The efficacy and safety of conventional first-line chemotherapeutic regimens for the treatment of advanced biliary tract carcinomas (ABTCs) have been unsatisfactory. We aimed to explore alternative chemotherapeutic regimens capable of providing improved efficacy and fewer side-effects. Multicentre, randomised, phase II clinical trial. Patients with unresectable advanced-stage tumors, or those who have developed recurrence or metastasis following initial radical surgery, between January 2021 and November 2022 were included. The participants were randomised to either a gemcitabine-cisplatin group (GC) or an albumin-paclitaxel-cisplatin group (NC). Progression-free survival (PFS) was the primary outcome, whereas overall survival (OS), and objective response rate (ORR) were the secondary outcomes. The trial enrolled 75 patients and had a median follow-up period of 11 months. The median PFS (mPFS) was 7.8 m (95 https://www.chictr.org.cn/showproj.html?proj=38440 .

Immune checkpoint inhibitors (ICIs) targeting programmed cell death protein 1 (PD-1) or programmed death ligand 1(PD-L1) respond well to deficient-microsatellite(dMMR) colorectal cancer and poorly to proficient-microsatellite (pMMR) CRC. Anti-vascular therapy is the standard backline treatment regimen for advanced metastatic colorectal cancer and also potentiates the immunotherapeutic efficacy of CRC by promoting immune cell infiltration and remodeling the tumor immune microenvironment (TIME). However, it is not clear whether combining radiotherapy, anti-vascular and anti-PD-1 can affect the efficacy of pMMR CRC. In this experiment, we investigated the antitumor efficacy of radiotherapy combined with fruquintinib and tirelizumab in pMMR CRC mice. CT26 cellular hormonal tumor corresponding to pMMR CRC. A mouse model with subcutaneous transplanted tumors is established, divided into control, radiotherapy (IR), fruquintinib + tirelizumab (F+T), and radiotherapy + fruquintinib + tirelizumab (IR+F+T) groups. Immunofluorescence (IF) experiments were conducted to investigate the number and function of tumor vessels. Immunohistochemistry (IHC) and flow cytometry (FC) were utilized to examine immune cell infiltration and alterations within the TIME. Compared to the control group, tumor growth was significantly inhibited after treatment. When compared to IR and F+T, IR+F+T demonstrated a remarkable suppression of tumor growth. The quantitative analysis results showed a significant decrease in Ki-67 positive cells in the target tumors with IR+F+T compared to IR and F+T. The TUNEL results indicated that treatment promoted tumor cell apoptosis, and the effect was further enhanced with triple combinational therapy. Both F+T and IR+F+T repressed CD31 expression and improved the ratio of α-SMA+/CD31+ in tumor tissue, yet there was no significant difference between the two groups. The immunohistochemistry and flow cytometry results demonstrated that triple combinational therapy increased tumor-infiltrating CD8+ T cells and significantly elevated the proportions of CD8, CD69, and CD86. Both F+T and IR+F+T boosted PD-L1 expression, with no significant difference between them. Combined irradiation on top of fruquintinib and tirelizumab treatment enhanced the efficiency in CT26 murine CRC syngeneic tumor model. There was no significant effect of radiotherapy on the anti-angiogenesis of fruquintinib and the promotion of normal vascular function. Irradiation promoted CD8+ T cell and dendritic cell infiltration and activation. Mingsheng Zhang, Qingqing Yu, Huiying Hou, Xiaoting Su, Qin Huang, Hong Qiu, Le Huang, Liang Zhuang, Qiang Fu, Yanmei Zou, Li Sun, Liu Huang, Shunfang Liu, Fei Liu, Xianglin Yuan. Efficacy and mechanism of radiotherapy combined with fruquintinib and tirelizumab in mCRC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 1828.

Oxaliplatin is a widely applied anti-cancer drug in clinics for colorectal cancer (CRC) treatment. Nonetheless, the treatment efficacy is always limited by the acquisition of chemoresistance in cancer cells. The deregulation of long non-coding RNA (lncRNA) FAL1 has been implicated in the tumorigenesis and progression of different malignancies. Nevertheless, the possible contribution of lnc-FAL1 in drug resistance development of CRC has not been investigated. Here, we reported the overexpression of lnc-FAL1 in CRC samples, and elevated lnc-FAL1 levels seemed to be associated with the poor survival in CRC patients. We further demonstrated that lnc-FAL1 promoted oxaliplatin chemoresistance in both cell and animal model. Additionally, lnc-FAL1 was mainly derived from exosomes secreted by cancer associated fibroblasts (CAFs), and lnc-FAL1-containing exosomes or lnc-FAL1 overexpression significantly inhibited oxaliplatin-induced autophagy in CRC cells. Mechanistically, lnc-FAL1 acted as a scaffold for the interaction between Beclin1 and TRIM3 to promote TRIM3-dependent Beclin1 polyubiquitination and degradation, thereby suppressing oxaliplatin-induced autophagic cell death. In summary, these data imply a molecular mechanism through which CAF-derived exosomal lnc-FAL1 contributes to the acquisition of oxaliplatin resistance in CRC.

Background: The overexpression of human antigen R (HuR) has been proven in various types of cancer and is associated with the poor survival lung cancer patients. HuR overexpression stabilizes the mRNA of tumor-promoting genes by binding with 3 '-UTR AU-rich elements. However, the role of HuR in the proliferation of lung cancer is unclear.Methods: HuR expression was assessed using immunohistochemistry of tumor tissue samples from ten patients with lung cancer and ten patients with benign lung disease. Gene, protein, mRNA, and lncRNA changes in A549 HuR knockdown (KD) cells were assessed by single-cell RNA sequencing analysis. Furthermore, cell proliferation, migration, and invasion were determined by Cell Counting Kit-8 (CCK-8) assays and Transwell assays with or without Matrigel. The cell cycle was assessed by propidium iodide staining. The protein level, mRNA level and half-life of PLK1 were detected by western blotting and RT-qPCR.Results: In clinical patients, the expression of HuR was significantly higher in lung cancer patients than in patients with benign lung disease. RNA sequencing analysis of A549 HuR knockdown cells revealed that the main function of HuR was related to ribonucleoprotein complex biogenesis. HuR was found to regulate signaling pathways mainly related to the spliceosome, RNA transport and the cell cycle. HuR KD suppressed the proliferation, migration and invasion of A549 cells, indicating its promotive role in these processes.Conclusion: These results demonstrate that HuR plays an important role in the progression of lung cancer.

目的:探讨结直肠癌(CRC)组织人源长寿保障基因2(LASS2)、同源异型盒基因B7(HOXB7)表达与凋亡指数(AJ)及预后的关系.方法:选择2013年10月至2015年4月期间在我院接受治疗的105例CRC患者作为研究对象.检测其CRC组织以及癌旁组织中LASS2、HOXB7表达以及AI,分析LASS2、HOXB7表达与临床病理特征的关系,采用Kaplan-Meier生存曲线分析不同LASS2、HOXB7表达患者总生存率的差异,Cox比例风险回归分析CRC患者预后的影响因素.结果:CRC组织中LASS2阳性率低于癌旁正常组织,而HOXB7阳性率高于癌旁正常组织(P＜0.05),CRC组织中AI低于癌旁正常组织(P＜0.05).经Spreaman相关性分析显示CRC组织LASS2阳性率和AI呈正相关关系,而HOXB7阳性率和AI呈负相关关系(P＜0.05).LASS2表达与临床分期、浸润深度和淋巴结转移有关(P＜0.05),而HOXB7表达与临床分期和淋巴结转移有关(P＜0.05).HOXB7表达阳性患者的生存率低于HOXB7表达阴性患者,而LASS2表达阳性患者的生存率高于LASS2表达阴性患者(P＜0.05).Cox比例风险回归分析结果显示,临床分期为Ⅲ期、有淋巴结转移、LASS2阴性表达、HOXB7阳性表达以及AI＜2.0％均是影响CRC患者预后的危险因素(P＜0.05).结论:在CRC组织中HOXB7阳性率升高,而LASS2阳性率以及AI下降,且与临床分期以及淋巴结转移密切相关.LASS2、HOXB7表达及AI与CRC患者的生存和预后联系密切.

Background Erlotinib, a small-molecule epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, demonstrated therapeutic efficacy against pancreatic cancer. However, acquired resistance to erlotinib in pancreatic cancer is widely observed, and the exact mechanisms have not been fully explored until now. We examined the role of circular RNA circ_0013587 in the acquired resistance to erlotinib in pancreatic cancer cells and explored the underlying mechanisms. Methods We selected erlotinib-resistant pancreatic cancer cells from the AsPC-1 cell line. The expression of circ_0013587 was examined by qRT-PCR assays. The effects of circ_0013587 on pancreatic cancer cell proliferation, invasion, and erlotinib resistance were assessed by cell functional assays. Bioinformatic analysis and dual-luciferase reporter assays identified circ_0013587 and E-cadherin as direct targets of miR-1227. Mouse xenograft models were employed to investigate the function of circ_0013587 in erlotinib resistance of tumors in vivo. Results Circ_0013587 expression was significantly reduced in erlotinib-resistant AsPC-1 cells. We found that increasing circ_0013587 levels in erlotinib-resistant AsPC-1 cells re-sensitized them, whereas reducing circ_0013587 levels in erlotinib-sensitive AsPC-1 cells made them resistant. Mechanically, circ_0013587 released E-cadherin from the suppression of miR-1227, leading to E-cadherin up-regulation. Rescue assays highlighted that circ_0013587 reversed erlotinib resistance in pancreatic cancer cells by increasing E-cadherin levels through reducing the expression of miR-1227. Furthermore, circ_0013587 overexpression sensitized erlotinib-resistant AsPC-1 cells to erlotinib in xenograft models. Conclusions Our results demonstrated that down-regulation of circ_0013587 contributes to acquired resistance to erlotinib in pancreatic cancer cells through mediating the miR-1227/E-cadherin pathway and that circ_0013587 is a potential target molecular to overcome erlotinib resistance.

China has a heavy burden of hepatocellular carcinoma, which is a serious threat to people′s life and health. However, the available drugs for advanced hepatocellular carcinoma in the past are limited and the efficacy is not satisfactory. In recent years, immunotherapy has a significant effects in some tumors. The authors introduce the efficacy of restart immunotherapy on an advanced hepatocellular carcinoma patient undergoing interruption of treatment due to corona virus disease 2019, in order to provide references for the diagnosis and treatment of this kind of patients.

目的 探讨3D打印技术联合案例教学法在头颈肿瘤临床教学中的应用效果.方法 选取2016年1月-2017年12月在某大学附属医院肿瘤科接受住院医师规范化培训的60名学员为教学对象,随机分为实验组(30例)和对照组(30例),实验组采用3D打印技术联合案例教学法教学,对照组进行传统讲授式教学.课程结束后,对两组学员进行统一考试统计成绩,发放调查问卷评估教学满意度,综合评价3D打印技术联合案例教学法的教学应用效果.结果 实验组和对照组学员性别、年龄和全省规范化培训学员统一招录总成绩差异无统计学意义(P>0.05);实验组学员的理论基础知识、典型病例分析、临床操作技能和常见影像阅片成绩均明显高于对照组,差异有统计学意义(P<0.05).同时,实验组在兴趣吸引力、理解记忆力、培养临床思维、知识层面扩展、医患沟通能力培养等教学满意度调查评估表各项评分均明显高于对照组,差异有统计学意义(P<0.05).结论 3D打印技术联合案例教学法在头颈肿瘤临床教学中的应用,有益于提升头颈肿瘤教学课程的教学质量和教学满意度,培养良好的临床思维和临床实践能力.

传统的肿瘤治疗方法依然存在肿瘤组织可及性差和药物不良反应普遍的问题.黄酮类化合物已被证实对多种类型肿瘤有效,但其安全性和作用部位特异性尚未被评估.然而,膳食黄酮类化合物因溶解度小、代谢快、口服吸收差等特点限制了其在体内抗肿瘤活性的发挥.此外,黄酮类化合物在某些情况下还能通过生物转化等作用与药物相互作用而影响生物利用度.纳米载体因可改变药物的药动学和药效学特征而被设计用于靶向药物传递,提高难溶性药物的生物利用度,将大分子传递到细胞内的作用位点,同时还能减少药物不良反应.体内、外研究均表明,纳米类黄酮制剂,特别是槲皮素、柚皮素、芹菜素、儿茶素和非瑟酮等在多种肿瘤的预防和治疗方面具有潜在作用,但其临床应用价值仍有待阐明.本文就纳米类黄酮制剂在提高生物利用度、肿瘤治疗效果和安全性方面的作用展开综述,为肿瘤治疗药物的开发利用提供新思路.

Non-small cell lung cancer (NSCLC) has the highest morbidity and mortality worldwide. OTU deubiquitinase 5 (OTUD5), a deubiquitinating enzyme, can enhance the stability of p53 and programmed cell death 5 (PDCD5), a protein related to the apoptosis, by deubiquitination. This study aimed to explore the biological function and underlying mechanism of OTUD5 in NSCLC. Western blot and qRT-PCR were used to detect the expression of OTUD5 protein and mRNA in NSCLC tissues and cells, respectively. RNAi was adopted to construct an OTUD5 low-expression model while the plasmids overexpressing p53 and PDCD5 were used to establish the overexpression models, respectively. CCK-8 assay, transwell assay, and apoptosis assay were carried out to analyze the changes in the proliferation, migration, and chemoresistance of A549 and HCC827 cells. The mechanism of OTUD5 in NSCLC was studied by Western blot. Down-regulated OTUD5 in NSCLC tissues was significantly correlated to a poor prognosis. The knockdown of OTUD5 inactivated p53 and PDCD5, promoting the proliferation and metastasis of NSCLC cells while inhibiting their apoptosis. OTUD5 knockdown also enhanced the resistance of NSCLC cells to doxorubicin and cisplatin. OTUD5 acted as a tumor suppressor in NSCLC by regulating the p53 and PDCD5 pathways.

目的 了解中华医学会医学伦理学分会临床伦理学小组中部分成员单位对临床伦理及其重要性认知的情况,为医院伦理工作的开展提供参考.方法 通过问卷调查,对6家医院的196名医务工作者进行医学伦理学基础知识及临床伦理问题的调查.结果 调查对象中有14.29％的调查对象不知道所在医院已成立了伦理委员会,且有32.14％的调查对象从来没有向伦理委员会提出过任何层面的申请;不同学历的医务工作者在伦理基础知识及临床伦理应用中的差异性没有统计学意义,但不同岗位的医务工作者在伦理基础知识及临床伦理应用中有着显著的统计学意义.结论 调查对象中临床医生能够更好地将医学伦理学的价值理论转化为临床伦理规范,在各项临床伦理认知的重要程度上有较好的表现,但还需加强对临床医生以外的各岗位医务工作者开展多层面多内容的伦理培训,提高医务人员对伦理委员会职能的认知.

目的 探讨尼美舒利联合奥沙利铂对人胃癌移植瘤裸鼠肿瘤生长及淋巴转移的影响.方法 取裸鼠40只,将人胃癌SGC-7901细胞株移植于裸鼠胃壁,建立人胃癌移植瘤裸鼠模型,建模成功后随机将裸鼠分为对照组(0.9％氯化钠溶液灌胃)、尼美舒利组(尼美舒利20 mg·kg-1·d-1灌胃)、奥沙利铂组(奥沙利铂10 mg/kg灌胃,每3天1次)、联合组(尼美舒利+奥沙利铂),每组10只,给药30 d后处死裸鼠,测定瘤体积及瘤重量,计算抑瘤率,并采用免疫组化法、实时荧光定量聚合酶链反应法(RT-PCR)测定人胃癌裸鼠移植瘤组织环氧化酶-2(COX-2)、血管内皮生长因子受体3(VEGFR-3)、血管内皮生长因子C(VEGF-C)、生存素(survivin)、β-连环素(β-catenin)蛋白及mRNA表达水平,采用酶联免疫吸附法(ELISA)测定血清肿瘤标志物癌胚抗原(CEA)、细胞角蛋白19可溶性片段抗原(CYFRA21-1)、鳞状细胞癌抗原(SCCAg)水平.结果 与对照组比较,尼美舒利组、奥沙利铂组和联合组裸鼠瘤体积缩小,瘤重量减轻(P<0.05),奥沙利铂组和联合组裸鼠瘤体积、瘤重量低于尼美舒利组,抑瘤率高于尼美舒利组(P<0.05),联合组裸鼠瘤体积、瘤质量低于奥沙利铂组,抑瘤率高于奥沙利铂组(P<0.05);与对照组比较,尼美舒利组、联合组裸鼠肿瘤组织COX-2、VEGF-C、VEGFR-3、Survivin、β-catenin染色阳性率均降低,奥沙利铂组COX-2、VEGF-C、VEGFR-3、Survivin、β-catenin染色阳性率高于尼美舒利组(P<0.05),联合组COX-2、VEGF-C、VEGFR-3、Survivin、β-catenin阳性率低于奥沙利铂组、尼美舒利组(P<0.05);与对照组比较,尼美舒利组、联合组COX-2、VEGF-C、VEGFR-3、Survivin、β-catenin mRNA降低,奥沙利铂组COX-2、VEGF-C、VEGFR-3mRNA上升,Survivin、β-catenin mRNA降低(P<0.05),尼美舒利组、联合组COX-2、VEGF-C、VEGFR-3、Survivin、β-catenin mRNA低于奥沙利铂组(P<0.05),联合组COX-2、VEGF-C、VEGFR-3 mRNA高于尼美舒利组(P<0.05),Survivin mRNA表达低于尼美舒利组(P<0.05);与对照组比较,尼美舒利组、奥沙利铂组、联合组裸鼠CEA、CYFRA21-1、SCCAg降低(P<0.05),奥沙利铂组、联合组裸鼠上述指标低于尼美舒利组,联合组上述指标又低于奥沙利铂组(P<0.05).结论 尼美舒利联合奥沙利铂相比二者单独使用,可更有效地抑制人胃癌移植瘤裸鼠肿瘤生长及淋巴结转移.

Objective The aim of the study was to evaluate the role of postoperative sequential chemotherapy and radiotherapy in patients with locally advanced gastric cancer.Methods From January 2003 to December 2010, 146 gastric cancer patients at our institution（Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China） received postoperative sequential chemotherapy and radiotherapy after radical surgery. Radiotherapy was administered as a dose of 4500 cGy in 25 fractions. For patients with positive margins, the dose was raised to 5040 cGy in 28 fractions. Three cycles of m FOLFOX or PF（cisplatin, 5-fluorouracil） chemotherapy regimen were applied before and after radiotherapy. Three-and 5-year survival rates were analyzed; any adverse effects with respect to hematology, hepatic and renal function, or the gastrointestinal tract that occurred during the treatment were evaluated.Results This cohort consisted of non-metastatic patients: 104 men and 42 women with a median age of 51.0 years. The full course of sequential chemotherapy and radiotherapy（4500–5040 cGy） was completed by 129 patients（88.4%）. Seventeen regional relapses（9.8%） and 46 distant relapses（23.8%） were recorded. Fifty patients（34.2%） died during follow-up. The 3-and 5-year overall survival rates（OS） were 60% and 54%, and disease-free survival rates（DFS） were 53% and 47%, respectively. There were no significant differences in survival rate with respect to age, sex, histopathology, N stage, site of the tumor, or margin status. Multivariate analysis showed that only the depth of tumor invasion（T stage） was an independent prognostic factor for OS（P = 0.009） and DFS（P = 0.006）. The rates of grades 3 and 4 neutropenia and vomiting were 9.6% and 3.4%, respectively, during the treatment.Conclusion Postoperative sequential chemotherapy with an m FOLFOX or PF regimen and radiotherapy were found to be an effective means of treating advanced gastric cancer patients with T3–T4 disease. The adverse effects of this treatment were tolerable.

Colorectal cancer (CRC) represents one of the most prevalent malignancies and the third leading cause of cancer death worldwide. Inorganic pyrophosphatase (PPA1) is an enzyme that catalyzes the hydrolysis of pyrophosphate to inorganic phosphate, therefore participates in the energy metabolism. Proteomic studies have demonstrated the up-regulated expression of PPA1 in various tumors, however, its expression pattern in CRC hasn't been reported. In the current study, we used RT-qCR, Western Blot and immunohistochemical (IHC) staining to explore the expression of PPA1 in 113 paired colon cancer tissues and adjacent normal tissues, which revealed that PPA1 was correlated with lymph node metastasis. The prognostic value of PPA1 was confirmed by Kaplan-Meier survival analysis and Cox regression analysis. We further purified PPA1 and obtained the phosphor-JNK1 protein and performed enzymatic studies, which identified that PPA1 can directly dephosphorylate pJNK1, while showed no catalytic activity towards pERK or p-p38 proteins. Moreover, overexpression of PPA1 enhanced cell viability through JNK-p53 signaling pathways, and it may also prevent cell apoptosis by inhibiting Bcl-2 and Caspase-3 cleavage. To our knowledge, this is the first study demonstrated the expression and clinical significance of PPA1 in colon cancer, which also provided evidence that figuring out PPA1 specific inhibitors can be invaluable in the future chemotherapy development towards colon cancer.

With the development of imaging technology,the detection rate of gallbladder benign lesions has increased year by year.And part of the diseases may evolve into gallbladder cancer through a series of pathophysiologic processes.There are some misunderstandings in the understanding of gallbladder benign lesions for surgeons,so it is difficult for the clinical decision-making.The relationship between gallbladder benign lesions and gallbladder cancer should be correctly understood.Surgeons can neither exaggerate the risk of gallbladder cancer nor miss optimal timing of operation.The key point of the diagnosis and treatment of gallbladder benign lesions should be based on making full use of imaging data and strictly grasp pre-and intraoperative indications,and it is important to identify the malignant transformation of gallbladder benign lesions as soon as possible and carry out standardized treatment.

Objective:To observe the effects of bone morphogenetic protein 4 (BMP4) on the expression of IL-1β and apoptosis in mouse models of unilateral ureteral obstruction (UUO).Methods:Thirty-two C57BL/6 mice were randomly divided into four groups:saline-sham operated group (n =8),saline-UUO group (n =8),BMP4 antibody-sham operated group (n =8),and BMP4 antibodyUUO group (n =8).Each group was given intraperitoneal injection of either saline or BMP4 antibody (200 μL/g) every day after operation for 7 days.The mice were sacrificed at 7 day to evaluate the expression of BMP4 in renal tissue of normal mouse by immunofluorescence.Fluorescent quantitative real-time PCR was used to detect the expression of IL-1β mRNA in each group.Besides,the renal cell apoptosis was evaluated by TUNEL-assay.Results:The expressions of BMP4 were mainly distributed in the renal tubules of mice.Real-time PCR showed that the expression of IL-1β mRNA and apoptosis rate in BMP4 antibody-sham operated group and saline-sham operated group were with no significant differences (P＞0.05).The expression of IL-1β mRNA and apoptosis rate in BMP4 antibody-UUO group were less than saline-UUO group (P＜0.05).Conclusion:BMP4 participates in the process of renal interstitial inflammation and cell apoptosis in obstructive nephropathy,it can be used as a therapeutic target for renal disease.

肺炎链球菌是儿童社区获得性肺炎最常见的病原菌之一，除了引起肺炎外，还可导致脓胸、化脓性脑膜炎、败血症等。部分严重感染患儿可发生多器官功能不全、全身炎症反应综合征等产生不良后果。严重感染后机体异常强烈的免疫反应可能激活淋巴组织细胞，吞噬血细胞，产生继发性噬血细胞综合征，导致全血细胞减少。若得不到及时有效的治疗，预后不良。现报告1例肺炎链球菌感染导致的噬血现象的病例，以加强对本类疾病的认识。

Systemic immune-inflammation index (SII), based on lymphocyte (L), neutrophil (N), and platelet (P) counts, was recently developed and reflects comprehensively the balance of host inflammatory and immune status. We explored its prognostic value in localized gastric cancer (GC) after R0 resection and the potential associations with Thymidine phosphorylase (TYMP), which was reported to increase the migration and invasion of gastric cancer cells. A total of 455 GC patients who received D2 gastrectomy were enrolled. Blood samples were obtained within 1 week before surgery to measure SII (SII = P × N/L). TYMP expression was measured on tumor sections by immunohistochemical analysis. Preoperative high SII indicated worse prognosis (HR: 1.799; 95% CI: 1.174-2.757; p = 0.007) in multivariate analysis and was associated with higher pathological TNM stage, deeper local invasion of tumor and lymph node metastasis (all p < 0.001). SII predicted poor overall survival in pathological TNM stage I subgroup also (p < 0.001). Furthermore we found that in high SII group, positive rate of TYMP expression increased (53.7% vs 42.7%, p = 0.046) and TYMP positive patients had higher SII score (median 405.9 vs. 351.9, p = 0.026). SII, as a noninvasive and low cost prognostic marker, may be helpful to identify higher-risk patients after R0 resection, even for stage I GC patients.

UGT1A1*28/*6 as predictors of severe irinotecan-related diarrhea (SIRD) were duplicated by many studies. However, some patients of lower risk genotype (UGT1A1*1/*1) still suffered SIRD and the extremely low frequency of UGT1A1*6/*6 limited its clinical usage. Previous studies proved that the transforming growth factor (TGFB) family may have some effect on MTX-induced mucositis. However, the associations between TGFB gene variants and SIRD have never been reported so far. Our aim was to improve the predictive value of UGT1A1 gene variants on SIRD.