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1. Singh RP, Tyagi A, Sharma G, Mohan S, Agarwal R: Oral silibinin inhibits in vivo human bladder tumor xenograft growth involving down-regulation of survivin. Clin Cancer Res; 2008 Jan 1;14(1):300-8
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  • [Title] Oral silibinin inhibits in vivo human bladder tumor xenograft growth involving down-regulation of survivin.
  • PURPOSE: Chemoprevention is an upcoming approach to control bladder cancer, which is one of the commonly diagnosed malignancies showing recurrence rate of 70% or even higher.
  • Recently, we observed the in vitro efficacy of silibinin, a flavanolignan, in human bladder transitional cell papilloma RT4 cells.
  • EXPERIMENTAL DESIGN: RT4 tumor xenograft was implanted s.c. in athymic nude mice, and then animals were oral gavaged with silibinin at 100 and 200 mg/kg doses, 5 days/week for 12 weeks.
  • Tumor growth, body weight, and diet consumption were recorded, and tumors were analyzed for proliferation, apoptosis, and angiogenesis biomarkers and molecular alterations by immunohistochemistry, immunoblot analysis, and ELISA. p53 small interfering RNA was used in cell culture to examine the role of p53 in survivin expression.
  • Silibinin moderately (P < 0.001) decreased cell proliferation and microvessel density and strongly (P < 0.001) increased apoptosis in tumors.
  • CONCLUSION: These findings identified in vivo antitumor efficacy of silibinin against human bladder tumor cells involving down-regulation of survivin and an increase in p53 expression together with enhanced apoptosis.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carcinoma, Transitional Cell / drug therapy. Microtubule-Associated Proteins / drug effects. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Animals. Apoptosis / drug effects. Blotting, Western. Cell Proliferation / drug effects. Down-Regulation. Enzyme-Linked Immunosorbent Assay. Humans. Immunohistochemistry. Inhibitor of Apoptosis Proteins. Male. Mice. Mice, Nude. Neovascularization, Pathologic / drug therapy. Repressor Proteins. Silymarin / administration & dosage. Tumor Suppressor Protein p53 / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 18172282.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102514; United States / NCI NIH HHS / CA / R03 CA99079
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Birc5 protein, mouse; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Repressor Proteins; 0 / Silymarin; 0 / Tumor Suppressor Protein p53; 4RKY41TBTF / silybin
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2. Arnold LL, Eldan M, Nyska A, van Gemert M, Cohen SM: Dimethylarsinic acid: results of chronic toxicity/oncogenicity studies in F344 rats and in B6C3F1 mice. Toxicology; 2006 Jun 1;223(1-2):82-100
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  • The incidence of vacuolation of the epithelium in the urinary bladder was increased in both sexes, but was not associated with cytotoxicity, necrosis or hyperplasia.
  • Based on non-neoplastic lesions found in the urinary bladder, the NOEL for mice was assessed to be 40 ppm in males and 8 ppm in females.
  • Papillomas and carcinomas with degeneration of the urothelium, necrosis and urothelial cell hyperplasia, were found in the urinary bladders of both sexes.
  • In male rats, one papilloma was found in each of the 10 and 40 ppm groups; one urothelial cell carcinoma was found in the 2 ppm group and two in the 100 ppm group.
  • Four papillomas and six urothelial cell carcinomas were found in the female 100 ppm group.
  • Non-neoplastic treatment-related kidney lesions were confined to the 40 and 100 ppm levels and included necrosis, pyelonephritis, medullary nephrocalcinosis and tubular cystic dilation, hyperplasia of the epithelial lining of the papilla, and pelvic urothelial cell hyperplasia.
  • Based on the kidney and bladder lesions, the NOEL for non-neoplastic and neoplastic lesions was considered to be 10 ppm in males and females.
  • Based on these studies, DMA(V) is carcinogenic only in rats and only at relatively high doses, with the urinary bladder as the target organ.
  • [MeSH-major] Cacodylic Acid / toxicity. Carcinogens / toxicity. Herbicides / toxicity. Urinary Bladder Neoplasms / chemically induced. Urothelium / drug effects
  • [MeSH-minor] Administration, Oral. Animals. Dose-Response Relationship, Drug. Female. Male. Mice. Mice, Inbred Strains. No-Observed-Adverse-Effect Level. Rats. Rats, Inbred F344. Sex Factors. Species Specificity. Toxicity Tests, Chronic

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  • (PMID = 16677751.001).
  • [ISSN] 0300-483X
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Herbicides; AJ2HL7EU8K / Cacodylic Acid
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3. Swaminathan S, Torino JL, Burger MS: Human urinary bladder epithelial cells lacking wild-type p53 function are deficient in the repair of 4-aminobiphenyl-DNA adducts in genomic DNA. Mutat Res; 2002 Jan 29;499(1):103-17
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  • [Title] Human urinary bladder epithelial cells lacking wild-type p53 function are deficient in the repair of 4-aminobiphenyl-DNA adducts in genomic DNA.
  • The effect of the tumor suppressor gene TP53 on repair of genomic DNA damage was examined in human urinary bladder transitional cell carcinoma (TCC) cell lines.
  • Utilizing TCC10 containing wild-type p53 (wt-p53) as the parental line, an isogenic set of cell lines was derived by retroviral infection that expressed a transdominant mutant p53 (Arg --> His at codon 273, TDM273-TCC10), or the human papilloma virus 16-E6 oncoprotein (E6-TCC10).
  • The amount of adducts in urothelial DNA ranged between 0.1 and 20 per 10(6) nucleotides, N-OAc-AABP yielding the highest levels, followed by N-OH-ABP and N-OH-AABP.
  • At the dose used for DNA repair studies, N-OH-AABP or N-OAc-AABP did not induce apoptosis in TCC10.
  • These results suggest that p53 might modulate the repair of DNA adducts generated from the human bladder carcinogen ABP in its target human uroepithelial cells.
  • [MeSH-major] Aminobiphenyl Compounds / chemistry. DNA Adducts / physiology. Deoxyguanosine / analogs & derivatives. Repressor Proteins. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Urinary Bladder / physiology
  • [MeSH-minor] Apoptosis / drug effects. Carcinogens / pharmacology. Cells, Cultured. Codon. DNA Repair / drug effects. DNA Repair / physiology. Epithelial Cells / drug effects. Epithelial Cells / pathology. Epithelial Cells / physiology. Humans. Mutation. Oncogene Proteins, Viral / genetics. Oncogene Proteins, Viral / metabolism

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  • (PMID = 11804609.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-82035; United States / NIEHS NIH HHS / ES / ES-09090
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Aminobiphenyl Compounds; 0 / Carcinogens; 0 / Codon; 0 / DNA Adducts; 0 / E6 protein, Human papillomavirus type 16; 0 / Oncogene Proteins, Viral; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53; 16054949HJ / 4-biphenylamine; 26541-56-0 / N-acetoxy-4-acetylaminobiphenyl; 4463-22-3 / N-hydroxy-4-acetylaminobiphenyl; 6810-26-0 / N-hydroxy-4-aminobiphenyl; 86408-34-6 / N-(deoxyguanosin-8-yl)-4-aminobiphenyl; G9481N71RO / Deoxyguanosine
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4. Sachs MD, Ramamurthy M, Poel Hv, Wickham TJ, Lamfers M, Gerritsen W, Chowdhury W, Li Y, Schoenberg MP, Rodriguez R: Histone deacetylase inhibitors upregulate expression of the coxsackie adenovirus receptor (CAR) preferentially in bladder cancer cells. Cancer Gene Ther; 2004 Jul;11(7):477-86
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  • [Title] Histone deacetylase inhibitors upregulate expression of the coxsackie adenovirus receptor (CAR) preferentially in bladder cancer cells.
  • Studies on bladder cancer cell lines have shown that low adenoviral (Ad) infectivity is associated with low-level coxsackie adenovirus receptor (CAR) expression.
  • Recently, we and others demonstrated a tumor stage- and grade-dependent downregulation of CAR expression in a large series of clinical bladder cancer specimens.
  • Here, we demonstrate adenoviral gene transfer can be markedly enhanced in bladder cancer cells by upregulation of CAR through the use of certain differentiating agents, including the histone deacetylase inhibitors (HDACI) trichostatin A and sodium phenylbutyrate.
  • Normal urothelial cells and CAR-positive papilloma cells (RT4) failed to demonstrate upregulation under the same conditions.
  • Upregulation was cell cycle dependent, associated with increased adenoviral gene transfer and persisted for at least 7 days after a single treatment.
  • Such upregulation, however, appears to be tumor cell specific, as other CAR-negative cell lines failed to demonstrate enhanced adenoviral gene transfer with the same treatments.
  • These results provide a rational basis for combining HDACI therapy with gene therapy as a method of augmenting activity in bladder cancer, but this strategy may not be universally applicable to other cell types.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Receptors, Virus / metabolism. Up-Regulation / drug effects. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Adenoviridae / genetics. Adenoviridae / metabolism. Cell Line, Tumor. Coxsackie and Adenovirus Receptor-Like Membrane Protein. Histone Deacetylases / metabolism. Humans. Transduction, Genetic. Transgenes / genetics

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  • (PMID = 15118762.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CLMP protein, human; 0 / Coxsackie and Adenovirus Receptor-Like Membrane Protein; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Receptors, Virus; EC 3.5.1.98 / Histone Deacetylases
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5. Palmeira C, Oliveira PA, Arantes-Rodrigues R, Colaço A, De la Cruz PL, Lopes C, Santos L: DNA cytometry and kinetics of rat urothelial lesions during chemical carcinogenesis. Oncol Rep; 2009 Jan;21(1):247-52
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  • [Title] DNA cytometry and kinetics of rat urothelial lesions during chemical carcinogenesis.
  • The aims of this study were to evaluate the DNA content of chemically-induced rat urothelial lesions and their relationship to the proliferation index and histological patterns.
  • Sixty female Fisher 344 rats were divided randomly into six groups, four groups were exposed to N-butyl-N-(4-hydroxybutyl) nitrosamine for a period of 10 and 20 weeks, and two groups of ten rats were used as control animals.
  • As regards the other histological lesions, the frequency of the aneuploidy varied depending on the lesion type: 20% of aneuploidy were nodular hyperplasia, 32% of aneuploidy were dysplasias, 25% of aneuploidy were papilloma, 44% of aneuploidy were papillary neoplasm of low malignant potential, 22% of aneuploidy were low-grade papillary carcinoma, 100% of aneuploidy were high-grade papillary carcinoma and 100% of the aneuploidy were invasive carcinoma.
  • DNA content and prolife-ration index have critical roles to play during urothelial carcinogenesis.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. DNA, Neoplasm / analysis. Ki-67 Antigen / metabolism. Urinary Bladder Neoplasms / chemically induced. Urinary Bladder Neoplasms / genetics
  • [MeSH-minor] Animals. Butylhydroxybutylnitrosamine / toxicity. Cell Proliferation / drug effects. Female. Ploidies. Rats. Rats, Inbred F344. Urothelium / pathology

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  • (PMID = 19082469.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Ki-67 Antigen; 3817-11-6 / Butylhydroxybutylnitrosamine
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6. Shi Y, Cui L, Dai G, Chen J, Pan H, Song L, Cheng S, Wang X: Elevated prostaglandin E2 level via cPLA2--COX-2--mPGES-1 pathway involved in bladder carcinogenesis induced by terephthalic acid-calculi in Wistar rats. Prostaglandins Leukot Essent Fatty Acids; 2006 May;74(5):309-15
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  • [Title] Elevated prostaglandin E2 level via cPLA2--COX-2--mPGES-1 pathway involved in bladder carcinogenesis induced by terephthalic acid-calculi in Wistar rats.
  • To investigate the prostaglandin E2 (PGE2) biosynthetic mechanism in bladder carcinogenesis, we established Wistar rat model of bladder papilloma and transitional cell carcinoma (TCC) induced by 5% terephthalic acid (TPA) treatment.
  • Proliferating cell nuclear antigen (PCNA) was determined by immunohistochemistry.
  • Bladder papilloma (100%, 8/8) was examined in rats after 24-week treatment, and bladder TCC (80%, 16/20) was found after 48-week treatment.
  • The incidence of bladder papilloma and TCC in test group was significantly higher than that in control group (P<0.01).
  • The mRNA levels of cPLA2, COX-2 and mPGES-1 in the bladder papilloma and TCC were significantly higher than those in normal bladder (P<0.01), while the mRNA levels of COX-1 and mPGES-2 in TCC were unchanged compared with normal bladder.
  • Bladder TCC exhibited a substantial expression of COX-2 protein.
  • On the contrary, normal bladder tissue barely expresses COX-2 protein.
  • PCNA labeling index (LI) and the level of PGE2 in bladder papilloma are much higher than those in normal bladder (P<0.01), but lower than those in bladder TCC (P<0.05).
  • In conclusion, increasing PGE2 level via cPLA2--COX-2--mPGES-1 pathway may play an important role in rat bladder carcinogenesis.
  • PGE2 may be a biomarker for the development of bladder TCC. cPLA2 and mPGES-1 may be targets for development of novel chemoprevention strategies for bladder TCC.
  • [MeSH-major] Cyclooxygenase 2 / metabolism. Dinoprostone / metabolism. Intramolecular Oxidoreductases / metabolism. Phospholipases A / metabolism. Phthalic Acids / toxicity. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Animals. Base Sequence. Blotting, Western. Carcinoma, Transitional Cell / chemically induced. Carcinoma, Transitional Cell / genetics. Carcinoma, Transitional Cell / metabolism. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Group IV Phospholipases A2. Immunohistochemistry. Isoenzymes / genetics. Isoenzymes / metabolism. Male. Molecular Sequence Data. Papilloma / chemically induced. Papilloma / genetics. Papilloma / metabolism. Phospholipases A2. Random Allocation. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Urinary Bladder Calculi / chemically induced. Urinary Bladder Calculi / genetics. Urinary Bladder Calculi / metabolism

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  • (PMID = 16621493.001).
  • [ISSN] 0952-3278
  • [Journal-full-title] Prostaglandins, leukotrienes, and essential fatty acids
  • [ISO-abbreviation] Prostaglandins Leukot. Essent. Fatty Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Phthalic Acids; 6S7NKZ40BQ / terephthalic acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.1.1.- / Phospholipases A; EC 3.1.1.4 / Group IV Phospholipases A2; EC 3.1.1.4 / Phospholipases A2; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.99.3 / prostaglandin-E synthase; K7Q1JQR04M / Dinoprostone
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7. Hernández Castrillo A, Villanueva Peña A, Diego de Rodríguez E, Colina Martín A, Corral Mones JM: [Hematuria during pregnancy caused by bladder tumour. Report of 2 cases]. Actas Urol Esp; 2005 Nov-Dec;29(10):981-4
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  • [Title] [Hematuria during pregnancy caused by bladder tumour. Report of 2 cases].
  • [Transliterated title] Hematuria durante la gestación debida a tumor vesical. Presentación de 2 casos.
  • Tumours of the urinary bladder are rare in pregnancy.
  • Tocolytics agents were employed.
  • The pathology diagnoses were inverted papilloma in the first case and papillary urothelial neoplasm of low malignant potential in the other one.
  • [MeSH-major] Hematuria / etiology. Papilloma, Inverted / complications. Pregnancy Complications, Neoplastic. Urinary Bladder Neoplasms / complications

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  • (PMID = 16447598.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas espanolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 12
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8. Tyagi AK, Agarwal C, Singh RP, Shroyer KR, Glode LM, Agarwal R: Silibinin down-regulates survivin protein and mRNA expression and causes caspases activation and apoptosis in human bladder transitional-cell papilloma RT4 cells. Biochem Biophys Res Commun; 2003 Dec 26;312(4):1178-84
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  • [Title] Silibinin down-regulates survivin protein and mRNA expression and causes caspases activation and apoptosis in human bladder transitional-cell papilloma RT4 cells.
  • Bladder cancer is the fourth and eighth most common cancer in men and women in the United States, respectively.
  • Survivin, a member of inhibitor of apoptosis protein (IAP) gene family, is deregulated in a wide range of malignancies, including carcinoma of the bladder urothelium.
  • Recent advances have identified survivin as a novel intervention target to induce apoptosis in cancer cells by phytochemicals or synthetic agents.
  • Human bladder transitional-cell papilloma RT4 cells were treated with silibinin and analyzed for survivin protein and mRNA levels by Western blotting and real-time RT-PCR, respectively.
  • Together, these findings suggest that more studies are needed to investigate in vivo effect of silibinin on survivin expression and associated biological effects in bladder cancer that could provide useful information for silibinin efficacy in the prevention/intervention of human bladder cancer.
  • [MeSH-major] Caspases / metabolism. Microtubule-Associated Proteins / metabolism. RNA, Messenger / metabolism. Silymarin / pharmacology. Urinary Bladder Neoplasms / metabolism. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Apoptosis / drug effects. Carcinoma, Transitional Cell / metabolism. Carcinoma, Transitional Cell / pathology. Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Enzyme Activation / drug effects. Humans. Inhibitor of Apoptosis Proteins. Neoplasm Proteins. Papilloma / metabolism. Papilloma / pathology

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  • (PMID = 14651997.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R03 CA99079
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Silymarin; 4RKY41TBTF / silybin; EC 3.4.22.- / Caspases
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9. Hurst RE, Kyker KD, Bonner RB, Bowditch RD, Hemstreet GP 3rd: Matrix-dependent plasticity of the malignant phenotype of bladder cancer cells. Anticancer Res; 2003 Jul-Aug;23(4):3119-28
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  • [Title] Matrix-dependent plasticity of the malignant phenotype of bladder cancer cells.
  • The purpose of this study was to investigate the effect of cancer- and normal basement membrane-derived extracellular matrix to modulate the phenotype of bladder cancer cell lines.
  • Five lines, varying in malignancy from papilloma to highly undifferentiated and invasive and immortalized human urothelial cells, were grown on two extracellular matrix preparations, Matrigel and SISgel.
  • Matrigel represents matrix remodeled by malignancy while SISgel, obtained from small intestine submucosa (SIS), represents the normal matrix supporting differentiated cell growth.
  • In contrast, when the same cells were grown on SISgel, they grew as a layer of cells one to 5 cells thick, failed to invade, and expressed cell-surface E-cadherin.
  • Unlike breast cancer cells, neutralization of beta 1, beta 4 and alpha 6 integrins altered cell-cell and cell-matrix adhesiveness but did not alter the phenotype.
  • In summary, the phenotype of bladder cancer cells growing in tissue-like 3-dimensional culture is highly plastic, and malignant properties such as invasion and papillary growth can be suppressed by the matrix.

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  • [Cites] Semin Cancer Biol. 1993 Aug;4(4):259-65 [8400148.001]
  • (PMID = 12926044.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA075322-03; United States / NCI NIH HHS / CA / R01 CA075322; United States / NCI NIH HHS / CA / CA 75322; United States / NCI NIH HHS / CA / R01 CA075322-03
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cadherins; 0 / Drug Combinations; 0 / Integrins; 0 / Laminin; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen
  • [Other-IDs] NLM/ NIHMS54141; NLM/ PMC2561328
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