Background: The present study analyzed the relationship between clinical features and the T790M mutation in non-small cell lung cancer (NSCLC) patients resistant to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) treatment. Methods: NSCLC patients with resistance to fi rst-generation EGFR-TKIs in which the disease control time was more than 6 months after initial TKI treatment were enrolled. T790M mutation analysis was performed using one of the following methods according to each manufacturer ’ s protocols: Cobas EGFR mutation test (41/105, 39.0%), digital PCR (42/105, 40.0%) or Scorpion ampli fi cation refractory mutation system (ARMS) (22/105, 21.0%). Sample type of T790M was from tissue only (53/105, 50.5%), plasma only (46/105, 43.8%), tissue and plasma (6/105, 5.7%). Results: Of 105 patients, 57 were T790M-positive and 48 were T790M-negative. T790M-positive patients had longer progression-free survival (PFS) after initial EGFR-TKI treatment (p = 0.019). T790M positivity was more frequent in patients treated with ge fi tinib than in those treated with icotinib (65% vs 40.54%, p = 0.018). The rate of T790M positivity was lower in patients with EGFR L858R (44.44%, 12/27) before TKI treatment than in those with EGFR 19del (72.0%, 36/50, p = 0.036). Patientswho achieved PR after initial EGFR-TKI treatment had a higher rate of T790M positivity than those with SD (75.76% vs 50%, p = 0.023). There was no relationship between T790M status and age, gender, primary site, metastasis site, or treatment before TKI. Conclusion: Progression-free survival (PFS), drug type, response to initial EGFR-TKI treatment, and EGFR status before initial EGFR treatment were associated with the frequency of T790M mutation.

Novel molecular markers are required for defining subsets of diffuse astrocytic tumor patients with differing prognoses. Here, we examined ATP2A2 expression in 109 human diffuse astrocytic tumor samples (39 grade II diffuse astrocytoma (DA), 19 grade III anaplastic astrocytoma (AA), 51 grade IV glioblastoma) and its correlation with patient clinicopathologic characteristics. ATP2A2 expression significantly correlated with tumor grade and survival (P<0.05). High ATP2A2 expression was detected in 35.3% (18/51) of glioblastoma patients, compared to 61.5% (24/39) in grade II, and 52.6% (10/19) in grade III astrocytoma patients (P=0.043). The median survival was 45±5.3 (95% CI, 34.7-55.3) months in patients with high ATP2A2 expression and 16±5.0 (95% CI, 6.3-25.7) months in patients with low ATP2A2 expression (P<0.0001). Additionally, high grade astrocytoma patients with high ATP2A2 expression showed longer survival (median, 31.0±4.9 months, 95% CI, 21.4-40.7) than those with low ATP2A2 expression (median: 13.0±1.6 months, 95% CI, 9.9-16.1; P=0.027). Furthermore, both ATP2A2 overexpression and IDH1 mutation were detected in secondary glioblastoma, AA developed from DA and oligodendrogiomas with IDH1 mutation. The MTT assays showed that lentiviral ATP2A2 overexpression significantly suppressed the clonogenic growth of glioblastoma U251MG cells (P<0.05). Xenografts stably overexpressing ATP2A2 were markedly smaller in size 4 weeks post inoculation (P<0.05). Our findings identified high ATP2A2 expression in a subset of astrocytoma patients that was associated with better prognosis and ATP2A2 suppressed astrocytoma growth.

The liver-enriched transcription factor Forkhead Box A2 (FOXA2) has been reported to be involved in bile acid homeostasis and bile duct development. However, the role of FOXA2 in liver fibrogenesis remains undefined. In this study, we found that the abundance of FOXA2 was significantly lower in fibrotic livers of patients and mice treated with CCl4 than in controls. Interestingly, the expression level of FOXA2 decreased in hepatocytes, whereas FOXA2 was elevated in hepatic stellate cells (HSCs) of mouse fibrotic livers. Hepatocyte-specific ablation of FOXA2 in adult mice exacerbated liver fibrosis induced by CCl4. Either lentivirus LV-CMV-FOXA2 mediated FOXA2 overexpression in the liver or adeno-associated virus AAV8-TBG-FOXA2-mediated hepatocyte-specific upregulation of FOXA2 alleviated hepatic fibrosis. Overexpression of FOXA2 in HSCs did not obviously affect hepatic fibrogenesis. Additionally, FOXA2 knockout in hepatocytes resulted in aberrant transcription of metabolic genes. Furthermore, hepatocyte-specific knockout of FOXA2 enhanced endoplasmic reticulum stress (ER stress) and the apoptosis of hepatocytes, whereas FOXA2 overexpression in hepatocytes suppressed ER stress and hepatocyte apoptosis in mouse fibrotic livers. In conclusion, our findings suggested that FOXA2-mediated hepatocyte protection has a therapeutic role in hepatic fibrosis, and thus may be a new, promising anti-fibrotic option for treating chronic liver diseases.

Hepatocyte nuclear factor 1α (HNF1α) is a liver‐enriched transcription factor that is critical for the maintenance of hepatocyte function. Our previous studies have demonstrated the therapeutic effects of HNF1α on hepatic fibrosis and hepatocellular carcinoma (HCC) in animals. In this study, we created hepatocyte‐specific Hnf1α knockout mice using the Cre‐loxP recombination system. The knockout mice display increased fatty acid synthesis in the liver. Moreover, these mice spontaneously develop HCC through fatty liver without cirrhosis. Inflammatory cytokines, such as tumor necrosis factor α and IL‐6, are upregulated and accompanied by increased phosphorylation of Akt, p‐65 and STAT3 in the livers of HNF1α knockout mice. Our findings suggest that HNF1α plays a crucial role in hepatocyte lipid metabolism and hepatocarcinogenesis.

Purpose: Clear cell sarcoma (CCS) is a rare high-grade malignant tumor accounting for less than 1% of all soft tissue sarcomas. CCS in the spine is much rarer and poorly understood. The objective of our study is to discuss clinical characteristics, surgical management and outcomes of spinal CCS.Methods: Between October 2011 and December 2014, five patients with spinal CCS underwent surgical treatment in our center. Five cases from literature focusing on the spinal CCS were also reviewed. We retrospectively analyzed clinical data and outcome of all ten patients to present our understanding of spinal CCS.Results: Three en bloc and two piecemeal resections were performed successfully. The syndromes of all the patients were obviously relieved after operation. The mean follow-up period was 24.4 months (range 10-41 months). Two patients died of lung metastasis 10 and 26 months after operation respectively. One patient was alive with tumor recurrence. Other two patients were alive with no evidence of disease at last follow-up.Conclusions: Prognosis of spinal CCS tend to be worse than CCS in common sites. En bloc resection could be regarded as the first treatment option. Tumor size, tumor location, preoperative neurological status and resection mode might be the potential prognostic factors of spinal CCS.

Early diagnosis of liver fibrosis is critical for early intervention and prognosis of various chronic liver diseases. Conventional repeated histological assessment is impractical due to the associated invasiveness. In the current study, we evaluated circulating miR-185 as a potential biomarker to predict initiation and progression of liver fibrosis. We found that miR-185 was significantly up-regulated in blood specimens from patients with HBV-liver fibrosis and rats with liver fibrosis, the miR-185 levels were correlated with liver fibrosis progression, but not with the different viral loads in HBV-infected patients. miR-185 was observed in collagen deposition regions during advanced liver fibrosis. We found that differences in miR-185 levels facilitated the discrimination between early-staged or advanced-staged liver fibrosis and the healthy controls with high specificity, sensitivity, and likelihood ratio using receiver-operator characteristic analysis. miR-185 targeted SREBF1, and increased expression of COL1A1 and a-SMA genes that are hallmarks of liver fibrosis. Our data supported that circulating miR-185 levels could be used as potential biomarkers for the early diagnosis of liver fibrosis.

Here we report that mice deficient for the proteasome activator, REGγ, exhibit a marked resistance to TPA (12-O-tetradecanoyl-phorbol-13-acetate)-induced keratinocyte proliferation, epidermal hyperplasia and onset of papillomas compared with wild-type counterparts. Interestingly, a massive increase of REGγ in skin tissues or cells resulting from TPA induces activation of p38 mitogen-activated protein kinase (MAPK/p38). Blocking p38 MAPK activation prevents REGγ elevation in HaCaT cells with TPA treatment. AP-1, the downstream effector of MAPK/p38, directly binds to the REGγ promoter and activates its transcription in response to TPA stimulation. Furthermore, we find that REGγ activates Wnt/β-catenin signalling by degrading GSK-3β in vitro and in cells, increasing levels of CyclinD1 and c-Myc, the downstream targets of β-catenin. Conversely, MAPK/p38 inactivation or REGγ deletion prevents the increase of cyclinD1 and c-Myc by TPA. This study demonstrates that REGγ acts in skin tumorigenesis mediating MAPK/p38 activation of the Wnt/β-catenin pathway.

Background: Non-small cell lung cancer (NSCLC) accounts for approximately 80% of lung carcinoma cases, which becomes more and more important in the field of lung carcinoma as well as primary lung carcinoma in females.Material/Methods: We analyzed the medical history of 62 female NSCLC patients. Immunohistochemistry was used to observe and compare the expression of EGFR. The chi-square test was conducted to analyze associations between EGFR expression and the different variables. The cumulative survival rate was determined by the Kaplan-Meier product-limit method. The prognosis of female patients with NSCLC was examined by using a multivariate Cox proportional hazard regression model.Results: The expression proportion of EGFR in Chinese female NSCLC patients was 70.97%, and it was remarkably higher in adenocarcinoma than in squamous cell carcinoma and bronchioloalveolar carcinoma. A positive correlation was observed between EGFR expression and tumor-node metastasis staging or lymph node metastasis. The Cox proportional risk model analysis showed a correlation between postoperative survival time of the patients and pathology of the tumor type and lymph node metastasis.Conclusions: Expression of EGFR was closely related to pathology of the tumor type, tumor-node metastasis staging, and lymph node metastasis, which could be used as a promising indicator of NSCLC in Chinese female patients.

miR-27a and BTG2 are implicated in gliomagenesis and glioma progression. However, hitherto, a link between miR-27a and BTG2 in glioma has not been reported. In the present study, we investigated the effects of miR-27a on the proliferation and invasiveness of glioblastoma cells in vitro and in a mouse xenograft model and further studied the relation between miR‑27a expression and its target gene BTG2, which was identified by computation prediction algorithms. Our MTT and clonogenic assays showed that miR-27a overexpression significantly increased the clonogenic growth of glioblastoma U87MG and U251MG cells. The Transwell assays further revealed that miR-27a overexpression markedly increased the number of migrated U87MG and U251MG cells. TargetScan and other prediction algorithms identified BTG2 as a target gene of miR-27a, which was confirmed by EGFP reporter and immunoblotting assays showing an inverse relation between miR-27a expression and endogenous BTG2 expression. BTG2 overexpression also increased the proliferation and invasiveness of glioblastoma cells and BTG2 functioned downstream of miR-27a in modulating the proliferation and migration of glioblastoma cells. In conclusion, miR-27a modulates human glioblastoma growth and invasion by targeting BTG2.

Previous studies from this laboratory indicated that microRNA-21 (miR-21) contributes to chemoresistance of glioblastoma multiforme (GBM) cells to teniposide, a type II topoisomerase inhibitor. We also showed that LRRFIP1 is a target of miR-21. In this study, we found that higher baseline LRRFIP1 expression in human GBM tissue (n=60) is associated with better prognosis upon later treatment with teniposide. Experiments in cultured U373MG cells showed enhanced toxicity of teniposide against U373MG cells transfected with a vector that resulted in LRRFIP1 overexpression (vs. cells transfected with control vector). Experiments in nude mice demonstrated better response of LRRFIP1 overexpressing xenografts to teniposide. These findings indicate that high baseline LRRFIP1 expression in GBM is associated with better response to teniposide, and encourage exploring LRRFIP1 as a target for GBM treatment.

Alveolar adenoma is an extremely rare and benign pulmonary neoplasm; it is always asymptomatic and is usually detected incidentally on routine chest X-radiography. Typically on imaging examinations, alveolar adenoma exhibits as a peripheral, solitary, cystic nodule in the lung, which may easily imitate other lung lesions, consequently leading to difficulties in the differential diagnosis of this condition. Surgical resection is the primary treatment option. The diagnosis of alveolar adenoma is mainly based on postoperative histopathology, with features of proliferative type 2 alveolar epithelial cells and septal mesenchyme. The present case was a 60-year-old woman with alveolar adenoma, combined with systemic mutifocal cystic lesions. She underwent surgery following the obvious enlargement of this mass and a cystic nodule 7 cm in maximum diameter was resected. Postoperative histopathology confirmed a diagnosis of alveolar adenoma; her prognosis was favourable. In addition to reporting a rare case of alveolar adenoma coexisting with multifocal cysts, the English-language literature was reviewed for similar cases of alveolar adenoma.

Objective To evaluate the clinical value of real-time fluorescent quantitative reverse transcription polymerase chain reaction(qRT-PCR) in detecting expression of estrogen receptor alpha(ERα),progesterone receptor(PR) and human epidermal growth factor receptor 2(Her2) genes in breast cancer tissues.Methods Totally 48 breast cancer tissues and 28 benign breast tumor tissues(control) were obtained from patients undergoing surgery in our hospital during Mar.2010 and Oct.2010.The expression of ERα,PR and Her2 protein was examined by immunohistochemistry(IHC) in breast cancer tissues and the expression levels of ERα,PR and Her2 mRNA were detected by real-time qRT-PCR in breast cancer tissues and benign breast tumor tissues.The values of these two methods in diagnosis of breast cancer were evaluated. Results The expressions of ERα and Her2 mRNA were significantly higher in the breast cancer tissues than in the controls(P0.05,P0.01),while the expression of PR mRNA had no significant difference between controls and breast cancer tissues.ERα,PR and Her2 protein expressions were associated with the TNM stage of breast cancer, with the former two being negatively associated with TNM stages(P0.05) and Her2 being positively associated with TNM stages(P0.05).The expressions of ERα and Her2 mRNA were significantly higher in breast cancer tissues of patients with lymph node metastasis than in those without lymph node metastasis(P0.05).The expression of PR mRNA was not significantly different in breast cancer tissues between patients with and without lymph node metastasis(P0.05).Real-time qRT-PCR in detecting ERα,PR and Her2 mRNA expression had similar capability with IHC method in evaluating the sensitivity,specificity of endocrine therapy;moreover,the two methods also had a consistent pathological diagnosis rates(P0.05).Conclusion ERα,PR and Her2 genes are important predictive markers for endocrine therapy or targeted therapy of breast cancer.Real-time qRT-PCR method can be used for clinical detection and research of ERα,PR and Her2 mRNA.

OBJECTIVE:To extract tumor interstitial fluid (TIF) from MKN-45 gastric cancer which is similar to "muddy phlegm" in Chinese medicine and observe influences of MKN-45 tumor interstitial fluid (MKN-45 TIF) intervention on metastasis of gastric cancer and on the expressions of vascular endothelial growth factor (VEGF), kinase insert domain containing receptor (KDR), epithelial-cadherin (E-cad), cyclooxygenase-2 (COX-2), intercellular adhesion molecule-1 (ICAM-1) and telomerase genes and proteins in primary tumor tissue.METHODS:An MKN-45 tumor-bearing model was established in 50 nude mice. The modeled animals were equally randomized to 5 groups: the simple tumor-bearing group (model group), the normal saline (NS) via tail vein injection (i.v.) group (NS i.v. group), MKN-45 TIF i.v. group (TIF i.v. group), NS intraperitoneal injection (i.p.) group (NS i.p. group), and MKN-45 TIF i.p. group (TIF i.p. group). The TIF and NS intervention groups received injection (i.p. or i.v.) of MKN-45 TIF or NS twice a week, 0.2 mL at a time. After 8 weeks, the primary tumors were removed, weighed and HE stained to observe tumor metastasis. The primary tumor tissues were analyzed by immunohistochemistry and real-time quantitative PCR to detect expressions of VEGF, KDR, E-cad, COX-2, ICAM-1, and telomerase genes and proteins in different groups.RESULTS:There were significant differences in tumor weight between TIF intervention groups and the model and NS intervention groups. Tumor metastasis was observed in all 5 groups, but the tumor metastasis rate in TIF intervention groups was significantly higher than those in the model and NS intervention groups. The gene and protein expressions of gastric cancer-related factors VEGF, KDR, COX-2, ICAM-1 and telomerase were unregulated while the gene and protein expressions of E-cad were downregulated in TIF intervention groups.CONCLUSIONS:TIF promotes tumor growth, invasion and metastasis of gastric cancer. These findings provide preliminary experimental clues for verifying the hypothesis of "tumor-phlegm microenvironment".

The mechanisms whereby hepatic fibrosis develops in chronic liver diseases remain incompletely defined. Here, we sought to examine whether microRNA (miRNA) became dysregulated in dimethylnitrosamine-induced hepatic fibrosis in rats. Our microarray analysis revealed that the miR-34 family was upregulated along with other miRNAs in liver fibrotic tissues. Six miRNAs, such as rno-miR-878, were downregulated. The findings were confirmed by RT-PCR assays. Gene ontology analysis further showed that many of these dysregulated miRNAs were involved in lipid/fatty acid metabolism. The acyl-CoA synthetase long-chain family member 1 (ACSL1) gene contained specific binding sites for miR-34a/miR-34c. Additional enhanced green fluorescence protein reporter activity assays indicated that the miR-34 family targeted ACSL1. Our RT-PCR and immunoblotting assays further demonstrated that both the mRNA and protein levels of ACSL1 were markedly reduced in fibrotic liver tissues. Our findings suggest that miRNA becomes dysregulated during hepatic fibrosis, and that the miR-34 family may be involved in the process by targeting ACSL1.

Objective To investigate the expression of ankyrin repeats in oral squamous cell carcinoma(OSCC) and its clinical significance.Methods The expression of gankyrin protein was detected by immunohistochemical method in 55 OSCC specimens and the corresponding para-cancer non-tumor tissues;the differential expression of gankyrin protein was analyzed in OSCC specimens of different pathological characteristics;we also analyzed the possible clinical value of the differential expression.Results Expression of gankyrin in the OSCC tissues was significantly stronger than that in the corresponding para-cancer non-tumor tissues(P=0.000).Gankyrin protein expression was significantly different between OSCC tissues of high,low and moderate differentiation(P=0.006).We also found that the expression of gankyrin was not associated with the sex,age,or lymphatic status of OSCC patients.Conclusion Gankyrin protein is over-expressed in OSCC tissues,which might be related to the differentiation degree of OSCC.

MED19 is a member of the Mediator that plays a key role in the activation and repression of signal transduction or the regulation of transcription in carcinomas. To tested the functional role of MED19 in human prostate cancer, we downregulated MED19 expression in prostate cancer cells (PC-3 and DU145) by lentivirus-mediated short hairpin (shRNA), and analyzed the effect of inhibition of MED19 on prostate cancer cell proliferation and tumorigenesis. The in vitro prostate cancer cell proliferation, colony formation, and in vivo tumor growth in nude mice xenografts was significantly reduced after the downregulation of MED19. Knockdown of MED19 caused S-phase arrest and induced apoptosis via modulation of Bid and Caspase 7. It was suggested that MED19 serves as a novel proliferation regulator that promotes growth of prostate cancer cells.

Hepatic stem cells (HSCs) are involved in repair of liver injury. Stem cells may have inhibitory effects on tumor cell growth and apoptosis. However, it is unknown whether HSCs regulate the biological functions of hepatocarcinoma cells, especially tumor cell growth and apoptosis. The present study was designed to determine the effects of hepatocytic precursor (stem-like) WB-F344 cells on the growth and apoptosis of hepatoma CBRH-7919 cells. Using a Transwell chamber culture system, we co-cultured WB-F344 cells and CBRH-7919 cells in serum-free conditioned medium at 3 different ratios: 1:1 (2 x 10(5): 2 x 10(5) cells/well), 1:5 (4 x 10(4): 2 x 10(5) cells/well), and 5:1 (2 x 10(5): 4 x 10(4) cells/well). We determined the effects of stem cells on tumor cells using in vivo xenograft assay in nude mice and determining gene expression by RT-PCR and Western blot analyses. With the increment proportion of the WB-F344 cells in the co-culture system, tumor formation was inhibited in nude mice. Moreover, down-regulation of bone morphogenetic protein 4 (BMP4), Bcl-2, and c-Myc and upregulation of PTEN also occurred along with the inhibitory effects. Western blotting showed that the TGF-beta/Smad pathway played a prominent role in tumor inhibition, which may have been mediated by the cytokines released from the stem cells. In conclusion, hepatocytic precursor (stem-like) WB-F344 cells inhibit the tumorigenicity of hepatoma CBRH-7919 cells, and the effect is mediated by TGF-beta/Smad signaling pathway.

ABCG2, which encodes an ATP-binding cassette transporter protein, is associated with the phenotype of cancer stem cells and is used to define the pluripotential side population cells by flow cytometry and slide-cytometry. MicroRNAs control a wide array of biological processes (e.g., cell differentiation, proliferation and apoptosis) whose dysregulation is a hallmark of cancer. MicroRNA-328 (miR-328) is underexpressed in many cancers including glioblastoma multiforme and contributes to tumor resistance to chemotherapy. ABCG2 is associated with multi-drug resistance and is also highly expressed in glioblastoma. Some preliminary studies have shown that ABCG2 is the target gene for miRNA-328. Thus, we hypothesize that modulating ABCG2 expression by targeting miRNA-328 in glioblastoma cancer stem cells could represent a promising strategy for therapeutic manipulation to increase the efficacy of chemotherapeutic agents for glioblastoma, a highly lethal type of cancer.

Dear Editor: I am Dr Xiao-Mei Ma, from the Department of Pathology in Changzheng Hospital at the Second Military Medical University, Shanghai, China. We present here a case report of a seminal vesicle cyst (SVC) in a young man with epididymal tissue in a dysgenetic kidney and ectopic ureteral insertion. SVCs are usually found in the second to fourth decades of life. SVCs can be congenital or acquired. Congenital SVCs seem to be invariably associated with renal dysplasia, hypoplasia, agenesis and duplication abnormalities in the same side, with the exception of two cases 1, 2. We report here a case report of a 26-year-old man who was referred to our hospital owing to absence of the left kidney, identified by sonography during a health examination. Magnetic resonance imaging (MRI) and magnetic resonance urography (MRU) showed a cyst expanding from the kidney fossa to the seminal vesicle fossa instead of the left kidney, ureter and seminal vesicle (Figure 1). His right urinary tract was normal. A solid mass was present in the left side of the bladder, and the left ureteral orifice could not be seen with a cystoscope. Laboratory tests of the blood and urine were normal. Clinical examination showed that the patient had a normal pair of testes, epididymis and penis. Figure 1 Magnetic resonance imaging (MRI) revealed that there was a cyst from the kidney fossa to the seminal vesicle fossa. (A): The seminal vesicle was cystic and compressed the bladder from outside (arrow pointing downward). The dilated ureter entered the expanded ... The surgeons performed a retroperitoneoscopy together with a small inclined inferior abdominal incision under general anaesthesia. At first, the patient was recumbent on his right arm. The cyst was resected in the postperitoneal region. There were three laparoscopic ports: a 12-mm trocar port at the left postaxillary line below the 12th rib, a 5-mm trocar port at the preaxillary line and 2 cm above the spina iliaca and a 10-mm trocar port at the preaxillary line below the arcus costarum. During the operation, the surgeons noticed that the cyst was just as shown by MRI and MRU. There were no vessels to the left kidney. The cyst was dissociated easily. The ectopic ureter opened in the seminal vesicle cyst, which was filled with chyliform fluid. At first, the surgeons suspected that the fluid was liquor puris, but it was later found to be semen with few sperm, which had poor vitality. Thereafter, the patient was moved to the Trendelenburg position. A small inclined inferior abdominal incision was made at the left lateral border of the rectus muscle. This cyst was resected completely. The total operating time was 120 min, with an estimated blood loss of 100 mL. The patient was able to eat and walk within 24 h after the operation. Macroscopically, the specimen was a membranous cyst filled with turbid fluid (Figure 2). It was 21.0 cm long and 1.5–6.0 cm in diameter. Figure 2 The specimen was a membranous cyst. One edge was the agenetic left kidney (arrowhead). Next to the agenetic left kidney was the dilated ureter (long arrow) and the seminal vesicle (short arrow). The image obtained by microscopy of the surgical specimen ... Microscopically, there were glomerulus, renal tubules and expanded epididymal ducts filled with abnormal sperm in the dysgenetic kidney (Figure 3). The dilated ureter was lined by urothelial epithelium. The seminal vesicle cyst wall consisted of a muscular layer lined by urothelial epithelium. Thus, the pathological diagnosis was epididymal tissue in the dilated portion of the dysgenetic kidney with an ipsilateral seminal vesicle cyst and ectopic ureteral insertion. Figure 3 (A): A glomerulus and renal tubules (arrows pointing right), as well as expanded epididymal ducts filled with abnormal sperm (arrow pointing left), were in the wall of the agenetic kidney (hematoxylin and eosin, original magnification, × 40). ... The patient recovered quickly and fathered a child who was born 2 years later. In this case, the patient had no history of infection. The left ureteral orifice was not in the bladder, but was inserted into the SVC. We found glomerulus and renal tubules in the specimen using microscopy. Those findings confirmed that the SVC of the patient was not acquired, but congenital, and that the left kidney was dysplastic. Until now, there have been only 27 papers about SVCs with renal dysplasia of a kidney bud 3 in the PubMed literature. There was a report of ectopic prostate glands and urothelial epithelium in a seminal vesicle cyst 4. This is the only case in the literature with epididymal tissue in the dysplastic kidney. The dysplastic kidney in our patient was a cystic with a thin wall. The cyst described in this case was probably the largest one out of all of the published cases. Seminal vesicle cysts accompanying renal dysplasia may be related to the dysregulation of the embryonic development of the distal mesonephric duct, which develops into the genitourinary system in humans. Thus, urinary malformations are associated with two-thirds of all the SVC cases, consisting mostly of ectopic ureteral insertion and ipsilateral renal dysgenesis/agenesis, and the epididymis developing from the mesonephric duct may partly reside in the kidney, as in this case. Sometimes there is a mass in the bladder because the SVC is compressing it from the outside. Surgeons usually misdiagnose such a mass as a tumour. There have indeed been reports of SVC associated with carcinoma of the bladder 5. After years of sexual activity, secretions reach the maximum level and are drained into the SVC, the ureter and the agenetic/dysgenetic kidney, which cause the cyst to fill with seminal fluid. The sperms are inactive or immature. Thus, the patients are usually infertile. Surgery is always a successful treatment for this condition, especially for patients with symptoms 6. There is a great danger of recurrence or infection in conventional treatment methods. Radical resection is effective. Laparoscopy together with small incision through a transperitoneal approach has gained acceptance because of the absolute advantages of lower postoperative pain, lower morbidity, shorter hospital stay and shorter convalescence. The use of laparoscopy for the management of a large seminal vesicle cyst with ipsilateral renal agenesis has been previously reported. Han et al. 7 reported a patient with a stone within the SVC; this patient was treated successfully with laparoscopic surgery. Taken together with our case, these reports indicate that the laparoscopic surgery may be the first choice for SVC patients who must have surgical treatment. However, the rarity of this condition makes extensive study of such cases impossible.