To describe the application of a three-anatomical-plane dissection (TAPD) technique for RCC-AHG and evaluate its feasibility and safety. Between June 2019 and October 2023, 42 patients undergoing PN using the TAPD technique at Ruijin Hospital were included. The data collected including patient demographic characteristics, oncological characteristics, perioperative and follow-up data on complications, renal function, recurrence and metastasis within 12 months after surgery. Patients underwent robotic or laparoscopic surgery by the transabdominal or retroperitoneal approach, depending on the tumor location. The three contact planes of the RCC-AHG tumor were anatomically dissected sequentially: the interface between the tumor and the perirenal fat (C1), the interface between the tumor and the renal hilum vessels (C2), and the interface between the tumor and the kidney parenchyma (C3). A total of 42 RCC-AHG patients were eventually enrolled. The median tumor diameter was 35.51 ± 13.99 cm; RENAL score: 9 (range: 8–11); no postoperative complications with Clavien–Dindo classification ≥ 2 (0.0

BACKGROUND:The advent of ultrasonic scalpels has remarkably advanced minimally invasive surgery; however, the Chinese market's reliance on imports highlights the urgent need for a cost-effective, efficient, and domestically produced surgical scalpel. This study aimed to compare SanAgileTMSA01 with the Johnson & Johnson GEN11, and HAR36 surgical devices. RESEARCH DESIGN AND METHODS:In total, 152 participants requiring urological or general laparoscopic surgery were randomly and equally divided between the two hospitals and randomized to the test and control groups. Clinical outcomes, adverse event rates, intraoperative bleeding, and surgery duration were compared between the two devices. RESULTS:The clinical application rate of both devices was 100%. There were no significant differences between the two groups in intraoperative bleeding, surgery duration, and incidence of adverse events. In the test group, five device-related adverse events occurred (6.58%), compared to two (2.63%) in the control group (no significant difference). The device-related adverse events did not result in any sequelae. CONCLUSIONS:The clinical performance of the SanAgileTMSA01 was comparable to that of the Johnson & Johnson GEN11 and HAR36. The SanAgileTMSA01 device may serve as a viable alternative ultrasonic surgical tool, thereby providing clinicians with additional options. TRIAL REGISTRATION:Registration number of Shanghai Medical Equipment Preparation 20,190,114.

The downregulated expression of forkhead box F1 (FOXF1) has been found in many malignant tumors but no research was done in bladder cancer (BC). The present study aimed to investigate the prognostic value and antitumor effects of FOXF1 in patients with BC. Herein, a retrospectively recruited BC cohort and public datasets were utilized to identify the predictive ability of FOXF1 and determine its association with the clinical characteristics of BC patients. It was found that the expression level of FOXF1 was notably lower in BC tissues than in para-cancerous mucosae. Low FOXF1 expression was associated with unfavorable clinicopathological features and poor prognosis. Furthermore, in BC cells, the mRNA and protein expression levels of FOXF1 were examined using reverse transcription-quantitative PCR and western blot analysis. Cell viability was examined using Cell Counting Kit-8, EdU and clonogenic capacity assays. Cell apoptosis was detected using flow cytometry. The results revealed that the activation of FOXF1 impaired cell viability and induced apoptosis in BC. The antitumor effects of FOXF1 were also validated using animal models. Subsequently, caspase-3 was spotted as a downstream gene of FOXF1 by using RNA sequencing and protein-protein interaction analyses. FOXF1 inhibited proliferation and induced apoptosis of BC cells via caspase signaling pathway. The present study demonstrates the expression patterns, prognostic predictive ability and antitumor effects of FOXF1 in BC. FOXF1 is a favorable biomarker for predicting clinical outcomes in patients with BC and represents a potential therapeutic target.

Abstract Objectives To predict CTLA4 expression levels and prognosis of clear cell renal cell carcinoma (ccRCC) by constructing a computed tomography‐based radiomics model and establishing a nomogram using clinicopathologic factors. Methods The clinicopathologic parameters and genomic data were extracted from 493 ccRCC cases of the Cancer Genome Atlas (TCGA)‐KIRC database. Univariate and multivariate Cox regression and Kaplan–Meier analysis were performed for prognosis analysis. Cibersortx was applied to evaluate the immune cell composition. Radiomic features were extracted from the TCGA/the Cancer Imaging Archive (TCIA) (n = 102) datasets. The support vector machine (SVM) was employed to establish the radiomics signature for predicting CTLA4 expression. Receiver operating characteristic curve (ROC), decision curve analysis (DCA), and precision‐recall curve were utilized to assess the predictive performance of the radiomics signature. Correlations between radiomics score (RS) and selected features were also evaluated. An RS‐based nomogram was constructed to predict prognosis. Results CTLA4 was significantly overexpressed in ccRCC tissues and was related to lower overall survival. A higher CTLA4 expression was independently linked to the poor prognosis (HR = 1.458, 95% CI 1.13–1.881, p = 0.004). The radiomics model for the prediction of CTLA4 expression levels (AUC = 0.769 in the training set, AUC = 0.724 in the validation set) was established using seven radiomic features. A significant elevation in infiltrating M2 macrophages was observed in the RS high group (p < 0.001). The predictive efficiencies of the RS‐based nomogram measured by AUC were 0.826 at 12 months, 0.805 at 36 months, and 0.76 at 60 months. Conclusions CTLA4 mRNA expression status in ccRCC could be predicted noninvasively using a radiomics model based on nephrographic phase contrast‐enhanced CT images. The nomogram established by combining RS and clinicopathologic factors could predict overall survival for ccRCC patients. Our findings may help stratify prognosis of ccRCC patients and identify those who may respond best to ICI‐based treatments.

Transcription deregulation is recognized as a prominent hallmark of carcinogenesis. However, our understanding of the transcription factors implicated in the dysregulated transcription network of clear cell renal carcinoma (ccRCC) remains incomplete. In this study, we present evidence that ZNF692 drives tumorigenesis in ccRCC through the transcriptional repression of essential genes. We observed overexpression of ZNF692 in various cancers, including ccRCC, and found that the knockdown or knockout of ZNF692 suppressed the growth of ccRCC. Genome-wide binding site analysis using ChIP-seq revealed that ZNF692 regulates genes associated with cell growth, Wnt signaling, and immune response in ccRCC. Furthermore, motif enrichment analysis identified a specific motif (5′-GCRAGKGGAKAY-3′) that is recognized and bound by ZNF692. Subsequent luciferase reporter assays demonstrated that ZNF692 transcriptionally represses the expression of IRF4 and FLT4 in a ZNF692 binding motif-dependent manner. Additionally, we observed MYC binding to the promoter regions of ZNF692 in most cancer types, driving ZNF692 overexpression specifically in ccRCC. Overall, our study sheds light on the functional significance of ZNF692 in ccRCC and provides valuable insights into its therapeutic potential as a target in cancer treatment.

Background: N6-methyladenosine (m6A) is the most common form of mRNA- and long noncoding RNA (lncRNA)-specific internal modification encountered in eukaryotes, with important effects on mRNA stability, translation, and splicing. The role of m6A-modified lncRNAs (m6A-lncRNAs) in bladder cancer (BLCA) is rarely reported. This study aimed to evaluate an efficient prognostic model of BLCA in patients, based on m6A-lncRNAs, and to discover potential biological targets. Methods: Differentially expressed lncRNAs were investigated in 433 BLCA samples derived from The Cancer Genome Atlas (TCGA) database. Kaplan–Meier and univariate Cox regression analyses were performed to screen for m6A-lncRNAs with prognostic roles in BLCA. We implemented Pearson correlation analysis to analyze 18 potentially prognostic lncRNAs and 20 known m6A-associated genes. Next, the data were imputed using least absolute shrinkage and selection operator (LASSO) Cox regression to establish an m6A-lncRNA prognostic signature. Results: We established an integrated risk score (RS) containing five m6A-lncRNAs and constructed a nomogram that had the ability to forecast the overall survival (OS) of patients with BLCA. We showed that the predictive accuracy of the RS for BLCA prognosis was high, which was confirmed by the area under the receiver operating characteristic (ROC) curve. We analyzed the correlation between tumor immune infiltrating cells and RS in high- and low-risk patients with BLCA and used tumor immune dysfunction and exclusion to predict the effect of immunotherapy. We screened out the most relevant modules of RS through the weighted gene co-expression network analysis network and explored their potential biological functions using GO and KEGG analyses. Conclusion: Our findings demonstrate that, compared with nomograms constructed using a single prognostic factor, the integrated RS represents a superior model for predicting survival in patients with BLCA, which may improve the clinical management of BLCA.

Background The aim of this study was to investigate the biological functions and underlying mechanisms of SIRT5 in clear cell renal cell carcinoma (ccRCC). Methods SIRT5 expression data in The Cancer Genome Atlas Kidney Clear Cell Carcinoma (TCGA-KIRC) were selected, and the correlations between SIRT5 expression and various clinicopathological parameters were analysed. SIRT5 expression in ccRCC tissues was examined using immunohistochemistry. Stable cell lines with SIRT5 knockdown were established. In vitro and in vivo experiments were conducted to investigate the functional roles of SIRT5 in the cellular biology of ccRCC, including cell viability assays, wound healing assays, soft agar colony formation assays, Transwell invasion assays, qRT-PCR, and Western blotting. In addition, microarrays, rescue experiments and Western blotting were used to investigate the molecular mechanisms underlying SIRT5 functions. Results SIRT5 expression was downregulated in ccRCC compared with normal tissues, which correlated with a poor prognosis of ccRCC. SIRT5 knockdown significantly increased cell proliferation, migration and invasion in vitro. In vivo experiments revealed that SIRT5 knockdown promoted ccRCC tumorigenesis and metastasis. Mechanistically, SIRT5 deglycosylated PDHA1 at K351 and increased PDC activity, thereby altering the metabolic crosstalk with the TCA cycle and inhibiting the Warburg effect. SIRT5 overexpression was related to low succinylation of PDHA1. Conclusions Downregulated SIRT5 expression in ccRCC accelerated the Warburg effect through PDHA1 hypersuccinylation and induced tumorigenesis and progression, indicating that SIRT5 may become a potential target for ccRCC therapy.

Background: The aim of this study is to investigate the biological functions and the underlying mechanisms of SIRT5 in clear cell renal cell carcinoma (ccRCC). Methods: The datasets of SIRT5 expression in The Cancer Genome Atlas Kidney Clear Cell Carcinoma (TCGA-KIRC) was selected and the correlation between SIRT5 and various clinicopathological parameters was analyzed. The SIRT5 expression in RCC tissues was examined by immunohistochemistry. The SIRT5 knockdown cell lines were constructed. In vitro and in vivo experiments were carried out to investigate the function of SIRT5 on cellular biology of RCC, including cell viability assay, wound-healing assay, soft agar colony formation assay, Transwell invasion assay, qRT-PCR, Western blot, etc. Besides, microarray, rescue experiment and Western blot were used to investigate the molecular mechanisms underlying the functions of SIRT5. Results: SIRT5 expression was downregulated in RCC tissues, and low expression of SIRT5 was correlated with poor prognosis of RCC. Knockdown of SIRT5 significantly prompted cell proliferation, migration, and facilitated invasion in vitro . In vivo experiments revealed that knocking down SIRT5 prompted ccRCC tumorigenesis and metastasis. SIRT5 deglycosylated PDHA1 at K351 and increased the activity of PDC, thus changing the metabolic pathway to the TCA cycle and inhibiting the Warburg effect. The overexpression of SIRT5 was related to the low succinylation of PDHA1. Conclusion: SIRT5 correlated with PDHA1 hyposuccinylation and progression in ccRCC, which suggested that SIRT5 might become a potential target for ccRCC therapy.

Abstract Aberrant epigenetic reprogramming represents a hallmark of renal cell carcinoma (RCC) tumorigenesis and progression. Whether there existed other epigenetic vulnerabilities that could serve as therapeutic targets remained unclear and promising. Here, we combined the clustered regularly interspaced short palindromic repeats functional screening results and multiple RCC datasets to identify JMJD6 as the potent target in RCC. JMJD6 expression correlated with poor survival outcomes of RCC patients and promoted RCC progression in vitro and in vivo. Mechanistically, aberrant p300 led to high JMJD6 expression, which activated a series of oncogenic crosstalk. Particularly, high‐throughput sequencing data revealed that JMJD6 could assemble super‐enhancers to drive a list of identity genes in kidney cancer, including VEGFA, β‐catenin, and SRC. Moreover, this JMJD6‐mediated oncogenic effect could be suppressed by a novel JMJD6 inhibitor (SKLB325), which was further demonstrated in RCC cells, patient‐derived organoid models, and in vivo. Given the probable overlapped crosstalk between JMJD6 signature and tyrosine kinase inhibitors downstream targets, targeting JMJD6 sensitized RCC to sunitinib and was synergistic when they were combined together. Collectively, this study indicated that targeting JMJD6 was an effective approach to treat RCC patients.

目的:检测缺氧诱导因子1α (hypoxia-inducible factor-1α,HIF-1α)在乳头状肾细胞癌(papillary renal cell carcinoma,PRCC)组织中的表达情况,分析其与微血管密度(microvessel density,MVD)间的关系,并探讨HIF-1α与患者预后间的关系.方法:应用免疫组织化学(免疫组化)技术检测PRCC组织和癌旁肾组织(对照)中HIF-1α及MVD表达,分析二者之间的相关性.采用Kaplan-Meier法和Logrank法对患者的生存数据进行分析,对有意义的因素行Cox模型多因素回归分析.结果:PRCC组织中HIF-1α的阳性表达率为42.17％(35/83),其中Ⅰ型、Ⅱ型PRCC组织中HIF-1α阳性表达率分别为32.65％、55.88％,二者间差异有统计学意义(P=0.035).Ⅱ型PRCC组织中的MVD高于Ⅰ型PRCC(40.74个/高倍镜比25.63个/高倍镜),在Ⅰ型和Ⅱ型PRCC中,HIF-1α的表达均与MVD呈正相关(γ=0.65).83例PRCC患者的5年生存率为89.16％(74/83),13例死亡的病例中,10例为Ⅱ型PRCC,采用Kaplan-Meier生存曲线分析显示,Ⅰ型PRCC患者的预后好于Ⅱ型PRCC(5年总体生存率87.8％比76.5％,P＜0.05).单因素分析显示,肾细胞癌Fuhrman核分级Ⅲ～Ⅳ级、肿瘤发生远处转移和HIF-1α阳性表达是PRCC患者预后不良的危险因素;多因素分析显示,Ⅱ型PRCC、Fuhrman核分级Ⅲ～Ⅳ级、肿瘤远处转移及HIF-1α阳性表达是PRCC预后不良的因素.结论:相对于Ⅰ型PRCC,HIF-1α在Ⅱ型PRCC组织中的阳性率更高,其阳性表达是PRCC患者预后不良的因素.

Renal cell carcinoma (RCC) is a heterogeneous histological disease and it is one of the most common kidney cancer. The treatment of RCC has been improved for the past few years, but its mortality still remains high. Chelerythrine (CHE) is a natural benzo[c]phenanthridine alkaloid and a widely used broad‐range protein kinase C inhibitor which has anti‐cancer effect on various types of human cancer cells. However, its effect on RCC has not been fully elucidated. In this study, we evaluated the effect and mechanism of CHE on RCC cells. Our study showed that CHE induced colony formation inhibition and G2/M cell cycle arrest in a dose‐dependent manner in RCC cells. In addition, CHE increased cellular ROS level, leading to endoplasmic reticulum (ER) stress, inactivating STAT3 activities and inducing apoptosis in RCC cells which were suppressed by NAC, a special ROS inhibitor. We further found that both knockdown of ATF4 protein and overexpression of STAT3 protein could reduce CHE‐induced apoptosis in Caki cells. These results demonstrated that the apoptosis induced by CHE was mediated by ROS‐caused ER stress and STAT3 inactivation. Collectively, our studies provided support for CHE as a potential new therapeutic agent for the management of RCC.

目的:研究ZNF692基因在肾透明细胞癌(clear cell renal cell carcinoma,ccRCC)中的表达特征及其与患者预后间的关系,并分析ZNF692基因相关的调控机制.方法:采用癌症基因组图谱(The Cancer Genome Atlas,TCGA)数据库进行生物信息数据挖掘,提取516例ccRCC样本,分析ZNF692的表达特征及水平与ccRCC预后之间的关联,进一步分析ZNF692表达水平与DNA拷贝数、甲基化及组蛋白修饰间的关联,探索ZNF692的上游调控机制.收集本院20例ccRCC患者资料,采用实时定量反转录聚合酶链反应(quantitative reverse transcription polymerase chain reaction,qRT-PCR)检测癌及配对癌旁组织中ZNF692基因的表达水平,分析ZNF692表达与ccRCC患者预后间的关系;敲低ccRCC细胞株786-O和769-P ZNF692基因后,观察细胞的增殖状态,分析ZNF692的功能.结果:数据挖掘及临床样本分析提示,相对于癌旁组织,ZNF692在肿瘤组织中高表达(P<0.05);ZNF692高表达的ccRCC患者总体生存期(Logrank统计分析,P<0.0001)及无事件生存期(Logrank统计分析,P<0.0001)低于低表达患者.数据库数据挖掘及临床样本分析提示ZNF692高表达与c-MYC转录激活相关;ZNF692转录调控处于高度转录活化的状态,组蛋白H3赖氨酸27位点乙酰化(H3K27ac)富集;敲低细胞株ZNF692基因后,ccRCC细胞增殖被显著抑制(P<0.05).结论:ZNF692作为潜在癌基因参与了ccRCC的发生、发展,且其在ccRCC中高表达与患者预后不良相关.

F-box and WD repeat domain containing 7 (Fbxw7) is an F-box protein that belongs to the SKP1-CUL1-F-box protein E3 ligase complex and is responsible for transferring the ubiquitin molecule to the substrate, which results in its recognition and subsequent degradation by proteasomes. Furthermore, it can identify a network of signaling proteins that function in cell growth, diversion and apoptosis. In the present study, Fbxw7 was downregulated in renal cell carcinoma (RCC) tissues compared with the adjacent non-tumor tissues and its expression was significantly associated with the tumor-node-metastasis stage, lymph node metastasis and distant metastasis in patients with RCC. Furthermore, multivariate Cox regression analyses indicated that Fbxw7 expression was an independent factor for the prediction of the overall survival of patients with RCC. A functional study demonstrated that downregulation of Fbxw7 facilitated tumor cell migration and invasion via the epithelial-mesenchymal transition (EMT). Therefore, the results of the current study indicted that Fbxw7 is an anti-oncogene that serves a notable function in RCC development by suppressing RCC metastasis and the EMT, indicating the potential therapeutic value of Fbxw7 in inhibiting metastasis in RCC.

The goal of this research was to study the relationships between maternally expressed gene 3 (MEG3), microRNA-7 (miR-7), and RASL11B, and explore their influence on the progression of clear cell renal cell carcinoma (CCRCC). Microarray analysis was conducted using the data provided by The Cancer Genome Atlas. The expression levels of MEG3 and miR-7 in CCRCC and adjacent tissue samples were ascertained by quantitative real-time polymerase chain reaction (qRT-PCR). The cell proliferation activity was unmasked by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and cell apoptosis and cell cycle were investigated by flow cytometry. A dual luciferase reporter assay was used to verify target relationships. Wound healing assay and transwell assay were used to detect cell migration and invasion ability. Decreased MEG3 expression was observed in CCRCC tissues and cells. Overexpression of MEG3 accelerated apoptosis; inhibited cell proliferation, migration and invasion; and induced G0/G1 phase cell cycle arrest in CCRCC. MiR-7, directly binding to MEG3, was overexpressed in the CCRCC tissues and could inhibitthe apoptosis and promote the migration and invasion of CCRCC cells. RASL11B, lowly expressed in CCRCC, was a target of miR-7. After the overexpression of RASL11B, G0/G1 phase cell cycle arrest was induced; cell apoptosis was promoted; and the proliferation, invasion, and migration of CCRCC cells were inhibited. MEG3 could up-regulate RASL11B to inhibit the cell proliferation, invasion, and migration; induce G0/G1 cell cycle arrest; and promotecell apoptosis by suppressing miR-7 in CCRCC.

Renal cell carcinoma (RCC) is one of the most common malignant tumors in urogenital system with an incidence accounting for about 3% of the whole body malignant tumor. NudC domain containing 1 (NudCD1), a new member of NudC family distributed in nucleus, is found to be upregulated in multiple tumors. However, its expression and role in RCC tissue has not been elucidated. NudCD1 expression in RCC tissue was measured by western blot and immunohistochemistry (IHC). NudCD1 level was elevated by overexpression vector to investigate its regulatory role on LIS1/Dynein signaling pathway. Cell morphology, intracellular localization, and cell division were observed by immunofluorescence together with delayed microscope photograph. The impact of NudCD1 overexpression on cell migration was assessed by Transwell assay. NudCD1 expression was significantly increased in RCC tissue compared with that in adjacent normal control. NudCD1/LIS1/Dynein signaling pathway was obviously upregulated in RCC tissue. Overexpression of NudCD1 level in A498 cell line markedly elevated NudCD1/LIS1/Dynein signaling pathway, suggesting they might be involved in RCC process. NudCD1 upregulation also caused abnormal microtubule fasciculus structure with multinuclear morphology, and promoted cell migration. NudCD1 expression was obviously increased in RCC and affected RCC cell division and migration possibly through activating NudCD1/LIS1/Dynein signaling pathway, indicating therapeutic targeting NudCD1 might be a new approach to inhibit RCC cell migration.

Study about blood pressure variation in the first 24 hours post-operation is limited in patients with adrenal aldosterone-producing adenoma. We aim to evaluate the potential predictors for postoperative hypertension urgency during the first 24 hours after laparoscopic adrenalectomy in patients with aldosterone-producing adenoma. Clinical data of 177 patients with aldosterone-producing adenoma were retrospectively collected from January 2009 to December 2015 and the potential factors that may influence postoperative blood pressure during the first 24 hours after surgery were analyzed. The factors included gender, age, body mass index, preoperative maximum systolic blood pressure, number of antihypertensive medicines, preoperative spironolactone treatment, duration of hypertension, surgical method and approach, adenoma diameter, preoperative proteinuria, estimated glomerular filtration rate, serum potassium and serum aldosterone. Univariate and multivariate regression analyses were used to evaluate the relationship between the above variables and postoperative hypertension urgency. We found that the proportion of patients with a higher systolic blood pressure ≥ 160 mmHg and ≥ 180 mmHg were significantly increased post-operation (both p < 0.001). In multivariate analysis, the maximum systolic blood pressure was an independent predictor of postoperative hypertension urgency, and the cut-off point was 157 mmHg with the sensitivity of 66% and specificity of 82%. Multivariable analysis also showed that preoperative maximum systolic blood pressure and number of antihypertensive medicines were independent risk factors for higher postoperative systolic blood pressure. This study was derived from a high volume adrenal tumor center, and these data may provide a potential tool to guide preoperative counseling.

Castleman tumor, a rare lymphoproliferative disorder, is one of the associated tumors in paraneoplastic pemphigus (PNP). Castleman tumor was a frequently reported neoplasm in association with paraneoplastic pemphigus which was caused by an autoimmune reaction originating from the B lymphocytes. Castleman tumor association with PNP is a rarely reported subtype of PNP in China. Early detection and removal of the tumor are crucial for the treatment of tumor- associated autoimmune disease. Here we described a case of a patient with PNP associated Castleman tumor in order to clearly understand and improve the prognosis of the disease. Pathologic evidence proved that it was the follicular dendritic cell sarcoma-like Castleman tumor.

Previous studies have indicated that high expression of lactate dehydrogenase A (LDHA) exists in many human cancers. Recently, several reports showed that silencing or inhibition of LDHA could suppress metastasis of human cancer including renal cell carcinoma (RCC). However, the mechanism remains unknown. The role of LDHA in RCC migration and invasion was investigated using immunohistochemistry, western blotting, Transwell and scratch assays, and in vivo experiment. The influence of LDHA on the Warburg effect was also investigated by LDHA activity and lactate production assay. LDHA was overexpressed in RCC tissues and predicted a worse survival following renal resection. Correlation analysis demonstrated that LDHA was negatively correlated with E-cadherin and positively with N-cadherin. Experimentally, both in vivo and in vitro experiments found downregulation of LDHA suppressed RCC cells migration and invasion by inhibiting EMT. In addition, results indicated LDHA could promote the Warburg effect. Further research presented that the LDHA inhibitor, oxamate, suppressed tumor metastasis by inhibiting LDHA activity and EMT. These results demonstrated that LDHA mediates tumor metastasis by promoting EMT in RCC, suggesting that LDHA could be a promising therapeutic target for RCC therapy.

ATP-binding cassette sub-family G member 2 (ABCG2) is a semi-transport protein that plays a major role in multidrug resistance. We aimed to evaluate the prognostic significance of ABCG2 expression in patients with clear cell renal cell carcinoma.