., 3.5 microm) analytical column and eluted with acetonitrile-water mobile (70:30, v/v) containing 0.1% formic acid. The analytes of interest were monitored by tandem mass spectrometry with electrospray positive ionization. The overall extraction efficiency was greater than 88% for OSI-774 and 62% for OSI-420, with values for within-day and between-day precision and accuracy of <15%. Compared to previous assays, this method is simple, specific, and reproducible and will be used to characterize the plasma pharmacokinetics of OSI-774 at doses of 50 to 150 mg to optimize treatment with this agent.     

特罗凯靶向治疗联合培美曲塞和顺铂对非小细胞肺癌患者血清肿瘤标志物、免疫球蛋白和T淋巴细胞亚群的影响

摘要 目的：探讨特罗凯靶向治疗联合培美曲塞和顺铂对非小细胞肺癌（NSCLC）患者血清肿瘤标志物、免疫球蛋白和T淋巴细胞亚群的影响。方法：选取2018年2月~2020年2月期间我院接收的NSCLC患者80例,采用抽签法分为对照组、观察组两组,各40例。对照组给予培美曲塞和顺铂化疗方案治疗,观察组在对照组基础上联合特罗凯靶向治疗,对比两组总有效率、血清肿瘤标志物、免疫球蛋白、T淋巴细胞亚群及不良反应发生率。结果：对比两组不良反应无差异（P>0.05）。治疗3个疗程后,对照组、观察组的临床总有效率分别为37.50%、60.00%,观察组的总有效率高于对照组（P<0.05）。治疗3个疗程,观察组CD3⁺、CD4⁺、CD4⁺/CD8⁺高于对照组,CD8⁺低于对照组（P<0.05）。治疗3个疗程,观察组免疫球蛋白G（IgG）、免疫球蛋白A（IgA）、免疫球蛋白M（IgM）高于对照组（P<0.05）。治疗3个疗程,观察组细胞角蛋白19片段（CYFRA21-1）、糖类抗原50（CA50）、癌胚抗原（CEA）低于对照组（P<0.05）。结论：特罗凯靶向治疗联合培美曲塞和顺铂治疗NSCLC患者,疗效较好,可能与该方案可降低患者血清肿瘤标志物含量、调节免疫应答等因素有关。     

Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

BackgroundLung adenocarcinomas from patients who respond to the tyrosine kinase inhibitors gefitinib (Iressa) or erlotinib (Tarceva) usually harbor somatic gain-of-function mutations in exons encoding the kinase domain of the epidermal growth factor receptor (EGFR). Despite initial responses, patients eventually progress by unknown mechanisms of “acquired” resistance.ConclusionIn patients with tumors bearing gefitinib- or erlotinib-sensitive EGFR mutations, resistant subclones containing an additional EGFR mutation emerge in the presence of drug. This observation should help guide the search for more effective therapy against a specific subset of lung cancers.     

Gefitinib-mediated Reactive Oxygen Specie (ROS) Instigates Mitochondrial Dysfunction and Drug Resistance in Lung Cancer Cells

Therapeutic benefits offered by tyrosine kinase inhibitors (TKIs), such as gefitinib (Iressa) and erlotinib (Tarceva), are limited due to the development of resistance, which contributes to treatment failure and cancer-related mortality. The aim of this study was to elucidate mechanistic insight into cellular perturbations that accompany acquired gefitinib resistance in lung cancer cells. Several lung adenocarcinoma (LAD) cell lines were screened to characterize epidermal growth factor receptor (EGFR) expression and mutation profile. To circumvent intrinsic variations between cell lines with respect to response to drug treatments, we generated gefitinib-resistant H1650 clone by long-term, chronic culture under gefitinib selection of parental cell line. Isogenic cells were analyzed by microarray, Western blot, flow cytometry, and confocal and transmission electron microscope. We observed that although chronic gefitinib treatment provided effective action against its primary target (aberrant EGFR activity), secondary effects resulted in increased cellular reactive oxygen species (ROS). Gefitinib-mediated ROS correlated with epithelial-mesenchymal transition, as well as striking perturbation of mitochondrial morphology and function. However, gefitinib treatment in the presence of ROS scavenger provided a partial rescue of mitochondrial aberrations. Furthermore, withdrawal of gefitinib from previously resistant clones correlated with normalized expression of epithelial-mesenchymal transition genes. These findings demonstrate that chronic gefitinib treatment promotes ROS and mitochondrial dysfunction in lung cancer cells. Antioxidants may alleviate ROS-mediated resistance.     

EGF receptor tyrosine kinase inhibitors diminish transforming growth factor-alpha-induced pulmonary fibrosis

Transforming growth factor-alpha (TGF-alpha) is a ligand for the EGF receptor (EGFR). EGFR activation is associated with fibroproliferative processes in human lung disease and animal models of pulmonary fibrosis. We determined the effects of EGFR tyrosine kinase inhibitors gefitinib (Iressa) and erlotinib (Tarceva) on the development and progression of TGF-alpha-induced pulmonary fibrosis. Using a doxycycline-regulatable transgenic mouse model of lung-specific TGF-alpha expression, we determined effects of treatment with gefitinib and erlotinib on changes in lung histology, total lung collagen, pulmonary mechanics, pulmonary hypertension, and expression of genes associated with synthesis of ECM and vascular remodeling. Induction in the lung of TGF-alpha caused progressive pulmonary fibrosis over an 8-wk period. Daily administration of gefitinib or erlotinib prevented development of fibrosis, reduced accumulation of total lung collagen, prevented weight loss, and prevented changes in pulmonary mechanics. Treatment of mice with gefitinib 4 wk after the induction of TGF-alpha prevented further increases in and partially reversed total collagen levels and changes in pulmonary mechanics and pulmonary hypertension. Increases in expression of genes associated with synthesis of ECM as well as decreases of genes associated with vascular remodeling were also prevented or partially reversed. Administration of gefitinib or erlotinib did not cause interstitial fibrosis or increases in lavage cell counts. Administration of small molecule EGFR tyrosine kinase inhibitors prevented further increases in and partially reversed pulmonary fibrosis induced directly by EGFR activation without inducing inflammatory cell influx or additional lung injury.     

FTIR spectra signatures reveal different cellular effects of EGFR inhibitors on nonsmall cell lung cancer cells

ATP‐analogue inhibitors, Gefitinib (Iressa) and Erlotinib (Tarceva) had been approved for advanced and metastatic nonsmall cell lung cancer (NSCLC) cells against tyrosine kinase domain of epidermal growth factor receptor (EGFR). Many techniques have been developed to better understand the drug mechanism which is multistep, time‐consuming and expensive. Herein, we performed Fourier‐transform infrared (FTIR) microscopy for evaluating the biochemical change on NSCLC (A549) cells after treatment. At levels that produced equivalent effects, Gefitinib dramatically induced cell apoptosis via impaired mitochondrial transmembrane potential. Whereas, Erlotinib had a slight effect on A549. Principal component analysis was performed to distinguish the effect of EGFR inhibitors on A549. FTIR spectra regions were divided into three regions: lipids (3000‐2800 cm^?1), proteins (1700‐1500 cm^?1) and carbohydrates and nuclei acids (1200‐1000 cm^?1). Biochemical changes can be evaluated by these spectral regions. This work may be a novel concept for utilizing FTIR spectroscopy for high‐throughput discriminative effects of a drug or compound and its derivatives on cells.     

The HDAC inhibitor,MPT0E028, enhances erlotinib-induced cell death in EGFR-TKI-resistant NSCLC cells

Epidermal growth factor receptor (EGFR), which promotes cell survival and division, is found at abnormally high levels on the surface of many cancer cell types, including many cases of non-small cell lung cancer. Erlotinib (Tarceva), an oral small-molecule tyrosine kinase inhibitor, is a so-called targeted drug that inhibits the tyrosine kinase domain of EGFR, and thus targets cancer cells with some specificity while doing less damage to normal cells. However, erlotinib resistance can occur, reducing the efficacy of this treatment. To develop more effective therapeutic interventions by overcoming this resistance problem, we combined the histone deacetylase inhibitor, MPT0E028, with erlotinib in an effort to increase their antitumor effects in erlotinib-resistant lung adenocarcinoma cells. This combined treatment yielded significant growth inhibition, induced the expression of apoptotic proteins (PARP, γH2AX, and caspase-3), increased the levels of acetylated histone H3, and showed synergistic effects in vitro and in vivo. These effects were independent of the mutation status of the genes encoding EGFR or K-Ras. MPT0E028 synergistically blocked key regulators of the EGFR/HER2 signaling pathways, attenuating multiple compensatory pathways (e.g., AKT, extracellular signal-regulated kinase, and c-MET). Our results indicate that this combination therapy might be a promising strategy for facilitating the effects of erlotinib monotherapy by activating various networks. Taken together, our data provide compelling evidence that MPT0E028 has the potential to improve the treatment of heterogeneous and drug-resistant tumors that cannot be controlled with single-target agents.