1.Recent advances in diagnosis of flat lesions of urinary bladder.
Liang CHENG ; Jia-wen XU ; Xiao-Dong TENG
Chinese Journal of Pathology 2010;39(9):577-581
Antigens, CD20
;
metabolism
;
Carcinoma in Situ
;
classification
;
diagnosis
;
metabolism
;
pathology
;
Diagnosis, Differential
;
Humans
;
Hyaluronan Receptors
;
metabolism
;
Hyperplasia
;
Precancerous Conditions
;
diagnosis
;
metabolism
;
pathology
;
Tumor Suppressor Protein p53
;
metabolism
;
Urinary Bladder
;
metabolism
;
pathology
;
Urinary Bladder Neoplasms
;
classification
;
diagnosis
;
metabolism
;
pathology
;
Urothelium
;
metabolism
;
pathology
2.Perivascular epithelial cell tumor of urinary bladder.
Fen ZHANG ; Yan-hui LIU ; Xin-lan LUO ; Heng-guo ZHUANG
Chinese Journal of Pathology 2009;38(2):131-132
Actins
;
metabolism
;
Adult
;
Female
;
Humans
;
Melanoma-Specific Antigens
;
metabolism
;
Microphthalmia-Associated Transcription Factor
;
metabolism
;
Perivascular Epithelioid Cell Neoplasms
;
metabolism
;
pathology
;
surgery
;
Urinary Bladder
;
metabolism
;
pathology
;
surgery
;
Urinary Bladder Neoplasms
;
metabolism
;
pathology
;
surgery
3.Recent advances in pathology and molecular genetics of small cell carcinoma of the urinary bladder.
Liang CHENG ; Wen-bin HUANG ; Jie CHEN
Chinese Journal of Pathology 2007;36(10):700-703
Biomarkers, Tumor
;
metabolism
;
Carcinoma, Small Cell
;
genetics
;
metabolism
;
pathology
;
Carcinoma, Squamous Cell
;
pathology
;
Chromosome Aberrations
;
Diagnosis, Differential
;
Humans
;
Keratins
;
metabolism
;
Lymphoma
;
pathology
;
Mucin-1
;
metabolism
;
Urinary Bladder
;
pathology
;
Urinary Bladder Neoplasms
;
genetics
;
metabolism
;
pathology
4.Pathologic diagnosis of benign glandular lesions of urinary bladder.
Chinese Journal of Pathology 2011;40(3):147-150
Adenoma
;
metabolism
;
pathology
;
Biomarkers, Tumor
;
metabolism
;
Cystadenocarcinoma
;
pathology
;
Cystitis
;
metabolism
;
pathology
;
Endometriosis
;
immunology
;
pathology
;
Fallopian Tube Neoplasms
;
pathology
;
Female
;
Humans
;
Intestines
;
pathology
;
Keratin-7
;
metabolism
;
Male
;
Metaplasia
;
pathology
;
Racemases and Epimerases
;
metabolism
;
Urinary Bladder Neoplasms
;
metabolism
;
pathology
;
Uterine Diseases
;
immunology
;
pathology
5.Malignant granular cell tumor of the urinary bladder.
Yan-zhen ZHUANG ; Xian-yi JIANG ; Pei-qiong CHEN
Chinese Journal of Pathology 2006;35(3):188-188
Cystectomy
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Fatal Outcome
;
Female
;
Glial Fibrillary Acidic Protein
;
metabolism
;
Granular Cell Tumor
;
pathology
;
secondary
;
surgery
;
Humans
;
Immunohistochemistry
;
Middle Aged
;
S100 Proteins
;
metabolism
;
Urinary Bladder
;
chemistry
;
pathology
;
surgery
;
Urinary Bladder Neoplasms
;
metabolism
;
pathology
;
surgery
;
Vaginal Neoplasms
;
metabolism
;
secondary
;
surgery
6.Expression and prognostic significance of survivin in the progression of bladder transitional cell cancer.
Yanbo, WANG ; Zhaohui, ZHU ; Fuqing, ZENG ; Liang, WANG ; Yu, WU ; Wei, XIA ; Shi'an XING
Journal of Huazhong University of Science and Technology (Medical Sciences) 2007;27(4):444-7
The expression of survivin, a member of inhibitor of apoptosis (IAP) family, was examined in bladder transitional cell cancer (BTCC) tissue and adjacent normal tissues to examine its clinical implication in the development of BTCC. Thirty specimens of bladder cancer were detected for the expression of survivin by using immunohistochemistry and real-time quantitative reverse transcription polymerase chain reaction (RT-QPCR) in BTCC tissue and adjacent normal tissues. Our results showed that the positive rate of survivin immunostaining specimen were 0 and 60% (18/30) in the adjacent normal tissues, bladder cancer, respectively. The-DeltaDeltaCT value of survivin in bladder cancer tissue was 10.2829 (9.0034-11.5624) times that in the adjacent normal tissues. The expressions of survivin were correlated with the pathological grades of tumor and clinical stages. It is concluded that there was only weak expression of survivin mRNA in the adjacent normal tissues, but the expression of survivin mRNA in bladder cancer tissue was much higher than that in the adjacent normal tissues and the expression of survivin was correlated with pathological grades and clinical stages of tumor.
*Carcinoma, Transitional Cell/metabolism
;
*Carcinoma, Transitional Cell/pathology
;
Microtubule-Associated Proteins/genetics
;
Microtubule-Associated Proteins/*metabolism
;
Prognosis
;
RNA, Messenger/genetics
;
RNA, Messenger/metabolism
;
Tumor Markers, Biological/genetics
;
Tumor Markers, Biological/*metabolism
;
Urinary Bladder Neoplasms/*metabolism
;
Urinary Bladder Neoplasms/*pathology
7.Hepatic and renal injury induced by Radix Aristolochiae or Guanxin Suhe Wan for a long-term in rats.
Hong-Xiang QIAO ; Yong-Ye LIU ; Li-Mao WU ; Lian-Da LI
China Journal of Chinese Materia Medica 2008;33(9):1044-1048
OBJECTIVETo evaluate the toxicity of Radix Aristolochiae supplied experimental evidence of rational use of drug in clinic.
METHODAfter treatment with small dose Radix Aristolochiae, Guanxin Suhe Wan (with Radix Aristolochiae) and Guanxin Suhe Wan (without Radix Aristolochiae) in different group for a long- term, respectively, the biochemical indicator of PT, ALT, AST, ALB, ALP, Crea and BUN were detected, and the kidney, liver, stomach and urinary bladder were examined by pathologic assaying.
RESULTIn Radix Aristolochiae group and Guanxin Suhe Wan (with Radix Aristolochiae) group, all of biochemical indicator were changed significantly, and hepatonecrosis, renal tubular necrosis, gastric carcinoma and bladder carcinoma were discovered.
CONCLUSIONRadix Aristolochiae and Guanxin Suhe Wan (with Radix Aristolochiae) can damage kidney and liver, and cause gastric carcinoma and bladder carcinoma by intensive toxicity.
Animals ; Aristolochia ; chemistry ; toxicity ; Drugs, Chinese Herbal ; toxicity ; Kidney ; drug effects ; metabolism ; pathology ; Liver ; drug effects ; metabolism ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Stomach Neoplasms ; chemically induced ; Urinary Bladder ; drug effects ; metabolism ; pathology ; Urinary Bladder Neoplasms ; chemically induced
8.Expression of OCT4 protein in bladder cancer and its clinicopathological implications.
Pengpeng ZHAO ; Chunxiao LIU ; Kai XU ; Shaobo ZHENG ; Hulin LI ; Yawen XU ; Abai XU ; Bingkun LI ; Peng HUANG
Journal of Southern Medical University 2012;32(5):643-646
OBJECTIVETo study the expression of OCT4 protein in bladder cancer and its correlation to the clinicopathologic features and prognosis of bladder cancer.
METHODSOCT4 mRNA and protein expression was detected in 5 bladder cancer cell lines (RT-4, Tcc-Sup, KK47, T24, and 5637) and 1 normal bladder cell lines by real-time PCR and Western blotting, respectively. Immunohistochemical analysis was used to detect the expression of OCT4 protein in 46 bladder cancer samples.
RESULTSAll the 5 bladder cancer cell lines expressed detectable levels of OCT4 mRNA and proteins, whereas the normal bladder cell line SV-HUC-1 was negative for OCT4 expression. The clinical bladder cancer tissues showed a high positivity rate of OCT4 expression (76.1%), which was not detected in normal bladder tissues. Specific OCT-4 signals were localized mainly in the nuclei of the cancer cells. The expression rate of OCT4 protein was significantly higher in bladder cancer tissue than in normal bladder epithelium (P<0.05), and showed a positive correlation to the grade of tumor differentiation and metastasis (P<0.05) but not to the patients' age, gender or TNM stage.
CONCLUSIONOCT4 protein expression is associated with tumor differentiation and metastasis in bladder cancer and may play an important role in the early diagnosis and prognostic evaluation of bladder cancer.
Cell Line, Tumor ; Humans ; Neoplasm Metastasis ; Neoplasm Staging ; Octamer Transcription Factor-3 ; metabolism ; Prognosis ; Urinary Bladder Neoplasms ; diagnosis ; metabolism ; pathology
9.Expression of Engrailed-2 and β-catenin in bladder urothelial carcinoma and their significance.
Yunfei LI ; Haitao LIU ; Xinghua DU ; Caiyong LAI ; Zexuan SU ; Shuangquan GAO
Journal of Southern Medical University 2013;33(9):1372-1376
OBJECTIVETo investigate the expressions of Engrailed-2 (EN2) and β-catenin in bladder urothelial carcinoma and explore their significance.
METHODSSixty bladder urothelial carcinoma samples of different grades and stages and 10 normal bladder mucosal tissues were examined for expressions of EN2 and β-catenin proteins and mRNA using immunochemistry, Western blotting and RT-PCR. RESULTS Compared to normal bladder mucosa, bladder urothelial carcinoma tissues showed significantly increased expressions of EN2 and β-catenin proteins (P<0.05), and the high-grade carcinoma tissues exhibited significantly stronger expressions than the low-grade ones (P<0.05); the expressions of the proteins increased also significantly with advanced pathological stages of bladder urothelial carcinoma (P<0.05). The expressions of EN2 and β-catenin mRNAs showed a consistent pattern of changes with their protein expressions.
CONCLUSIONThe expressions of EN2 and β-catenin are significantly increased in bladder urothelial carcinoma. EN2 may contribute to the development and progression of bladder urothelial carcinoma by activating Wnt/β-catenin signal pathway.
Adult ; Aged ; Aged, 80 and over ; Carcinoma ; metabolism ; pathology ; Female ; Homeodomain Proteins ; metabolism ; Humans ; Male ; Middle Aged ; Nerve Tissue Proteins ; metabolism ; Urinary Bladder Neoplasms ; metabolism ; pathology ; beta Catenin ; metabolism
10.SCF/c-Kit signaling promotes invasion of T24 cells via PI3K pathway.
Shujun GUO ; Xiangnan TAO ; Yimeng WANG ; Jie TANG ; Lin SHEN ; Chuanwang SONG
Journal of Southern Medical University 2014;34(4):507-510
OBJECTIVETo explore the role of SCF/c-Kit signaling in the invasion of bladder cancer T24 cells.
METHODSWestern blotting was used to detect the expression of c-Kit and PI3K pathway activation stimulated by stem cell factor (SCF) in T24 cells. The invasiveness of T24 cells before and after SCF stimulation and Wortmannin (aspecific PI3K inhibitor) treatment was evaluated using Transwell invasion assay (direct and indirect counting methods).
RESULTST24 cells expressed c-Kit protein and showed obvious Akt phosphorylation after stimulation with SCF (1 ng/ml) for 24 h. Compared to the control group, SCF stimulation (1 ng/ml) caused a greater number of T24 cells to migrate through the polycarbonate film (P<0.01), and this effect was blocked by the application of Wortmannin before the stimulation.
CONCLUSIONSCF/c-Kit signaling promotes the invasiveness of T24 cells, and this effect is mediated by the PI3K pathway.
Carcinoma, Transitional Cell ; metabolism ; pathology ; Cell Line, Tumor ; Humans ; Neoplasm Invasiveness ; Proto-Oncogene Proteins c-kit ; metabolism ; Signal Transduction ; Stem Cell Factor ; metabolism ; Urinary Bladder Neoplasms ; metabolism ; pathology