ERCC1 多态性与肺癌铂类化疗耐药的关系研究

目的:研究DNA切除修复交叉互补基因1(excision repair cross-complementing gene1,ERCC1)单核苷酸多态性与非小细胞肺癌铂类药物化疗敏感性的关系。方法:应用基因测序方法检测89例以铂类药物为主要化疗方案的非小细胞肺癌患者的ERCC1 Asn118Asn基因型,,比较不同基因型与化疗疗效的关系。结果:89例患者化疗总有效率为29.2%。携带ERCC1 CC基因型、含至少一个变异基因型(TC和TT基因型)患者的有效率分别为38.5%和61.5%(X2=2.151,p=0.142),基因型在化疗有效组和无效组之间的分布无差异(p>0.05)。结论:ERCC1Asn118Asn单核苷酸多态性可能与非小细胞肺癌对铂类药物化疗的敏感性无关。     

ERCC1多态性与肺癌铂类化疗耐药的关系研究

目的：研究DNA切除修复交叉互补基因1（excision repair cross-complementing gene1,ERCC1）单核苷酸多态性与非小细胞肺癌铂类药物化疗敏感性的关系。方法：应用基因测序方法检测89例以铂类药物为主要化疗方案的非小细胞肺癌患者的ERCC1 Asn118Asn基因型,,比较不同基因型与化疗疗效的关系。结果：89例患者化疗总有效率为29.2%。携带ERCC1 CC基因型、含至少一个变异基因型（TC和TT基因型）患者的有效率分别为38.5%和61.5%（X2=2.151,p=0.142）,基因型在化疗有效组和无效组之间的分布无差异（p〉0.05）。结论：ERCC1Asn118Asn单核苷酸多态性可能与非小细胞肺癌对铂类药物化疗的敏感性无关。     

吉西他滨联合顺铂序贯吉非替尼治疗晚期非小细胞肺癌

目的:观察吉西他滨联合顺铂序贯吉非替尼治疗晚期非小细胞肺癌的疗效与毒副反应。方法:71例经病理学诊断的晚期(Ⅲb-Ⅳ期)非小细胞肺癌患者,随机分成两组,观察组给予吉西他滨加顺铂化疗,序贯吉非替尼。对照组给予吉西他滨加顺铂化疗。结果:两组有效率(RR)为36.1%VS14.3%(P=0.0362);疾病控制率(DCR)比较x2=14.782,P<0.001;中位生存期(MST)为12.1月VS10.8月(P<0.05);有统计学差异;观察组除了皮疹、腹泻毒副反应较大外,其他与对照组相仿。结论:吉西他滨联合顺铂序贯吉非替尼治疗晚期非小细胞肺癌有较好的疗效和安全性,可以扩大样本继续观察。     

斑蝥酸钠联合化疗方案对非小细胞肺癌患者microRNA-21与SIRT1表达影响的研究

为研究斑蝥酸钠联合化疗方案治疗非小细胞肺癌患者疗效,分析其对microRNA-21与SIRT1表达的影响。本研究将86例晚期非小细胞肺癌患者依据数字随机法平均分为两组:对照组采用紫杉醇加顺铂化疗,观察组采用斑蝥酸钠联合紫杉醇加顺铂化疗,比较两组患者治疗疗效及microRNA-21与SIRT1表达量变化情况。观察组治疗有效率67.4%,显著高于对照组(44.2%)(字2=4.71,p=0.03);非小细胞肺癌患者癌组织中的microRNA-21表达量为(4.67±1.25),显著高于癌旁组织表达量为(2.45±1.08)(t=8.81,p=0.00);非小细胞肺癌患者癌组织中SIRT1表达阳性率为62.8%(39.5%~76.4%),显著高于癌旁组织表达率为42.5%(25.1%~54.1%)(t=10.94,p0.05);治疗前,两组患者癌组织中microRNA-21表达量和SIRT1表达阳性率(%)无统计学差异(p0.05),经治疗后均显著下降(p0.05),但观察组下降程度显著高于对照组(p0.05);治疗后观察组免疫功能指标显著升高,且观察组治疗后CD~(4+)/CD~(8+)和NK细胞显著高于对照组(p0.05);观察组临床症状改善情况和生活质量改善程度均优于对照组,差异具有统计学意义(p0.05);观察组胃肠道反应率和白细胞下降率分别为13.9%和9.3%,对照组分别为39.5%和30.2%,两组差异具有统计学意义(p0.05)。由此得出结论,斑蝥酸钠联合化疗方案治疗非小细胞肺癌患者,能够有效抑制microRNA-21和SIRT1的表达,提高治疗疗效,改善患者生活质量和免疫功能,降低不良反应率,具有增效减毒的作用,从而改善预后。     

培美曲塞+顺铂方案诱导化疗联合同期放化疗对局部晚期非小细胞肺癌的近期疗效及安全性观察

目的:探究培美曲塞+顺铂方案诱导化疗联合同期放化疗对局部晚期非小细胞肺癌的近期疗效及安全性。方法:收集我院肿瘤科2009年7月到2011年7月住院治疗的局部晚期非鳞癌非小细胞癌患者54例,按照随机数字表法分为研究组和对照组,每组27例,研究组给予培美曲塞+顺铂方案诱导化疗联合同期放化疗,对照组仅给予培美曲塞+顺铂方案化疗联合同期放疗,治疗2个周期,随访2年,对比两组患者的近期疗效及安全性。结果:研究组的近期有效率和控制率分别为55.56%、77.78%,高于对照组的50.33%和59.26%,有效率和控制率差异具有统计学意义(P0.05)。随访2年,研究组的中位生存期为12.77个月,1年生存率为48.15%,高于对照组中位生存期11.28个月,1年生存率40.74%,但差异无统计学意义(P0.05),研究组2年生存率为43.46%,高于对照组的25.38%,差异具有统计学意义(P0.05);研究组白细胞减少以及脱发发生率分别为37.0%、25.9%,低于对照组的81.5%和55.5%,差异具有统计学意义(均P0.05);研究组中血小板减少、血红蛋白减少、呕吐、肝功能损害、肾功能损耗、皮疹等发生率分别为40.7%、22.2%、59.2%、11.1%、7.4%、14.8%,高于对照组中各不良反应发生率分别为33.3%、18.5%、55.5%、14.8%、11.1%、7.4%,但两组间差异无统计学意义(P0.05)。结论:培美曲塞+顺铂方案诱导化疗联合同期放化疗对局部晚期非小细胞肺癌治疗效果明显,且不良反应少,可作为临床上晚期非小细胞肺癌化疗一线药物。     

培美曲塞联合顺铂化疗对晚期非小细胞肺癌患者疗效及血清肿瘤标志物的影响

目的:探究培美曲塞联合顺铂化疗对晚期非小细胞肺癌患者疗效及血清肿瘤标志物的影响。方法:选取于2012年7月~2016年2月期间我院收治的89例非小细胞肺癌患者为研究对象,采用随机数字法将研究对象分为观察组(45例)和对照组(44例);观察组采用培美曲塞联合顺铂化疗,对照组采用多西他赛联合顺铂化疗,观察并比较两组患者治疗前后细胞角质素片段抗原(CYRAF211)、血清癌胚抗原(CEA)、糖类抗原125(CA125)、神经元特异性烯醇化酶(NSE)表达水平。结果:观察组疗效优于对照组,比较有统计学差异(Z=1.940,P=0.026),观察组治疗的总有效率(55.66%)显著高于对照组(36.37%),差异有统计学意义(χ2=5.432,P=0.034);化疗后,两组CEA、CYFRA21-1、CA125及NSE水平均较化疗前较有显著下降,同时观察组各指标水平均显著低于对照组(P0.05);化疗前,Ⅲ期患者肿瘤标志物CEA、CYFRA21-1、CA125及NSE水平均显著低于Ⅳ期患者(P0.05);化疗后,Ⅲ期和Ⅳ期患者肿瘤标志物CEA、CYFRA21-1、CA125及NSE水平较治疗前均有显著降低(P0.05),且Ⅲ期水平显著低于Ⅳ期(P0.05)。结论:培美曲塞联合顺铂治疗晚期非小细胞肺癌具有显著疗效,血清CEA、CYFRA21-1、CA125及NSE水平经化疗后显著降低,可作为分期和评价化疗疗效的可靠指标。     

传统CA V 方案与金喜素联合顺铂治疗小细胞 肺癌疗效回顾对比分析

目的：分组比较传统CAV方案（环磷酰胺＋阿霉素＋长春新硷）和金喜素和顺铂方案对小细胞肺癌患者的治疗效果。方法：通过分组对比分析164例小细胞肺癌患者连续三次应用传统CAV（环磷酰胺、阿霉素、长春新硷）方案和连续三次应用金喜素联合顺铂方案化疗,检测肿块横径与直径缩小程度。比较两个方案对小细胞肺癌的治疗作用。结果：金喜素联合顺铂方案对小细胞肺癌总有效率达56.5％,传统CAV方案总有效率41.8％,两组比较有明显统计学意义（x^2=18.4〉16．27,v=3,p〈0．001）,两组毒副反应比较无统计学意义（x^2=5.62〈9．49,v=4,p〉0．05）。结论：金喜素联合顺铂方案对小细胞肺癌较传统CAV方案有更明显的疗效,值得临床应用。     

不同化疗方案联合手术治疗非小细胞肺癌的临床疗效及对患者免疫功能的影响分析

目的:探讨分析不同化疗方案联合手术治疗非小细胞肺癌的临床疗效以及对患者免疫功能的影响。方法:经病理学证实的非小细胞肺癌患者94例,随机数字表法将其分为顺铂组与洛铂组,各47例。2组患者均采取手术治疗,并术前行辅助化疗。其中顺铂组采取紫杉醇+顺铂方案,洛铂组接受紫杉醇+洛铂方案。比较治疗前后2组患者临床疗效及KPS评分,并对Ig A、Ig G、Ig M、CD4+及CD8+指标水平进行分析。结果:洛铂组有效率(CR+PR)为87.2%(41/47),与顺铂组[80.8%(38/47)]差异无统计学意义(P0.05)。洛铂组术后KPS评分及CD4+水平高于顺铂组(P0.05),但CD8+水平低于顺铂组(P0.05),差异有统计学意义;2组患者手术前后Ig A、Ig G及Ig M均无统计学意义(P0.05)。洛铂组毒副反应发生率低于顺铂组(P0.05)。结论:含洛铂术前辅助化疗方案有助于改善非小细胞肺癌患者的免疫功能,降低化疗的毒副反应。     

ERCC1 codon118基因表达在预测三代含铂方案治疗晚期非小细胞肺癌疗效中的意义

目的:探讨ERCC1codon118基因表达对预测三代含铂方案治疗晚期非小细胞肺癌疗效的影响。方法:对我院收治的240例晚期非小细胞肺癌患者进行ERCC1codon118基因多样性检测,以及对各基因型对三代含铂方案治疗晚期非小细胞肺癌疗效进行比较。结果:C/C组与C/T组+T/T组患者其肿瘤分化程度、临床分期、肿瘤大小、血管侵犯等基本资料无明显的相关性(P>0.05);C/C组患者其无进展生存时间以及生存时间、1年、2年以及3年生存率为13.2±5.4月、25.4±4.3月、62.88%、23.48%以及14.39%,明显高于对照组的6.2±4.3月、10.5±3.2月、26.85%、8.33%、1.85%。结论:ERCC1codon118基因表达可能与预测三代含铂方案治疗晚期非小细胞肺癌敏感性有关。     

培美曲塞单药或联合铂类治疗晚期复治非小细胞肺癌54例临床观察

目的:培美曲塞是一种多靶点抗叶酸化疗药,目前已成为晚期非小细胞肺癌二线治疗的标准药物.本研究回顾分析培美曲塞单药或联合铂类治疗晚期复治非小细胞肺癌的疗效及不良反应.方法:对既往至少接受过1个标准含铂方案化疗的54例晚期非小细胞肺癌怠者,分为单药治疗组21例,联合铂类治疗组33例.单药治疗组给予培美曲塞单药治疗,培美曲塞500mg/m2,第1天,21天为1个周期;联合铂类治疗组给予培美曲塞联合顺铂或卡铂,培美曲塞500mg/m2,第1天,顺铂75 mg/m2或卡铂AUC=5,第1天,21天为1个周期.评价疗效及不良反应.结果:54例患者均可评价疗效.单药治疗组PR 1例,RR4.8%,SD10例,疾病控制率(DCR)52.4%,PD10例(47.6%).中位无进展生存期3.8个月;联合治疗组PR4例,RR12.1%,SD20例,疾病控制率(DCR)72.7%,PD9例(27.3%).中位无进展生存期4.8个月.与药物相关的不良反应主要为:Ⅰ/Ⅱ度骨髓抑制、胃肠道反应.结论:培美曲塞或与铂类联合治疗晚期复治非小细胞肺癌有效,不良反应轻微、可耐受.     

培美曲塞联合顺铂治疗晚期非小细胞肺癌的临床疗效观察

目的:探讨培美曲塞联合顺铂治疗晚期非小细胞肺癌(NSCLC)的临床疗效。方法:随机选取我院肿瘤科晚期NSCLC患者177例,随机将其分为3组,培美曲塞联合顺铂治疗(PP组)72例,多西他赛联合顺铂治疗(DP组)53例,吉西他滨联合顺铂治疗(GP组)52例,比较三组治疗方法的临床疗效与不良反应之间的差异,根据临床疗效将PP组分为有效组与无效组,分析培美曲塞联合顺铂治疗晚期NSCLC的影响因素。结果:PP组疾病控制率(DCR)与客观有效率(ORR)均显著高于GP组(均P0.05);PP组与DP组近期疗效之间的比较无显著差异(均P0.05)。PP组的药物毒副作用均显著优于DP组与GP组(均P0.05)。PP组的中位生存期显著高于DP组与GP组(均P0.05),在无吸烟、腺癌与IV期晚期NSCLC患者中,培美曲塞联合顺铂治疗有效率更高。结论:培美曲塞治疗晚期NSCLC的疗效佳,与多西他赛相当并显著优于吉西他滨治疗,药物毒副作用小,且受吸烟状况、病理类型与临床分期影响。     

ERCC1和RRM1在非小细胞肺癌组织中的表达及意义

目的:观察非小细胞肺癌中ERCC1和RRM1表达,并探讨其临床意义。方法:选择本院及西安交通大学第一附属胸外二科于2013年1月-2013年6月收治的经术后病理证实为非小细胞癌肺癌患者40例作为研究对象,均采取免疫组化技术测定组织中ERCC1和RRM1表达水平,并分析ERCC1和RRM1表达水平与患者年龄、病理分期、是否淋巴结转移等相关因素之间的关系。结果:40例非小细胞肺癌患者中,ERCC1表达阴性28例(70.0%),阳性12例(30.0%);RRM1表达阴性9例(22.5%),阳性31例(77.5%)。ERCC1和RRM1表达阴性非小细胞肺患者生存期均优于表达阳性患者,均P0.05。患者非小细胞癌TNM分期及淋巴结转移转移情况与ERCC1及RRM1表达情况具有相关性,均P0.05。结论:非小细胞肺癌ERCC1和RRM1表达水平测定有助于预后情况,具有重要临床价值。     

Prognostic Value of EGFR Mutation and ERCC1 in Patients with Non-Small Cell Lung Cancer Undergoing Platinum-Based Chemotherapy

Background

In order to improve the outcome of patients with non-small cell lung cancer (NSCLC), a biomarker that can predict the efficacy of chemotherapy is needed. The aim of this study was to assess the role of EGFR mutations and ERCC1 in predicting the efficacy of platinum-based chemotherapy and the outcome of patients with NSCLC.

Methods

We conducted a retrospective study to analyze the relationships between EGFR mutations or ERCC1 expression and progression-free survival (PFS) in patients with NSCLC who received platinum-based chemotherapy. EGFR mutation status was determined using the peptide nucleic acid-locked nucleic acid polymerase chain reaction clamp method, and immunohistochemistry was used to examine the expression of ERCC1 in tumor samples obtained from the patients.

Results

Among the NSCLC patients who received platinum-based chemotherapy, the median PFS was significantly better in those who had never smoked and those with exon 19 deletion, and the median overall survival (OS) was significantly better in those who had never smoked, those with exon 19 deletion, and women. Cox regression analysis revealed that exon 19 deletion and having never smoked were significantly associated with both PFS and OS. Subset analysis revealed a significant correlation between ERCC1 expression and EGFR mutation, and ERCC1-negative patients with exon 19 deletion had a longer PFS than the other patients; ERCC1-positive patients without exon 19 deletion had a shorter PFS than the other patients.

Conclusions

Our results indicate that among NSCLC patients receiving platinum-based chemotherapy, those with exon 19 deletion have a longer PFS and OS. Our findings suggest that platinum-based chemotherapy is more effective against ERCC1-negative and exon 19-positive NSCLC.     

Examination of ERCC1 expression in lung cancer patients treated with platinum-based chemotherapy

Platinum-based chemotherapies are widely used in the treatment of lung cancer. However, little is known about their effect in the expression of certain tissue biomarkers. We have studied the ERCC1 (excision repair cross-complementation group 1) expression in tissue samples of patients treated with neoadjuvant chemotherapy. Fifty lung cancer tissue blocks of 25 patients (15 males, 10 females) were studied. They included 25 bronchoscopic biopsies (14 squamous cell carcinomas and 11 adenocarcinomas) together with their corresponding surgical biopsies after neoadjuvant chemotherapy. Immunohistochemistry was performed on formalin-fixed, paraffin-embedded tissues to study the expression of ERCC1. Staining scores (0-300) were calculated by multiplying the percentage of positive tumor cells (0-100) by the staining intensity (0-3). All but one bronchosopic squamous cell carcinoma tissues (13/14) expressed ERCC1. Four of these cases became negative after neoadjuvant therapy, and in 8 cases the level of expression decreased. In the adenocarcinoma group all but one bronchosopic tissues (10/11) expressed ERCC1. Six of these cases became negative after neoadjuvant therapy, and in 4 cases the level of expression decreased. Comparison of staining scores before and after chemotherapy revealed more pronounced decrease in adenocarcinomas and in female patients. There was no newly expressed ERCC1-positive case in the surgical biopsy group. The results of the present study suggest that platinum-based chemotherapy affects the expression of tissue biomarker (ERCC1) which may have predictive value, and probably induces a selection of tumor cells with more aggressive phenotype. This knowledge might be of importance when designing treatment protocols for non-small cell lung cancer patients.     

Association of ERCC1-C118T and -C8092A polymorphisms with lung cancer risk and survival of advanced-stage non-small cell lung cancer patients receiving platinum-based chemotherapy: A pooled analysis based on 39 reports

The published data on the predictive role of ERCC1 polymorphisms in lung cancer risk and survival of patients with advanced non-small cell lung cancer (NSCLC) receiving platinum-based chemotherapy remains inconsistent. The aim of this meta-analysis was to determine the role of ERCC1 gene polymorphisms (C118T and C8092A) in this clinical situation. Eligible studies were included and assessed for quality using multiple search strategies. Thirty-nine published papers involving 9615 cases (4606 with Stage III/IV disease) and 5542 controls were included in the analysis. Pooled odds ratios (OR) or hazard ratios (HR) with 95% confidence intervals (CI) were used to estimate risk. ERCC1-C118T was associated with lung cancer risk. The OR was 0.90 (95% CI: 0.81–0.99, p = 0.043) in an additive genetic model (C allele vs. T allele) and 0.77 (95% CI: 0.63–0.95, p = 0.013) in a recessive genetic model (CC/CT vs. TT). The corresponding risk was 0.74 (95% CI: 0.58–0.94, p = 0.013) based on a homozygous comparison (CC vs. TT). No significant correlation was found for ERCC1 C8092A and there was no obvious relationship between ERCC1 C118T/C8092A polymorphisms and objective response to platinum-based chemotherapy. Overall survival (OS) of patients with non-small cell lung cancer (NSCLC) receiving platinum-based chemotherapy was significantly related to ERCC1 C118T (HR: 1.29, 95% CI: 1.07–1.56, p = 0.007, CT/TT vs. CC). There was no relationship between ERCC1 C8092A and survival (HR: 1.32, 95% CI: 0.84–2.10, p = 0.23, CA/AA vs. CC). These findings suggest that ERCC1 C118T polymorphisms may serve as a biomarker for lung cancer risk and have prognostic value in patients with advanced non-small cell lung cancer (NSCLC) undergoing platinum-based treatment. Further studies with larger numbers of subjects from a worldwide arena are needed to validate the associations.     

吉非替尼联合GP化疗方案治疗晚期非小细胞肺癌的效果及对血清CEA、SCC、NSE、CYFRA21-1水平的影响

目的:研究吉非替尼联合吉西他滨和顺铂(GP)化疗方案治疗晚期非小细胞肺癌的效果及对血清癌胚抗原(Carcinoembbryonic antigen,CEA)、鳞状细胞癌相关抗原(Squamous cell carcinoma,SCC)、神经元特异烯醇化酶(Neuron-specific enolase,NSE)、细胞角蛋白19片段(Cytokeratin-19-fragment,CYFRA21-1)水平的影响。方法:选取2016年6月～2018年6月我院收治的晚期非小细胞肺癌患者110例,采用随机数字表法将患者分为两组,每组55例。对照组患者给予GP化疗方案,观察组在对照组的基础上给予吉非替尼。比较两组患者的临床治疗效果,治疗前后血清肿瘤标志物水平和生活质量的变化以及不良反应发生情况。结果:治疗后,观察组疾病控制率为86.67%,对照组为74.55%,观察组显著高于对照组(P0.05);两组治疗后血清CEA、SCC、NSE和CYFRA21-1水平均较治疗前显著下降,且观察组以上指标均显著低于对照(P0.05);两组治疗后FACT-L各项评分包括躯体状况、社会家庭状况、情感状况、肺癌特异性模块和功能状况评分均较治疗前显著升高,且观察组以上指标均显著高于对照(P0.05)。治疗期间,观察组患者白细胞减少、血小板减少、肝肾功能异常的发生率显著低于对照组(P0.05),两组贫血、恶心呕吐的发生率比较无统计学差异(P0.05)。结论:与GP化疗方案相比,吉非替尼联合GP化疗方案可更显著提高晚期非小细胞肺癌患者的治疗效果,改善其生活质量,且安全性较高,可能与其降低血清CEA、SCC、NSE和CYFRA21-1水平有关。     

不同放化疗模式治疗中晚期非小细胞肺癌的疗效分析

目的:探讨同步和序贯放疗联合不同化疗方案对治疗中晚期非小细胞肺癌近期疗效、远期生存及毒性反应的影响。方法:将45例III-IV期非小细胞肺癌患者随机归入两组,同步放化疗组22例;序贯放化疗组23例。全组病例依据病情分别选择艾素和顺铂、吉西他滨和顺铂、长春瑞滨和顺铂或培美曲塞和顺铂方案化疗。比较两组近期疗效、远期生存率及毒性反应。结果:同步组近期有效率为81.8%高于序贯组73.9%,但无统计学差异(P0.05);两组均有随放疗剂量增加有效率升高趋势。NP和TP方案两组近期疗效相近(P0.05)。同步组和序贯组1年生存率分别为90.9%和86.9%(P0.05);2年生存率分别为72.7%和52.2%(P0.05)。毒性反应主要为骨髓抑制、放射性食管炎和肺炎。同步组毒副反应发生率高于序贯组,但无统计学差异(P0.05)。结论:同步放化疗治疗中晚期非小细胞肺癌近期疗效及远期生存率有优于序贯放化疗的趋势,但毒副反应发生相对增多。联合治疗模式下,分期越早,患者远期生存时间越长。近期疗效有随放疗剂量增高而提高趋势,但放疗剂量、病理类型、化疗方案等对患者远期生存无明显统计学差异。     

CITED2 silencing sensitizes cancer cells to cisplatin by inhibiting p53 trans-activation and chromatin relaxation on the ERCC1 DNA repair gene

In this study, we show that silencing of CITED2 using small-hairpin RNA (shCITED2) induced DNA damage and reduction of ERCC1 gene expression in HEK293, HeLa and H1299 cells, even in the absence of cisplatin. In contrast, ectopic expression of ERCC1 significantly reduced intrinsic and induced DNA damage levels, and rescued the effects of CITED2 silencing on cell viability. The effects of CITED2 silencing on DNA repair and cell death were associated with p53 activity. Furthermore, CITED2 silencing caused severe elimination of the p300 protein and markers of relaxed chromatin (acetylated H3 and H4, i.e. H3K9Ac and H3K14Ac) in HEK293 cells. Chromatin immunoprecipitation assays further revealed that DNA damage induced binding of p53 along with H3K9Ac or H3K14Ac at the ERCC1 promoter, an effect which was almost entirely abrogated by silencing of CITED2 or p300. Moreover, lentivirus-based CITED2 silencing sensitized HeLa cell line-derived tumor xenografts to cisplatin in immune-deficient mice. These results demonstrate that CITED2/p300 can be recruited by p53 at the promoter of the repair gene ERCC1 in response to cisplatin-induced DNA damage. The CITED2/p300/p53/ERCC1 pathway is thus involved in the cell response to cisplatin and represents a potential target for cancer therapy.