• Title/Summary/Keyword: bladder cell

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ppGalNAc T1 as a Potential Novel Marker for Human Bladder Cancer

  • Ding, Ming-Xia;Wang, Hai-Feng;Wang, Jian-Song;Zhan, Hui;Zuo, Yi-Gang;Yang, De-Lin;Liu, Jing-Yu;Wang, Wei;Ke, Chang-Xing;Yan, Ru-Ping
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.11
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    • pp.5653-5657
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    • 2012
  • Objectives: To investigate the effect of glycopeptide-preferring polypeptide GalNAc transferase 1 (ppGalNAc T1 ) targeted RNA interference (RNAi) on the growth and migration of human bladder carcinoma EJ cells in vitro and in vivo. Methods: DNA microarray assays were performed to determine ppGalNAc Ts(ppGalNAc T1-9) expression in human bladder cancer and normal bladder tissues. We transfected the EJ bladder cancer cell line with well-designed ppGalNAc T1 siRNA. Boyden chamber and Wound healing assays were used to investigate changes of shppGalNAc T1-EJ cell migration. Proliferation of shppGalNAc T1-EJ cells in vitro was assessed using [3H]-thymidine incorporation assay and soft agar colony formation assays. Subcutaneous bladder tumors in BALB/c nude mice were induced by inoculation of shppGalNAc T1-EJ cells and after inoculation diameters of tumors were measured every 5 days to determine gross tumor volumes. Results: ppGalNAc T1 mRNA in bladder cancer tissues was 11.2-fold higher than in normal bladder tissues. When ppGalNAc T1 expression in EJ cells was knocked down through transfection by pSUPER-shppGalNAc T1 vector, markedly reduced incorporation of [3H]-thymidine into DNA of EJ cells was observed at all time points compared with the empty vector transfected control cells. However, ppGalNAc T1 knockdown did not significantly inhibited cell migration (only 12.3%). Silenced ppGalNAc T1 expression significantly inhibited subcutaneous tumor growth compared with the control groups injected with empty vector transfected control cells. At the end of observation course (40 days), the inhibitory rate of cancerous growth for ppGalNAc T1 knockdown was 52.5%. Conclusion: ppGalNAc T1 might be a potential novel marker for human bladder cancer. Although ppGalNAc T1 knockdown caused no remarkable change in cell migration, silenced expression significantly inhibited proliferation and tumor growth of the bladder cancer EJ cell line.

Cytologic Findings of Primary Small Cell Carcinoma of the Urinary Bladder - A case report - (방광에 발생한 원발성 소세포암종의 세포학적 소견 -1 예 보고-)

  • Kwon, Mi-Seon;Ahn, Geung-Hwan;Chung, Jin-Haeng;Lee, Seung-Sook;Koh, Jae-Soo
    • The Korean Journal of Cytopathology
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    • v.12 no.2
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    • pp.121-125
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    • 2001
  • Primary small cell carcinoma of the urinary bladder is a rare malignant tumor. A more rapidly fatal course may be seen in advanced stages of small cell carcinoma as compared to similar stages of urothelial carcinoma. It is very important to recognize this distinct form of bladder cancer by urinary cytology The differential diagnosis of small cell carcinoma of the urinary bladder includes metastatic small cell carcinoma, urothelial carcinoma, and primary or secondary malignant lymphoma. This article highlights the urinary cytologic diagnosis of a case of primary small cell carcinoma. A 59-year-old male presented with gross hematuria for five months. Urinary cytology showed high cellularity consisting of tiny monotonous tumor cells in the necrotic background. The tumor cells occurred predominantly singly, but a few in clusters. The cytoplasm was so scanty that only a very narrow rim of it was seen. The nuclei were oval or round and had finely stippled chromatin. Rarely, the nuclei contain visible nucleoli. Frequently cell molding was noted in clusters. Many single cells demonstrated nuclear pyknosis or karyorrhexis. The histologic findings of transurethral resection and partial cystectomy specimen were those of small cell carcinoma. Cytologic distinction may be very difficult but careful attention to clinical features and cellualr details can classify these neoplasms correctly.

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Capsaicin-Induced Apoptosis and Reduced Release of Reactive Oxygen Species in MBT-2 Murine Bladder Tumor Cells

  • Lee, Ji-Seon;Chang, Jong-Sun;Lee, Ji-Youl;Kim, Jung-Ae
    • Archives of Pharmacal Research
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    • v.27 no.11
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    • pp.1147-1153
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    • 2004
  • Bladder cancer is a common cancer with high risk of recurrence and mortality. Intravesicle chemotherapy after trans-urethral resection is required to prevent tumor recurrence and progression. It has been known that antioxidants enhance the antitumor effect of bacillus Calmette-Guerin (BCG), the most effective intravesical bladder cancer treatment. Capsaicin, the major pungent ingredient in genus Capsicum, has recently been tried as an intravesical drug for overactive bladder and it has also been shown to induce apoptotic cell death in many cancer cells. In this study, we investigated the apoptosis-inducing effect and alterations in the cellular redox state of capsaicin in MBT-2 murine bladder tumor cells. Capsaicin induced apoptotic MBT-2 cell death in a time- and dose-dependent manner. The capsaicin-induced apoptosis was blocked by the pretreatment with Z-VAD-fmk, a broad-range caspase inhibitor, or Ac-DEVD-CHO, a caspase-3 inhibitor. In addition to the caspase-3 activation, capsaicin also induced cytochrome c release and decrease in Bcl-2 protein expression with no changes in the level of Bax. Furthermore, capsaicin at the concentration of inducing apoptosis also markedly reduced the level of reactive oxygen species and lipid peroxidation, implying that capsaicin may enhance the antitumor effect of BCG in bladder cancer treatment. These results further suggest that capsaicin may be a valuable intravesical chemotherapeutic agent for bladder cancers.

Mechanisms of proton secretion by carbonic anhydrase-containing cells in turtle bladder (Turtle Bladder의 탄산탈수효소를 함유한 세포에 의한 Proton 분비기작)

  • Jeon, Jin-Seok
    • Applied Microscopy
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    • v.22 no.2
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    • pp.84-96
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    • 1992
  • This study was carried out to examine the $H^+$ transport mechanism by observing the properties of cellular membrane having an ${\alpha}$ type of carbonic anhydrase (CA)-containing cells in turtle urinary bladder. The urinary bladder consists of a heterogenous population of cells. As a result of fine observation with traditional thin-section electron microscopy. the bladder epithelium has three different cell types on mucosal surface. They are a basal cell, a granular cell and a third type of CA-rich cell. The CA-rich cells are divided into two distinct smaller groups within them and called them ${\alpha}$ type and ${\beta}$ type of CA cells. The ${\alpha}$ type of CA cells are responsible for the proton secretion using the proton pumps on the apical plasma membrane, while the ${\beta}$ type of CA cells secrete bicarbonate via an oppositely-directed proton pumps in their basolateral plasma membrane. After performing the freeze-fracture technique, it was shown that there were distributed a large number of intramembranous particles having a special structure on the apical membrane of ${\alpha}$ type of CA-rich cells in the process of their $H^+$ secretion. In turtle bladder ${\alpha}$ type of CA-rich cells, this particle was the only prominent structure in the apical membrane. These intramembrane rod-shaped particles probably represent the integral membrane components of the proton pump. This result may explain that carbonic anhydrase within epithelial cell of urinary bladder takes part in formation of $H^+$ and bicarbonate, that active transport of $H^+$ is done, and that the reabsorption of bicarbonate suggests transport mechanism containing $H^+$ secretion. However, it seems that more studies are required for considering their regular transport pathway.

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The Diagnoses and Surgical Treatment of Transitional Cell Carcinoma in the Urinary Bladder in a Dog (방광에 발생한 이행상피암종의 진단과 수술적 처치)

  • 김성미;장화석;송영성;김혜진;김순신;김휘율
    • Journal of Veterinary Clinics
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    • v.21 no.1
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    • pp.62-65
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    • 2004
  • A 13-year-old, male Maltese was refered to Veterinary Teaching Hospital of Konkuk University with inappropriate urination and hematuria. CBC, serum chemistry profile, urinalysis and urine culture were performed. Malignant cells were found in the urine sediment. Thoracic and abdominal radiography, retrograde positive-contrast cystography, retrograde double-contrast cystography, excretory urography, ultrasonography were performed. On the retrograde positive-contrast cystography examination, irregular filling defects were present on the left side of the cranial part of the bladder. Partial cystectomy performed and then medical therapy was conducted. On histopathological examinations, the lesion was confirmed as a transitional cell carcinoma of the urinary bladder.

Analyzing the factors that contribute to the development of embryological classical type of bladder exstrophy

  • Ria Margiana;Widya Juwita;Khoirul Ima;Zakiyatul Faizah;Supardi Supardi
    • Anatomy and Cell Biology
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    • v.56 no.4
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    • pp.421-427
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    • 2023
  • Bladder exstrophy is a rare congenital condition of the pelvis, bladder, and lower abdomen that opens the bladder against the abdominal wall, produces aberrant growth, short penis, upward curvature during erection, wide penis, and undescended testes. Exstrophy affects 1/30,000 newborns. The bladder opens against the abdominal wall in bladder exstrophy, a rare genitourinary condition. This study is vital to provide appropriate therapy choices as a basis to improve patient outcomes. This study may explain bladder exstrophy and provide treatment. Epispadias, secretory placenta, cloacal exstrophy, and other embryonic abnormalities comprise the exstrophy-spades complex. The mesenchymal layer does not migrate from the ectoderm and endoderm layers in the first trimester, affecting the cloacal membrane. Embryological problems define the exstrophy-aspidistra complex, which resembles epimedium, classic bladder, cloacal exstrophy, and other diseases. Urogenital ventral body wall anomalies expose the bladder mucosa, causing bladder exstrophy. Genetic mutations in the Hedgehog cascade pathway, Wnt signal, FGF, BMP4, Alx4, Gli3, and ISL1 cause ventral body wall closure and urinary bladder failure. External factors such as high maternal age, smoking moms, and high maternal body mass index have also been associated to bladder exstrophy. Valproic acid increases bladder exstrophy risk; chemicals and pollutants during pregnancy may increase bladder exstrophy risk. Bladder exstrophy has no identified cause despite these risk factors. Exstrophy reconstruction seals the bladder, improves bowel function, reconstructs the vaginal region, and restores urination.

Cyclooxygenase-2 Expression in Urinary Bladder Transitional Cell Carcinoma and its Association with Clinicopathological Characteristics

  • Tabriz, Hedieh Moradi;Olfati, Golrokh;Ahmadi, Seyed Ali;Yusefnia, Sudabeh
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.8
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    • pp.4539-4543
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    • 2013
  • Background: Transitional cell carcinoma (TCC) is the most predominant type of urinary bladder tumor. As cyclooxygenase (COX)-2 is recently introduced as an attractive target molecule in bladder TCC, we evaluated the immunohistochemical expression of this marker and its association with several clinicopathological characteristics. Materials and Methods: This cross-sectional study was performed in the Pathology department of Sina Hospital in Tehran, Iran during 2006-2011. Ninety-two paraffin embedded blocks were selected from patients with urinary bladder TCC who underwent cystectomy or transurethral resection (TUR). Then, we assessed COX-2 expression by immunohistochemical staining using antibody against COX-2. Staining in more than 5% of tumor cells was considered as positive expression. Results: COX-2 was expressed in 50 % of our patients. This marker was markedly expressed in high grade bladder TCC (62.1%) versus other grades and there was statistically a significant difference in COX-2 expression between various grades (p=0.008). In addition, patients' age, lymphatic and perineurial invasion were associated with the expression of COX-2 (p=0.001, 0.015 and 0.039, respectively). However, other parameters such as stage, tumor size, venous invasion and lymph node metastasis did not show any significant relationship with this marker (all, p>0.05). Conclusions: COX-2 was expressed in urinary bladder TCC especially in high grade forms, advocating its probable role in the differentiation of this tumor. Accordingly, COX-2 could be a valuable biological target molecule in the evaluation and treatment of patients with bladder TCC.

Apoptin Induces Apoptosis in Human Bladder Cancer EJ and BIU-87 Cells

  • Zhan, Hui;Wang, Jian-Song;Wang, Hai-Feng;Zuo, Yi-Gang;Wang, Chun-Hui;Ding, Ming-Xia
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.1
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    • pp.135-138
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    • 2012
  • Objective: To investigate whether apoptin is a apoptosis-inducing protein with a potential for bladder cancer therapy. Methods: We constructed a PCDNA3/Apoptin eukaryotic expression vector, and transfected this vector into bladder cancer cell lines BIU-87 and EJ, then observed the results by RT-PCR, transmission electron microscopy, MTT assay and the flow cytometry (TUNEL method). Results: PCDNA3/Apoptin successfully induced a high level apoptosis in both bladder cancer cell lines, compared with the controls (p<0.05). Conclusions: Apoptin can induce high level apoptosis in human bladder cancer EJ and BIU-87 cells, which suggests a potential for human bladder cancer therapy.

OK-432 Suppresses Proliferation and Metastasis by Tumor Associated Macrophages in Bladder Cancer

  • Tian, Yuan-Feng;Tang, Kun;Guan, Wei;Yang, Tao;Xu, Hua;Zhuang, Qian-Yuan;Ye, Zhang-Qun
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.11
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    • pp.4537-4542
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    • 2015
  • OK-432, a Streptococcus-derived anticancer immunotherapeutic agent, has been applied in clinic for many years and achieved great progress in various cancers. In the present study, we investigated its anticancer effect on bladder cancer through tumor associated macrophages (TAMs). MTS assay validated OK-432 could inhibit proliferation in both T24 and EJ bladder cell lines. OK-432 also induced apoptosis of bladder cancer cells in vitro. Consequently, we demonstrated that OK-432 could suppress the bladder cancer cells migration and invasion by altering the EMT-related factors. Furthermore, using SD rat model, we revealed that OK-432 inhibited tumor growth, suppressed PCNA expression and inhibited metastasis in vivo. Taken together, these findings strongly suggest that OK-432 inhibits cell proliferation and metastasis through inducing macrophages to secret cytokines in bladder cancer.

New Techniques for the Detection of the Malignant Cells in Urine Cytology (요 세포검사의 최근 검사기법)

  • Gong, Gyung-Yub
    • The Korean Journal of Cytopathology
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    • v.17 no.1
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    • pp.18-26
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    • 2006
  • Transitional cell carcinoma of the urinary bladder is common in the genitourinary tract. The gold standard for the diagnosis of bladder cancer has been cystoscopy, along with urine cytology. Cystoscopy is an invasive and relatively expensive technique. By comparison, urine cytology is easy to perform and specific for a diagnosis of bladder cancer, although less sensitive, especially in low-grade tumors. For this reason, there has been a need for superior noninvasive technology to increase our confidence in being able to detect bladder cancer. There are many reports of the various urinary tests that are available to facilitate the diagnosis. In this article, I reviewed the literature on urinary markers and tests that may be clinically useful, including fluorescence in situ hybridization, uCyt+/Immunocyte, the $BTA^{(R)}$ test, the NMP 22TM, the $FDP^{(R)}$ test, the telomerase activity test, the HA and HAse tests, and flow cytometry. Most of these tests have a higher sensitivity and specificity than cytology. However, urine cytology has the highest specificity, especially in individuals with a high-grade tumor. We conclude that no urinary markers or tests can replace the role of cystoscopy along with cytology in the diagnosis of transitional cell carcinoma of the bladder. However, some markers could be used adjunctively to increase the diagnostic accuracy during screening or during the postoperative follow-up examination of patients with bladder cancer.